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News INFECTION | +60 articles

mr peabody

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Aug 31, 2016
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Anti-HIV-1 activity of the iboga alkaloid congener 18-MC*

Silva, Cirne-Santos, Frugulhetti, Galvo-Castro, Saraiva, Kuehnem, Bou-Habib

Infection by the HIV-1 virus is a global health problem affecting more than 42 million people worldwide. HIV-1 persistently replicates in the lymphoid tissues, leading to a progressive deterioration of the immune system. An effective vaccine against HIV-1 infection has not been developed yet.

Two decades after the discovery of the first cases of AIDS, the clinical use of the abundant anti-retroviral repertoire has decreased the morbidity and mortality of HIV-1 infection. However, this treatment does not completely eradicate HIV-1 from the infected tissues, and its long-term use is restricted by metabolic disorders and toxicities, emergence of drug-resistant viruses and complex administration. Thus, the search for other anti-retroviral compounds is critical, and numerous new anti-HIV-1 agents that target different phases of viral replication cycle are under development or in clinical trials.

The Iboga-type indole alkaloid coronaridine is found in many species of the plant kingdom and has been studied for its potential anti-addictive properties. Because of the side effects such as tremor, cerebellar neurotoxicity and bradycardia associated with COR, chemical structure modifications were made to reduce its side effects, which was attained with a meth-oxylation at carbon-18, resulting in the Iboga analogue 18-methoxycoronaridine (18-MC).

Since many alkaloids have been described as capable of inhibiting HIV-1 infection in vitro, we investigated whether 18-MC is also endowed with anti-retroviral properties. We found that 18-MC inhibits HIV-1 replication in human peripheral blood mononuclear cells and in monocyte-derived macrophages, and that this activity is at least partially mediated by reducing the activity of the HIV-1 enzyme reverse transcriptase.


Results and discussion

In this paper, we report that the indole alkaloid congener 18-MC inhibits HIV-1 infection. The infection assays were performed with primary cells to avoid the genotypic and phenotypic changes that might occur during viral passages in tumor cell lines. We also used primary isolates, which are closer to the viral population present in HIV-1-infected patients.

In preliminary experiments, we found that naturally occurring COR decreased the infection in a dose dependent manner. Since 18-MC is an improved molecule of the natural compound coronaridine, presenting little to none of the adverse effects associated with the original molecule, we continued our anti-retroviral studies using the new alkaloid congener 18-MC.

Our present results warrant further investigation on the mechanisms by which 18-MC decreases HIV-1 replication in vitro. Considering that 18-MC demonstrates a vigorous leishmanicidal activity in vitro, its potential therapeutic properties may be uniquely useful for the treatment of HIV-1-infected individuals as well as patients co-infected with Leishmania and HIV-1.

*From the article here :
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mr peabody

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Aug 31, 2016
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Study urges life-saving drug treatment to combat Ukraine's HIV epidemic

by Brita Belli, Yale University | Medical Xpress | Jan 3 2019

Ukraine has the second-largest HIV epidemic in Eastern Europe and Central Asia, accounting for 9% of new infections in the region in 2016. In 2018, 240,000 people were living with HIV. Annual new HIV infections in Ukraine — home to Eastern Europe and Central Asia's second largest HIV epidemic — have risen from 9,500 in 2010 to 12,000 in 2018.

Researchers at Yale have found that scaling up the use of methadone and buprenorphine - medications for treating opioid use disorder known as opioid agonist therapies (OATs) - could greatly reduce HIV transmission rates and prevent deaths in Ukraine, where the disease is epidemic among people who inject drugs, according to a new study published in The Lancet.

The researchers found that treating at least 20% of people with opioid use disorder who inject drugs — the minimum recommended by the World Health Organization — could, over 10 years, prevent more than 10,000 new HIV infections and nearly 18,000 new deaths.

Currently, only 2.7 percent of people who inject drugs in Ukraine receive OATs, despite their proven effectiveness.

"Opioid agonist treatments are one of the most effective treatments for opioid use disorder and preventing HIV infections," said co-author Lynn Madden, a Yale postdoctoral associate in internal medicine and head of a foundation focused on substance use disorders and mental illness. "In addition to treating opioid dependence, it substantially reduces drug use and injection frequency, lowers HIV transmission rates, and prevents death, including death due to overdose," she said.

Senior author Alexei Zelenev, Yale associate research scientist in medicine, said "the healthcare system in Ukraine needs modernization, and HIV testing needs to be expanded, as only 56 percent of the population with HIV are aware of their infected status."

"High prevalence in people who inject drugs, criminalization of drug users, large injection networks, and suboptimal access to evidence-based treatment for opioid use disorder contribute to ongoing HIV transmission,"
he said.

Researchers obtained HIV epidemic profiles and regional data—including OAT treatment—for 23 regions in the Ukraine. Their mathematical model evaluated the efficiency of current OAT treatment programs and assessed the effect of expanding those programs to treat 20 percent of the drug-injecting population.

Taking into account regional differences, the study showed that scaling up OAT in regions with large populations of people who inject drugs—like Dnipropetrovsk, Odessa, and Kyiv—would lead to the greatest reductions in infections and death, but that smaller regions not covered by the U.S. President's Emergency Plan for AIDS Relief (PEPFAR) remain highly vulnerable to HIV outbreaks and need to be considered when allocating resources. PEPFAR is the U.S. government's response to the global HIV/AIDS epidemic.

"Scaling up OAT programs requires initiative on several fronts," said Zelenev.

"In addition to expanding capacity at existing treatment sites," he said, "expansion of addiction treatment into primary care clinics, as well as through take-home pharmacy prescriptions, can offer pathways for increased access to effective treatment."

"The expansion of OAT has not been adequate,"
he said.

Amid the ongoing military conflict with Russia, Ukraine faces a difficult financial situation that exacerbates the public health crisis.

Frederick Altice, professor of medicine, epidemiology and public health at Yale, and a co-author, said "the study reveals the importance of scaling up evidence-based treatments to prevent new HIV infections and death."

"Ukraine is a major country in the Eastern European and Central Asian region, the only region globally where new HIV infections and HIV-related deaths remain increasing,"
he said.

"Findings from this study have important implications for other countries throughout the region where the HIV epidemic is similar. In nearby Russia, new HIV infections and deaths are increasing faster than in any other country in the region due to their complete bans on OATs—one of the greatest HIV prevention tools we have available to us."

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mr peabody

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Aug 31, 2016
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Emory University School of Medicine

In animal models, a 'shocking' step toward a potential HIV cure

by Emory University | Medical Xpress | 22 Jan 2020

It's a leading research strategy for eliminating HIV from the body: "shock and kill." The idea is to activate the dormant virus from within the immune cells where it hides, then eliminate it. One obstacle has been finding a safe way to wake up the virus.

In two complementary Nature papers, researchers now report that they have come closer to that goal. The papers are from researchers at the Yerkes National Primate Research Center of Emory University and the University of North Carolina at Chapel Hill, funded by the National Institutes of Health.

The papers rely on studies involving two animal models of HIV infection. Each study took a different approach. But both yielded promising results, disrupting viral latency at levels not seen before.

That means that the virus came out of its hiding places, even in the presence of antiretroviral drugs that had stopped it from replicating for months.

The findings do not represent a cure and follow-up studies in animals, as well as clinical studies in humans, are needed and planned. But the results represent an advance because they could potentially be combined with other approaches directed against the virus, the scientists say.

"If our goal is to cure HIV/AIDS, then we have to disrupt viral latency," says Guido Silvestri, MD, co-senior author of one of the Nature papers. "What we're doing now is a new combination approach that provides unprecedented levels of virus reactivation."

Silvestri is interim chair of pathology and laboratory medicine at Emory University School of Medicine, chief of microbiology and immunology at Yerkes National Primate Research Center, and a Georgia Eminent Research Scholar.

Past results of latency reversal experiments were not as sustained and extensive, says co-senior author J. Victor Garcia, Ph.D., director of the International Center for the Advancement of Translational Science and professor at the University of North Carolina School of Medicine.

"Previously, no one had successfully demonstrated systemic HIV induction in humans or an animal model with human cells, and then replicated this success in a completely different species infected with a different virus," Garcia says.

Ann Chahroudi, MD, Ph.D., co-senior author on both papers, says the studies described in the two papers take different approaches. She is associate professor of pediatrics and director of the Center for Childhood Infections & Vaccines at Emory and Children's Healthcare of Atlanta.

Both approaches were tested at Yerkes in monkeys infected with SIV, a close relative of HIV, and treated with antiretroviral drugs. At UNC, tests were also conducted in mice transplanted with human immune cells.

One paper describes a drug called AZD5582, which activates an intracellular pathway that leads to HIV and SIV reactivation. AZD5582 appears to be safe and relatively non-toxic in non-human primates. In 12 monkeys treated with the drug, just one experienced a temporary fever and loss of appetite. With the aim of beginning clinical trials, researchers at UNC and Qura Therapeutics—a partnership between UNC and ViiV Healthcare—are investigating compounds related to AZD5582.

"AZD5582 was remarkable in its ability to reactivate latent SIV from resting CD4+ T cells, and to induce continued virus production in the blood when monkeys were still receiving daily antiretroviral therapy," says Chahroudi.

In the study described in the second paper, researchers stimulated the cells that are the main viral hosts (CD4+ T cells) while also depleting another kind of immune cell (CD8+ T cells), which normally keeps the virus in check.

The combination of immune interventions was especially potent; both the stimulation and depletion components were necessary to see SIV re-emerge,” Silvestri says. His lab had previously observed a similar but smaller effect with CD8 depletion alone. “That means that CD8 T cells must have a role in keeping the virus inactive, which needs to be understood better,” he says.

"The old paradigm is that you need CD8 cells to clear other infected cells," Silvestri says. "We're showing that CD8 cells are also involved in repressing latency reversal."

The main obstacle to a cure for HIV infection is the reservoir: immune cells that harbor the inactive virus when someone is being treated with antiretroviral drugs. Neither intervention—drug or immune stimulation/depletions—reduced the size of the reservoir, because once the animals were taken off antiretroviral drugs, viral levels did rebound. The scientists think the initial viral reactivation needs to be combined with other modes of treatment, such as antibodies directed against the virus itself.

"The exciting thing about these papers being published together are the concordance of the results in two animal models with both approaches, and the opening up of new avenues for research towards the goal of an HIV cure," said Chahroudi.

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mr peabody

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Aug 31, 2016
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Infections account for 13% of all cancer cases*

by Roxanne Nelson, RN, BSN | Medscape | Jan 21 2020

An estimated 13% of all cancer cases in 2018 may be attributable to infections, concludes a new global survey. This equates to about 2.2 million cancer cases diagnosed worldwide.

The primary causes were Helicobacter pylori, human papillomavirus (HPV), hepatitis B virus (HBV), and hepatitis C virus (HCV).

Of note, a third of global cancer cases attributable to infection are in China, which accounted for 42% of cancers caused by H pylori and for 69% of those caused by HBV.

"The present work estimates for the first time incidence rates of infection-attributable cancer in 2018 at an individual country level," write the authors, led by Catherine de Martel, MD, of the Infections and Cancer Epidemiology Group at the International Agency for Research on Cancer, France.

"Our study can help to raise awareness and inform recommendations for action against cancer, which tends to be viewed as a non-communicable disease," they add.

A causal association between certain infections and human malignancies is already well established, the authors comment. Previous research by de Martel and her group found that H pylori, HBV, HCV, and HPV were responsible for 2 million of 12.7 million cancer cases. Most of these were gastric, hepatic, and cervix uteri cancers.

For the current analysis, the authors used the GLOBOCAN 2018 database of cancer incidence and mortality rates. They estimated the attributable percentages and global incidence for specific cancers that have already been associated with infectious pathogens. The absolute numbers and ASIR were calculated at the country level and were stratified by sex, age group, and country.

Their results showed that H pylori was responsible for 810,000 new cancer cases in 2018, primarily underlying noncardia gastric adenocarcinoma. This was followed by HPV, responsible for 690,000 new cases, primarily causing cervix uteri carcinoma.

HBV contributed to 360,000 new cases, and HCV was responsible for 160,000 new cases, both primarily causing hepatocellular carcinoma.

Other infectious agents - Epstein-Barr virus, human T-cell lymphotropic virus, human herpesvirus, and parasitic infections - contributed to the remaining 210,000 new cases.

Variation by sex and income

Overall, men and women were equally affected by cancers caused by infections, but the types of pathogens and cancers varied by sex.

There was also considerable variation by geographic region. Eastern Asia had the highest rates of infection, followed closely by sub-Saharan Africa. Conversely, the lowest number of cases was in northern Europe and western Asia.

China accounted for 35% of the new infection-attributable cases in 2018. Of those, 340,000 were linked to H pylori, and 250,000 to HBV. South Korea also had a very high incidence of cancer caused by H pylori infection, as did Japan. There was also a high incidence of cancer cases related to HBV in South Korea.

Cervix uteri carcinoma accounts for approximately 80% of cancers that could be attributed to HPV. Women were the most affected by HPV, accounting for 90% of the 690,000 attributed cases globally. These proportions were highest in the lowest-income countries.

In contrast, the proportions of the other types of HPV-related anogenital cancers, along with head and neck cancers, were higher in high-income countries, with a greater proportion seen in men.

"It should be emphasized that the data we present here are a snapshot of the burden of cancer attributable to infections worldwide in 2018, and comparisons with previous results are not possible because of changes in data sources, notably for cancer incidence estimates, as well as other methodological modifications," the authors wrote.

*From the article here :
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mr peabody

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Aug 31, 2016
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Evelyn Ayo, a vaccinator at the Reproductive Health Uganda clinic in Gulu, administers an HPV vaccine.

Women can be protected from cervical cancer – so why aren't we doing it?

by Nelly Mugo | The Guardian | 24 Feb 2020

Amid a global shortage of HPV vaccine, more must be done to steer supplies towards those most at risk: girls in poor countries.

For too many women, cervical cancer is a death sentence. But it doesn’t have to be. A life-saving preventative vaccine can dramatically cut cases and put the world on track to eliminate this deadly disease.

The UK first began offering a vaccine against HPV – the primary cause of cervical cancer – in 2008. According to a 2018 study by Public Health England, infections of certain cancer-causing types of HPV have since fallen by 86 percent among 16- to 21-year-old women. A study conducted in Scotland last year found that the vaccine reduced pre-cancerous cervical lesions by up to 90 percent.

But such impact has been largely confined to wealthy countries, where the vaccine is widely available. Today, 90 percent of all cervical cancer deaths around the world occur in developing countries, many of which have yet to introduce inoculation. Just 21 low-income countries have the vaccine.

While demand for the vaccine is high, efforts to roll it out in developing countries have been threatened by a global supply shortage. With limited doses available, millions of women and girls are left without protection against a largely preventable disease, simply because of where they live.

Last summer, the UK announced the expansion of their HPV vaccination programme to include boys. Other countries, including the US, Germany and Australia, have implemented similar policies. The US also recommends the vaccine for certain women up to 45.

Encouraging more people to get vaccinated is unquestionably a positive thing. But, in the context of a global shortage, expanding the population that receives inoculation could mean girls and women in poorer countries are left behind.

It should be noted that vaccinating girls against HPV protects boys too, through herd immunity: when enough girls in a community are protected, the virus can’t spread from person to person and everyone is safeguarded.

The effects of the vaccine shortage are compounded by lack of access to timely screening and treatment options in low- and middle-income countries. Reliable preventive care services to spot cancer early, like pap smears and visual inspection with acetic acid, are often unavailable. This can mean that cancer diagnoses are often made too late, if at all.

Even when cervical cancer is diagnosed, many areas do not have healthcare facilities with cancer specialists, or the equipment for treatments like radiation and chemotherapy. These services are also expensive, putting them out of reach for many. Without access to the HPV vaccine, girls and women in the regions of highest need are left without any tools to protect themselves.

In November, the World Health Organization’s strategic advisory group of immunisation experts recommended that all countries temporarily postpone the implementation of HPV vaccination strategies for boys and older age groups. The expert group also suggested that countries consider adopting a vaccination schedule where the second dose is administered three to five years after the first, as appropriate to the national context. Deferring the second dose for younger girls does not affect the vaccine’s effectiveness and will make more doses available now, when they are urgently needed.

Implementing these recommendations and steering vaccine supply toward countries at high risk could save hundreds of thousands of lives.

The HPV vaccine shortage has an end in sight – new manufacturers are entering the market and more doses will be available eventually, though probably not until 2024 at the earliest. But millions of girls should not have to wait years to receive the life-saving benefits of HPV vaccination.

To create a future where girls and women don’t have to bear the burden of cervical cancer, leaders need to take steps to ensure that the limited doses we have go to the regions where they can save the most lives. Countries must also invest in life-saving services like cervical cancer screening and treatment programmes that can protect women who haven’t received the vaccine.

If we take these actions, we’ll be sending a clear message that the lives of girls and women in poorer countries really are equal to those in rich ones.

From the article here: https://www.theguardian.com/global-...from-cervical-cancer-so-why-arent-we-doing-it

Drop in HPV seen after just one shot of HPV vaccine

by Will Boggs MD | Medscape | 30 Dec 2019

Even a single dose of human papillomavirus (HPV) vaccine is associated with a reduced prevalence of HPV infection among U.S. women, according to findings from the National Health and Nutritional Examination Survey.

"Getting adolescents to initiate their first dose should be a priority, with the goal that they will complete the recommended series," Dr. Ashish A. Deshmukh from UTHealth School of Public Health, in Houston, Texas, told Reuters Health by email. "Our findings are promising; however, they are not suggestive that only one dose is adequate until we get further definite answers from currently ongoing trials."

While about two-thirds of adolescents in the U.S. have received at least one dose of the HPV vaccine, only about half have completed the three-dose series.

Dr. Deshmukh's team used NHANES 2009 to 2016 data to investigate HPV-infection prevalence among U.S. women by the number of vaccine doses received.

Among the 1,620 women included in the study, 1,004 were unvaccinated, while 106 had received one dose, 126 had received two and 384 had received three.

The prevalence of infection with HPV 18 was significantly lower among women who received the vaccine than among unvaccinated women, the researchers reported.

The predicted probability of infection with these HPV types remained significantly higher in unvaccinated women (8 percent) than in women who received the vaccine.

The predicted probability of infection with these HPV types was significantly greater among black women (11 percent) than among white women (7 percent) and among women with more than five lifetime male sexual partners (12 percent) than among women with fewer lifetime male partners (3 percent).

"If a single dose of HPV vaccine could provide protection for a long-enough duration similar to currently recommended 2 or 3 doses, then receiving the vaccine will be a more achievable metric of population coverage," Dr. Deshmukh said. "The implication of our findings will be greater in low-resource countries where cervical cancer still remains one of the leading causes of cancer mortality."

"Yet, the HPV-vaccination coverage is extremely poor, as getting adolescents to receive their first dose itself is a big hurdle, and in many countries, as generally, there is not adequate infrastructure to provide the recommended vaccine series,"
he said.

Dr. Deshmukh added, "Continued and effective physician recommendation has a great potential to overcome the existing hurdles, mainly parental indecision about both vaccine initiation and completion."

Dr. Margaret Stanley of the University of Cambridge, in the UK, who has researched various aspects of HPV infection, told Reuters Health by email, "These observations should be placed in context with other studies, but my view is that the available evidence is that immunization with even 1 dose of HPV vaccine at high coverage over 80 percent of sexually naïve adolescents is protective against vaccine-type persistent HPV infection for at least 10 years. However, for policy changes and implementation of a 1-dose schedule, evidence from randomized controlled trials will be necessary."

"The name of the game is to get HPV vaccine into as many 9- to 15-year-old boys and girls as possible, even if it's only one dose,"
she said.

From the article here: https://www.medscape.com/viewarticl...CPEDIT_TEMP2&uac=341393BJ&impID=2278909&faf=1

Yale University

Scientists find a new way to block cancer-causing HPV virus

by Anne Doerr | Yale University | 24 Mar 2020

The human papillomavirus (HPV) is the main cause of several cancers, including cervical cancer, which kills almost 300,000 women around the world each year. Although vaccines offer a proven first line of defense against HPV infection, researchers continue to look for additional options to guard against the virus.

In a new study published today in the Proceedings of the National Academy of Sciences, Yale Cancer Center (YCC) researchers have demonstrated in principle a new biological approach that can stop HPV infection. This method may eventually aid in treating not only HPV, but other viruses, as well as non-viral diseases that are currently thought to be "undruggable," said the researchers.

"We show that very short peptides [fragments of a protein] can block the HPV virus from infecting cells," said senior author Daniel DiMaio, M.D., Ph.D., deputy director of YCC, the Waldemar Von Zedtwitz Professor of Genetics, and professor of molecular biophysics and biochemistry and of therapeutic radiology. "This research confirms our model for how HPV infects cells. It also shows that the intracellular trafficking of a virus could be the target for a new anti-viral approach."

HPV is carried into the cell by a membrane-bound sac called an endosome. An HPV protein known as L2 contains a segment known as a "cell-penetrating peptide" that sticks through the membrane of the endosome into the cell's interior. There, a sequence of L2 next to the cell-penetrating peptide binds to a cell protein called retromer. Retromer then delivers the virus into a cellular transport mechanism known as the retrograde pathway that drops off the virus in the nucleus, where it can begin making copies of itself.

Previous research by DiMaio's lab found that the core machinery of the cell-penetrating peptide is surprisingly short. Peptides are composed of amino acids, and a sequence of only six amino acids was needed for the peptide to penetrate cell membranes, while a sequence of only three amino acids was required to bind to the retromer protein.

"We realized that we could synthesize a short peptide that should be enough to get through the cell membrane, bind the retromer and block infection, so we decided to test that," DiMaio said. "The first peptide we tried worked."

When the investigators added the synthesized cell-penetrating peptides into a culture medium of human cells, they saw that the peptides did enter the cytoplasm and bind to the retromer. When the scientists then infected the cells with HPV, the virus could no longer bind to the retromer and leave the endosome because the retromer was tied up by the peptide, and infection was blocked.

The Yale researchers demonstrated that this peptide inhibition persists even after the peptides are removed. "We don't actually know how long the peptide is active, but the effect may be irreversible," DiMaio added. "It also looks like the virus disappears from the cell. The cell has some way to sense that the infection is not proceeding normally, so it gets rid of the virus."

"In follow-up experiments conducted with colleagues at the University of Wisconsin, the scientists showed that this cell-penetrating peptide also inhibited HPV infection in mice. This basic research may point toward new types of anti-HPV treatments, which are needed,"
DiMaio said.

Although vaccines will always be the best foundation to prevent HPV infections, DiMaio said, "the vast majority of people worldwide are not vaccinated, especially in the developing world where most cases of cervical cancer occur. Additionally, current vaccines don't guard against all strains of HPV," he said.

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mr peabody

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Aug 31, 2016
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Paraíba strain of Zika virus responsible for microcephaly in Brazilian newborns*

by Tamara Bhandari | Washington University School of Medicine | 19 Feb 2020

Due to the Zika virus, more than 1,600 babies were born in Brazil with microcephaly, or abnormally small heads, from September 2015 through April 2016. The epidemic took health professionals by surprise because the virus had been known since 1947 and was not linked to birth defects.

As scientists scrambled to figure out what was going on, one fact stood out: 83% of microcephaly cases came from northeastern Brazil, even though Zika infections were recorded nationwide.

Researchers from Washington University School of Medicine in St. Louis have since learned that the strain of virus circulating in the northeastern Brazilian state of Paraíba in 2015 was particularly damaging to the developing brain. Kevin Noguchi, Ph.D., an assistant professor of psychiatry and the study's senior author, spoke about the findings, which are available online in The Journal of Neuroscience.

How did you determine that the Paraíba strain was unusually harmful?

We studied two strains of Zika virus—one from an outbreak in French Polynesia in 2013 that was associated with a low risk of microcephaly, and another from Paraíba in 2015. We infected one group of newborn mouse pups with one strain and a second group with the other strain. The brains of newborn mice are at a similar stage of development to a second-trimester human fetus, when Zika virus causes considerable damage. Each strain led to about the same number of deaths, but the brain damage in the surviving mice was dramatically different. The mice infected with the French Polynesian strain seemed to successfully fight off the infection within about two weeks, and we did not see any additional signs of damage after that. In contrast, we saw neurodegeneration in the mice infected with the Paraíba strain up to 30 days later, and they had smaller brains.

Is that why babies born in Paraíba were at high risk of microcephaly?

Maybe. It tells us that the strain from Paraíba was more capable of causing severe brain damage than the one from French Polynesia. It doesn't rule out other possibilities.

For instance, other environmental factors in Paraíba—such as dengue or other viruses that were circulating at the same time—could have affected Zika's ability to overwhelm the body's defenses and cause severe brain damage.

What is it about the Paraíba strain that made it so dangerous?

That's our next step. We have started a collaboration with Dr. Luis Martínez-Sobrido, Ph.D., and his colleagues at the University of Rochester. They found a mutation in the Paraíba strain that may affect its virulence, or the ability to cause disease.

If the Paraíba strain is so harmful, why didn't it cause an epidemic of microcephaly the next year?

Everyone was bracing for another massive increase in microcephaly the next year, but it didn't happen. We also saw more limited increases of microcephaly in other parts of Latin America and the Caribbean, even as the virus spread into those areas. Nobody really knows why. It could be that pregnant women started wearing more insect repellant and putting screens on their windows. In Brazil, it could be that so many people got infected the first year that many pregnant women were immune the next year. It's also possible that the virus was just too virulent for its own good. If you kill your host, you also kill the opportunity to get passed on to the next person. So it could be that Zika reached peak virulence in 2015 and then evolved to be less virulent over time. That's another thing we'd like to find out.

*From the article here :
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mr peabody

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HCV screening recommended for all US adults aged 18-79

by Marcia Frellick | Medscape | 2 Mar 2020

The US Preventive Services Task Force has expanded its recommendation for one-time hepatitis C virus (HCV) screening to include all asymptomatic US adults ages 18-79 years, including pregnant women, who do not have known liver disease.

It is a B-level recommendation, indicating that screening for HCV will have a substantial net benefit. The B level is also important because the Affordable Care Act requires that private insurers and Medicaid cover preventive services recommended at an A or B level by the USPSTF with no deductibles or copayments.

"HCV is associated with more deaths than the top 60 other reportable infectious diseases combined, including HIV," the group, led by Douglas K. Owens, MD, Stanford University, California, stated.

Among reasons for the change, authors cite the almost 3.8-fold increase in cases in the last decade, largely because of more injection drug use and better monitoring.

Owens and colleagues noted that research indicates the most important risk factor for HCV is injection drug use.

"In the United States, recent increases in HCV incidence have predominantly been among young persons who inject drugs (PWID). Approximately one third of PWID aged 18 to 30 years are infected with HCV, and 70% to 90% of older PWID are infected," they said.

Patients need to know the test is voluntary

The authors point out it is important for clinicians to let patients know that screening is voluntary and to communicate what HCV is, how it is acquired, what a positive or negative test means, and potential harms and benefits of treatment.

The USPSTF also suggested that clinicians consider screening patients considered high risk (past or current injection drug users even if they fall outside the recommended age range).

The recommendations come in light of several developments over the past decade.

One is the convincing evidence that the newer direct-acting antiviral (DAA) regimens result in cure rates above 95% for adults ages 18-79 years, and the "adequate evidence of sustained virologic response in adolescents."

In addition, the duration of treatment has declined. Whereas older, interferon-based regimens required as long as 48 weeks of treatment, DAA-based regimens require just 8 to 12 weeks of therapy.

Additionally, screening and treatment rates have varied widely. Screening rates have been high in healthcare systems serving insured people, some academic medical centers, and Veterans Health Administration centers.

However, the authors said, "national HCV screening rates in community health centers and from the National Health Interview Study were 8.3% and 17.3%, respectively; one study of four safety-net primary care practices serving low-income and uninsured or underserved populations found that only 0.8% of persons born in 1945 through 1965 were screened over a 1-year period."

The USPSTF did not find evidence of harm in screening in any new studies.

Test can give results quickly

Kalyan R. Bhamidimarri, MD, MPH, chief of the division of hepatology at the University of Miami in Florida, told Medscape Medical News that although much of the testing will fall on primary care physicians, rapid testing with a swab or finger stick can mean results are quickly available.

At their facility, they give patients a fingerstick test in the waiting room so results are ready to discuss during appointments, he said.

"Even if rapid testing is not available and the blood sample needs to be sent out," he said, "testing is able to capture more than 98% of HCV infection, and false-positives are very, very low."

He pointed out that primary care offices are already on alert to watch for signs of fatty liver disease, which has become an epidemic.

Bhamidimarri said the USPSTF move was important because while hepatitis C infections have decreased in the baby boomer group covered by the previous recommendations, they have increased in other groups as opioid use has increased, particularly in young people.

"The biggest challenge with hepatitis C is underscreening and undiagnosis," said Bhamidimarri, an associate professor of clinical medicine at the university.

He said acute infections have risen sharply in recent years and warns that without screening and treatment they will become chronic.

"So we are going to see another peak where individuals will have cirrhosis and will need a liver transplant sometime in the future," he said. "If this goes untreated we will see a major public health burden later on. In all these years they are untreated, they are going to horizontally spread the infection to others."

The broad screening that the USPSTF recommends is also important because it gets around possible stigma. Just asking people if they have risk factors won't work because people may come to appointments with a significant other and don't want to admit behaviors or talk about them with physicians, Bhamidimarri said.

Consistent with other recommendations

The USPSTF recommendation is very similar to the draft update of guidelines by the Centers for Disease Control and Prevention (CDC), which recommends screening for HCV at least once in a lifetime for all adults 18 years old and over.

The CDC's draft guidelines continue, "All persons with risk factors (eg, persons with HIV, prior recipients of blood transfusions, persons who have ever injected drugs and shared needles, and persons who are born to an HCV-infected mother) should be tested for HCV, with periodic testing while risk factors persist."

The American Association for the Study of Liver Diseases and the Infectious Diseases Society of America recommends one-time, opt-out HCV screening for everyone at least 18 years old and one-time testing for all people younger than 18 years at increased risk of exposure. They also recommend periodic screening for people with increased risk of exposure as well as yearly HCV tests for all people who inject drugs and HIV-infected men who have unprotected sex with men.

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mr peabody

Moderator: Music Discussion, PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

The bushmeat trade.

Is our destruction of nature responsible for Covid-19?

by John Vidal | The Guardian | 18 Mar 2020

As habitat and biodiversity loss increase globally, the coronavirus outbreak may be just the beginning of mass pandemics.

Mayibout 2 is not a healthy place. The 150 or so people who live in the village, deep in the great Minkebe Forest in northern Gabon, are used to occasional bouts of diseases such as malaria, dengue, yellow fever and sleeping sickness. Mostly they shrug them off.

But in January 1996, Ebola, a deadly virus then barely known to humans, unexpectedly spilled out of the forest in a wave of small epidemics. The disease killed 21 of 37 villagers who were reported to have been infected, including a number who had carried, skinned, chopped or eaten a chimpanzee from the nearby forest.

I travelled to Mayibout 2 in 2004 to investigate why deadly diseases new to humans were emerging from biodiversity “hotspots” such as tropical rainforests and bushmeat markets in African and Asian cities.

It took a day by canoe and then many hours along degraded forest logging roads, passing Baka villages and a small goldmine, to reach the village. There, I found traumatised people still fearful that the deadly virus, which kills up to 90% of the people it infects, would return.

Villagers told me how children had gone into the forest with dogs that had killed the chimp. They said that everyone who cooked or ate it got a terrible fever within a few hours. Some died immediately, while others were taken down the river to hospital. A few, like Nesto Bematsick, recovered. “We used to love the forest, now we fear it,” he told me. Many of Bematsick’s family members died.

Only a decade or two ago it was widely thought that tropical forests and intact natural environments teeming with exotic wildlife threatened humans by harbouring the viruses and pathogens that lead to new diseases in humans such as Ebola, HIV and dengue.

But a number of researchers today think that it is actually humanity’s destruction of biodiversity that creates the conditions for new viruses and diseases such as Covid-19, the viral disease that emerged in China in December 2019, to arise – with profound health and economic impacts in rich and poor countries alike. In fact, a new discipline, planetary health, is emerging that focuses on the increasingly visible connections between the wellbeing of humans, other living things and entire ecosystems.

Is it possible, then, that it was human activity, such as road building, mining, hunting and logging, that triggered the Ebola epidemics in Mayibout 2 and elsewhere in the 1990s and that is unleashing new terrors today?

“We invade tropical forests and other wild landscapes, which harbour so many species of animals and plants – and within those creatures, so many unknown viruses,” David Quammen, author of Spillover: Animal Infections and the Next Pandemic, recently wrote in the New York Times. “We cut the trees; we kill the animals or cage them and send them to markets. We disrupt ecosystems, and we shake viruses loose from their natural hosts. When that happens, they need a new host. Often, we are it.”

Bats are trapped in nets to be examined for possible viral load in Gabon.

Increasing threat

Research suggests that outbreaks of animal-borne and other infectious diseases such as Ebola, Sars, bird flu and now Covid-19, caused by a novel coronavirus, are on the rise. Pathogens are crossing from animals to humans, and many are able to spread quickly to new places. The US Centers for Disease Control and Prevention (CDC) estimates that three-quarters of new or emerging diseases that infect humans originate in animals.

Some, like rabies and plague, crossed from animals centuries ago. Others, such as Marburg, which is thought to be transmitted by bats, are still rare. A few, like Covid-19, which emerged last year in Wuhan, China, and Mers, which is linked to camels in the Middle East, are new to humans and spreading globally.

Other diseases that have crossed into humans include Lassa fever, which was first identified in 1969 in Nigeria; Nipah from Malaysia; and Sars from China, which killed more than 700 people and travelled to 30 countries in 2002–03. Some, like Zika and West Nile virus, which emerged in Africa, have mutated and become established on other continents.

Kate Jones, chair of ecology and biodiversity at UCL, calls emerging animal-borne infectious diseases an “increasing and very significant threat to global health, security and economies.”

Amplification effect

In 2008, Jones and a team of researchers identified 335 diseases that emerged between 1960 and 2004, at least 60% of which came from animals.

Increasingly, says Jones, these zoonotic diseases are linked to environmental change and human behaviour. "The disruption of pristine forests driven by logging, mining, road building through remote places, rapid urbanisation and population growth is bringing people into closer contact with animal species they may never have been near before," she says.

The resulting transmission of disease from wildlife to humans, she says, is now “a hidden cost of human economic development. There are just so many more of us, in every environment. We are going into largely undisturbed places and being exposed more and more. We are creating habitats where viruses are transmitted more easily, and then we are surprised that we have new ones.”

Jones studies how changes in land use contribute to the risk. “We are researching how species in degraded habitats are likely to carry more viruses which can infect humans,” she says. “Simpler systems get an amplification effect. Destroy landscapes, and the species you are left with are the ones humans get the diseases from.”

“There are countless pathogens out there continuing to evolve which at some point could pose a threat to humans,”
says Eric Fevre, chair of veterinary infectious diseases at the University of Liverpool’s Institute of Infection and Global Health. “The risk [of pathogens jumping from animals to humans] has always been there.”

The difference between now and a few decades ago, Fevre says, is that diseases are likely to spring up in both urban and natural environments. “We have created densely packed populations where alongside us are bats and rodents and birds, pets and other living things. That creates intense interaction and opportunities for things to move from species to species,” he says.

The disruption of pristine forests driven by logging, mining, road building, rapid urbanisation
and population growth is bringing people into closer contact with wildlife, increasing the risk
of disease.

Tip of the iceberg

“Pathogens do not respect species boundaries,” says disease ecologist Thomas Gillespie, an associate professor in Emory University’s department of environmental sciences, who studies how shrinking natural habitats and changing behaviour add to the risk of diseases spilling over from animals to humans.

“I am not at all surprised about the coronavirus outbreak,” he says. “The majority of pathogens are still to be discovered. We are at the very tip of the iceberg.”

Humans, says Gillespie, are creating the conditions for the spread of diseases by reducing the natural barriers between host animals – in which the virus is naturally circulating – and themselves. “We fully expect the arrival of pandemic influenza; we can expect large-scale human mortalities; we can expect other pathogens with other impacts. A disease like Ebola is not easily spread. But something with a mortality rate of Ebola spread by something like measles would be catastrophic,” Gillespie says.

Wildlife everywhere is being put under more stress, he says. “Major landscape changes are causing animals to lose habitats, which means species become crowded together and also come into greater contact with humans. Species that survive change are now moving and mixing with different animals and with humans.”

Gillespie sees this in the US, where suburbs fragment forests and raise the risk of humans contracting Lyme disease. “Altering the ecosystem affects the complex cycle of the Lyme pathogen. People living close by are more likely to get bitten by a tick carrying Lyme bacteria,” he says.

Yet human health research seldom considers the surrounding natural ecosystems, says Richard Ostfeld, distinguished senior scientist at the Cary Institute of Ecosystem Studies in Millbrook, New York. He and others are developing the emerging discipline of planetary health, which looks at the links between human and ecosystem health.

“There’s misapprehension among scientists and the public that natural ecosystems are the source of threats to ourselves. It’s a mistake. Nature poses threats, it is true, but it’s human activities that do the real damage. The health risks in a natural environment can be made much worse when we interfere with it,” he says.

Ostfeld points to rats and bats, which are strongly linked with the direct and indirect spread of zoonotic diseases. “Rodents and some bats thrive when we disrupt natural habitats. They are the most likely to promote transmissions [of pathogens]. The more we disturb the forests and habitats the more danger we are in,” he says.

Felicia Keesing, professor of biology at Bard College, New York, studies how environmental changes influence the probability that humans will be exposed to infectious diseases. “When we erode biodiversity, we see a proliferation of the species most likely to transmit new diseases to us, but there’s also good evidence that those same species are the best hosts for existing diseases,” she wrote in an email to Ensia, the nonprofit media outlet that reports on our changing planet.

Dead pangolins seized by authorities in North Sumatra. Disease ecologists argue that viruses
and other pathogens are likely to move from animals to humans in wildlife markets.

The market connection

Disease ecologists argue that viruses and other pathogens are also likely to move from animals to humans in the many informal markets that have sprung up to provide fresh meat to fast-growing urban populations around the world. Here, animals are slaughtered, cut up and sold on the spot.

The “wet market” (one that sells fresh produce and meat) in Wuhan, thought by the Chinese government to be the starting point of the current Covid-19 pandemic, was known to sell numerous wild animals, including live wolf pups, salamanders, crocodiles, scorpions, rats, squirrels, foxes, civets and turtles.'

Equally, urban markets in west and central Africa sell monkeys, bats, rats, and dozens of species of bird, mammal, insect and rodent slaughtered and sold close to open refuse dumps and with no drainage.

“Wet markets make a perfect storm for cross-species transmission of pathogens,” says Gillespie. “Whenever you have novel interactions with a range of species in one place, whether that is in a natural environment like a forest or a wet market, you can have a spillover event.”

The Wuhan market, along with others that sell live animals, has been shut by the Chinese authorities, and last month Beijing outlawed the trading and eating of wild animals except for fish and seafood. But bans on live animals being sold in urban areas or informal markets are not the answer, say some scientists.

“The wet market in Lagos is notorious. It’s like a nuclear bomb waiting to happen. But it’s not fair to demonise places which do not have fridges. These traditional markets provide much of the food for Africa and Asia,” says Jones.

“These markets are essential sources of food for hundreds of millions of poor people, and getting rid of them is impossible,” says Delia Grace, a senior epidemiologist and veterinarian with the International Livestock Research Institute, which is based in Nairobi, Kenya. She argues that bans force traders underground, where they may pay less attention to hygiene.

A bushmeat stall with pangolins, bush rats and tiger cats for sale on the roadside outside Bata
in Equatorial Guinea.

Fevre and colleague Cecilia Tacoli, principal researcher in the human settlements research group at the International Institute of Environment and Development (IIED), argue in a blog post that rather than pointing the finger at wet markets, we should look at the burgeoning trade in wild animals.

“It is wild animals rather than farmed animals that are the natural hosts of many viruses,” they write. “Wet markets are considered part of the informal food trade that is often blamed for contributing to spreading disease. But … evidence shows the link between informal markets and disease is not always so clear cut.”

Changing behaviour

So what, if anything, can we do about all of this?

Jones says that change must come from both rich and poor societies. Demand for wood, minerals and resources from the global north leads to the degraded landscapes and ecological disruption that drives disease, she says. “We must think about global biosecurity, find the weak points and bolster the provision of health care in developing countries. Otherwise we can expect more of the same,” she adds.

“The risks are greater now. They were always present and have been there for generations. It is our interactions with that risk which must be changed,” says Brian Bird, a research virologist at the University of California, Davis School of Veterinary Medicine One Health Institute, where he leads Ebola-related surveillance activities in Sierra Leone and elsewhere.

“We are in an era now of chronic emergency,” Bird says. “Diseases are more likely to travel further and faster than before, which means we must be faster in our responses. It needs investments, change in human behaviour, and it means we must listen to people at community levels.”

A poster in Beijing promoting wildlife as friends instead of food, after a crackdown on
wild animal markets following the coronavirus outbreak.

Getting the message about pathogens and disease to hunters, loggers, market traders and consumers is key, Bird says. “These spillovers start with one or two people. The solutions start with education and awareness. We must make people aware things are different now. I have learned from working in Sierra Leone with Ebola-affected people that local communities have the hunger and desire to have information,” he says. “They want to know what to do. They want to learn.”

Fevre and Tacoli advocate rethinking urban infrastructure, particularly within low-income and informal settlements. “Short-term efforts are focused on containing the spread of infection,” they write. “The longer term – given that new infectious diseases will likely continue to spread rapidly into and within cities – calls for an overhaul of current approaches to urban planning and development.”

The bottom line, Bird says, is to be prepared. “We can’t predict where the next pandemic will come from, so we need mitigation plans to take into account the worst possible scenarios,” he says. “The only certain thing is that the next one will certainly come.”

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mr peabody

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Staff member
Aug 31, 2016
Frostbite Falls, MN

Scientists conclude that coronavirus is the product of natural evolution

by The Scripps Research Institute | Medical Xpress | 17 Mar 2020

The novel SARS-CoV-2 coronavirus that emerged in the city of Wuhan, China, last year and has since caused a large scale COVID-19 epidemic and spread to more than 70 other countries is the product of natural evolution, according to findings published today in the journal Nature Medicine.

The analysis of public genome sequence data from SARS-CoV-2 and related viruses found no evidence that the virus was made in a laboratory or otherwise engineered.

"By comparing the available genome sequence data for known coronavirus strains, we can firmly determine that SARS-CoV-2 originated through natural processes," said Kristian Andersen, Ph.D., an associate professor of immunology and microbiology at Scripps Research and corresponding author on the paper.

In addition to Andersen, authors on the paper, "The proximal origin of SARS-CoV-2," include Robert F. Garry, of Tulane University; Edward Holmes, of the University of Sydney; Andrew Rambaut, of University of Edinburgh; W. Ian Lipkin, of Columbia University.

Coronaviruses are a large family of viruses that can cause illnesses ranging widely in severity. The first known severe illness caused by a coronavirus emerged with the 2003 Severe Acute Respiratory Syndrome (SARS) epidemic in China. A second outbreak of severe illness began in 2012 in Saudi Arabia with the Middle East Respiratory Syndrome (MERS).

On December 31 of last year, Chinese authorities alerted the World Health Organization of an outbreak of a novel strain of coronavirus causing severe illness, which was subsequently named SARS-CoV-2. As of February 20, 2020, nearly 167,500 COVID-19 cases have been documented, although many more mild cases have likely gone undiagnosed. The virus has killed over 6,600 people.

Shortly after the epidemic began, Chinese scientists sequenced the genome of SARS-CoV-2 and made the data available to researchers worldwide. The resulting genomic sequence data has shown that Chinese authorities rapidly detected the epidemic and that the number of COVID-19 cases have been increasing because of human to human transmission after a single introduction into the human population. Andersen and collaborators at several other research institutions used this sequencing data to explore the origins and evolution of SARS-CoV-2 by focusing in on several tell-tale features of the virus.

The scientists analyzed the genetic template for spike proteins, armatures on the outside of the virus that it uses to grab and penetrate the outer walls of human and animal cells. More specifically, they focused on two important features of the spike protein: the receptor-binding domain (RBD), a kind of grappling hook that grips onto host cells, and the cleavage site, a molecular can opener that allows the virus to crack open and enter host cells.

Evidence for natural evolution

The scientists found that the RBD portion of the SARS-CoV-2 spike proteins had evolved to effectively target a molecular feature on the outside of human cells called ACE2, a receptor involved in regulating blood pressure. The SARS-CoV-2 spike protein was so effective at binding the human cells, in fact, that the scientists concluded it was the result of natural selection and not the product of genetic engineering.

This evidence for natural evolution was supported by data on SARS-CoV-2's backbone—its overall molecular structure. If someone were seeking to engineer a new coronavirus as a pathogen, they would have constructed it from the backbone of a virus known to cause illness. But the scientists found that the SARS-CoV-2 backbone differed substantially from those of already known coronaviruses and mostly resembled related viruses found in bats and pangolins.

"These two features of the virus, the mutations in the RBD portion of the spike protein and its distinct backbone, rules out laboratory manipulation as a potential origin for SARS-CoV-2" said Andersen.

Josie Golding, Ph.D., epidemics lead at UK-based Wellcome Trust, said the findings by Andersen and his colleagues are "crucially important to bring an evidence-based view to the rumors that have been circulating about the origins of the virus (SARS-CoV-2) causing COVID-19."

"They conclude that the virus is the product of natural evolution,"
Goulding adds, "ending any speculation about deliberate genetic engineering."

Possible origins of the virus

Based on their genomic sequencing analysis, Andersen and his collaborators concluded that the most likely origins for SARS-CoV-2 followed one of two possible scenarios.

In one scenario, the virus evolved to its current pathogenic state through natural selection in a non-human host and then jumped to humans. This is how previous coronavirus outbreaks have emerged, with humans contracting the virus after direct exposure to civets (SARS) and camels (MERS). The researchers proposed bats as the most likely reservoir for SARS-CoV-2 as it is very similar to a bat coronavirus. There are no documented cases of direct bat-human transmission, however, suggesting that an intermediate host was likely involved between bats and humans.

In this scenario, both of the distinctive features of SARS-CoV-2's spike protein—the RBD portion that binds to cells and the cleavage site that opens the virus up—would have evolved to their current state prior to entering humans. In this case, the current epidemic would probably have emerged rapidly as soon as humans were infected, as the virus would have already evolved the features that make it pathogenic and able to spread between people.

In the other proposed scenario, a non-pathogenic version of the virus jumped from an animal host into humans and then evolved to its current pathogenic state within the human population. For instance, some coronaviruses from pangolins, armadillo-like mammals found in Asia and Africa, have an RBD structure very similar to that of SARS-CoV-2. A coronavirus from a pangolin could possibly have been transmitted to a human, either directly or through an intermediary host such as civets or ferrets.

Then the other distinct spike protein characteristic of SARS-CoV-2, the cleavage site, could have evolved within a human host, possibly via limited undetected circulation in the human population prior to the beginning of the epidemic. The researchers found that the SARS-CoV-2 cleavage site, appears similar to the cleavage sites of strains of bird flu that has been shown to transmit easily between people. SARS-CoV-2 could have evolved such a virulent cleavage site in human cells and soon kicked off the current epidemic, as the coronavirus would possibly have become far more capable of spreading between people.

Study co-author Andrew Rambaut cautioned that it is difficult if not impossible to know at this point which of the scenarios is most likely. If the SARS-CoV-2 entered humans in its current pathogenic form from an animal source, it raises the probability of future outbreaks, as the illness-causing strain of the virus could still be circulating in the animal population and might once again jump into humans. The chances are lower of a non-pathogenic coronavirus entering the human population and then evolving properties similar to SARS-CoV-2.

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mr peabody

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Aug 31, 2016
Frostbite Falls, MN
Poultry worker’s death highlights spread of coronavirus in meat plants

by Miriam Jordan and Caitlin Dickerson | NY Times | 9 April 2020

Some employees are coming in sick, and one woman died after being ordered back to work. “Our work conditions are out of control,” a longtime Tyson employee said.

Annie Grant, 55, had been feverish for two nights. Worried about the coronavirus outbreak, her adult children had begged her to stay home rather than return to the frigid poultry plant in Georgia where she had been on the packing line for nearly 15 years.

But on the third day she was ill, they got a text from their mother. “They told me I had to come back to work,” it said.

Ms. Grant ended up returning home, and died in a hospital on Thursday morning after fighting for her life on a ventilator for more than a week. Two other workers at the Tyson Foods poultry plant where she worked in Camilla, Ga., have also died in recent days.

“My mom said the guy at the plant said they had to work to feed America. But my mom was sick,” said one of Ms. Grant’s sons, Willie Martin, 34, a teacher in South Carolina. He said he watched on his phone as his mother took her last breath.

The coronavirus pandemic has reached the processing plants where workers typically stand elbow-to-elbow to do the low-wage work of cutting, deboning and packing the chicken and beef that Americans savor. Some plants have offered financial incentives to keep them on the job, but the virus’s swift spread is causing illness and forcing plants to close.

Smithfield Foods’ pork plant in Sioux Falls, S.D., announced Thursday that it would close temporarily, after more than 80 employees tested positive for the coronavirus. Workers have come down with Covid-19 in several poultry plants in Alabama, Georgia and Tennessee.

JBS USA, the world’s largest meat processor, confirmed the death of one worker at a Colorado facility and shuttered a plant in Pennsylvania for two weeks. Cargill this week also closed a facility in Pennsylvania, where it produces steaks, ground beef and ground pork. Tyson halted operations at a pork plant in Iowa after more than two dozen workers tested positive.

Industry analysts said the plant closures were unlikely to result in serious disruptions to the food supply.

But if the pandemic keeps plants shuttered for an extended period, some products could become harder to find in stores, said Christine McCracken, a meat industry analyst at Rabobank in New York. “If workers don’t feel safe, they may not come back, and we don’t have a large pool of people that are lining up to work in these plants,” she said.

At some plants, workers have staged walkouts over concerns that they are not being properly protected. But an untold number remain on the job, most of them African-Americans, Latinos and immigrants.

The Trump administration has urged food-supply workers to step up to meet growing demand. “You are vital,” Vice President Mike Pence said on Tuesday. “You are giving a great service to the people of the United States of America and we need you to continue, as a part of what we call critical infrastructure, to show up and do your job.”

Mr. Pence said the administration would work “tirelessly” to ensure the workers’ safety.

There is no evidence that the coronavirus can be transmitted through food, but public health experts have advised consumers to wipe down packaging because the virus could survive on those surfaces for days.

Several major meat-processing outfits are offering workers cash incentives to continue showing up for work.

At the Tyson plant in Camilla, the company offered its 2,100 workers a $500 bonus if they worked in April, May and June without missing a day.

Many of the employees live a 15-minute drive away in Albany, Ga., which has emerged as one of the epicenters of the coronavirus outbreak.

“How many more have to fight for their life, how many more families got to suffer before they realize we are more important than their production,” said Tanisha Isom, 36, a de-boner on line four at the Camilla plant. She recently learned that she had bronchitis and missed two weeks of work.

She has continued to cough, she said, with a low-grade fever and fatigue — and hopes to finally get tested for the coronavirus later this week.

“We are crying out for help but no one is listening,” said Ms. Isom, who has worked at Tyson for years and earns $12.95 an hour.

“Our work conditions are out of control. We literally work shoulder to shoulder daily,” she said. She said that two people she works closely with are currently fighting for their lives.

Gary Mickelson, a spokesman for Tyson Foods, said the company was taking the temperature of workers before they entered and had implemented social-distancing measures. These included dividers between work stations and slower production lines to widen the space between workers.

If there is a confirmed case at one site, “we notify anyone who has been in close contact with the person and instruct them to go home and self-quarantine,” he said. He noted that workers who are sick continue to be paid while off the job.

He also said that Tyson was coordinating with federal agencies to secure “an adequate supply of protective face coverings for production workers” and other protective coverings.

But workers and union leaders said the response by Tyson and other chicken companies, which produce the bulk of the nation’s meat supply, has been inadequate.

The Retail, Wholesale and Department Store Union, which represents thousands of poultry processing workers in the South, said that it had been “imploring” producers to take steps to protect workers’ safety while securing the nation’s food supply chain.

“Day after day we hear reports of our members contracting the Covid-19 virus and even succumbing to it,” said Stuart Appelbaum, the union’s president. “The poultry industry can and must do better to swiftly protect workers.”

“Saying you are still scrambling for protective supplies when much of the supply chain has been protecting workers for weeks is a pathetic excuse for companies that make billions in profits annually,”
he said.

Fatalities among workers have lent urgency to the demands for protection.

Cameron Bruett, a spokesman for JBS, confirmed that an older man who had worked for 30 years at its beef plant in Greeley, Colo., recently died from complications of Covid-19.

Operations have been halted at a plant the company operates in Souderton, Pa., until April 16, after several managers displayed “flulike symptoms,” he said.

In at least seven states, workers at Cargill, the nation’s third-largest meat producer, have tested positive for the virus, according to Dan Sullivan, a company spokesman.

Mr. Sullivan confirmed that Cargill had closed a plant in Hazleton, Pa., after several employees tested positive.

The federal government has deemed food-industry workers essential, and Cargill has encouraged employees to stay on the job through the pandemic with extra pay and bonus offers. Workers are eligible for up to 80 hours of paid leave for any virus-related absence.

But some employees say they, like Ms. Grant in Georgia, feel pressure to come to work, and others say they cannot afford to remain at home past any paid sick leave.

Jose Aguilar, a representative of the union in Alabama, said "many immigrant workers might not be eligible for unemployment benefits or payments from the federal stimulus package.:

“For the immigrant population, it’s really sad because right now, there are a lot of people who don’t have a choice,”
he said. “Almost everybody is going to work because they need money.”

A woman who has worked for 20 years at Pilgrim’s Pride in Guntersville, Ala., said "the virus was spreading in the meat packing area, where employees work side by side and social distancing is nearly impossible. Recently, the company took measures to bolster safety, she said.

“There are people cleaning the plant; they are checking our temperatures every time we come in the morning; they’re doing all that. They’re starting to give us masks,” said the woman, who asked not to be named for fear of retribution from her employer.

“But of course we’re worried because the truth is we don’t know if more people are going to get sick,” she said.

Pilgrim’s Pride did not respond to a request for comment. The company’s Facebook page said that workers who show symptoms were being told to stay home.

On Facebook, several employees of the Tyson plant in Camilla questioned why those who had been working alongside people who tested positive had not been told to stay away. Others expressed frustration that the facility remained open at all.

Shynekia Emanuel, who works nights on the deboning line in Camilla, said that "shift supervisors — the same people who had been checking workers’ temperatures — tested positive for the virus."

A company spokesman said Tyson would not discuss specific employees.

Mr. Emanuel, who said that he was particularly vulnerable to the virus because he has Crohn’s disease, will not report to work again until the pandemic has passed.

“Enough is enough,” he said. “Nobody wants to risk their lives over some chicken. Sorry. My life and my son’s life is way more important.”

Before checking herself into a hospital, Ms. Grant had told her children that several co-workers on her line had been absent.

“If they had taken proper precautions, they would have prevented people from getting it,” her son said. “This just isn’t right. It’s about saving multiple lives.”

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mr peabody

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Staff member
Aug 31, 2016
Frostbite Falls, MN

A medical staffer holds the hand of a patient in the Bassini Hospital near Milan, Italy.
One key thing to understand about the deadliness of the coronavirus is how it infects
the body and how our body responds to fight it.

Experts warn covid-19 attacks much more than the lungs

By Adam Miller | CBC Health | 17 April 2020

Understanding how COVID-19 attacks the human body is essential to developing an effective treatment or vaccine to stop the global pandemic — but there's still so much we don't know about how it can kill us.

As researchers around the world race to understand the illness, they are compiling and sharing their early observations of patients hit by a virus that has sickened more than two million people. The findings are preliminary, but they can help point researchers in the right directions.

They have seen that in severe cases, COVID-19 invades our respiratory cells and triggers an immune system response that targets those infected cells, destroys lung tissue and ultimately clogs our airways, cutting off our oxygen supply.

That's when organ failure can also occur, causing severe damage to the kidneys, liver and heart, similar to other infections like sepsis.

But they will look to determine whether the virus is targeting and shutting down organs in a new way or just behaving like other infections that cause such common complications.

Why COVID-19 can be so deadly

One key thing to understand about the deadliness of the coronavirus is how it infects the body and how our body responds to fight it.

Cytokines are small molecules released by the immune system that travel throughout the body to co-ordinate an immune response against an infection or injury — even with something as mild as a common fever.

But if the immune system overproduces them in response to the infection, they can cause "cytokine storms" that can rampage through the bloodstream and severely damage the body.

Dr. Douglas Fraser, an ICU doctor at London Health Sciences Centre and a researcher at Western University in London, Ont., has been studying that exaggerated immune response by collecting blood from critically ill COVID-19 patients in an effort to find new ways to treat the disease.

"The immune response to this particular disease is very different than what we've seen in other infected patients that end up in the ICU," he said. "It's a unique response and it's going to require unique therapies."

Fraser said his research shows there are different types of cytokines released in the body at unusual times and levels in response to COVID-19 compared with those that are typically found in critically ill patients from more common diseases.

"What we're seeing seems to be occurring in all of the very sick patients: those who are requiring the ICU admissions, those who are requiring assistance with their breathing and those that are ultimately dying," he said.

Kidneys tied to severe complications

Kidney infection was an "important complication" in a preliminary publication of a recent observational study of 287 COVID-19 patients in China, which found almost one in five had some stage of sudden or "acute" kidney infection — putting them at "substantially higher" risk of death.

While it's not yet known what rate of Canadian COVID-19 patients have acute kidney infections, the majority occur in severely ill patients, said Dr. Jeffrey Perl, a nephrologist at St Michael's Hospital in Toronto and an assistant medical professor at the University of Toronto.

"As people's blood pressure gets very low from a very massive, overwhelming inflammatory immune response, the kidneys are starved of blood," he said, adding that it can often lead to the need for a dialysis machine to clean the patient's blood.

To give an idea of how serious a complication it can be, Perl said the mortality rate for patients who had developed acute kidney injury from SARS in 2003 was 92 per cent, compared to just eight per cent in those who didn't.

"Chronic kidney patients are also at higher risk of death with COVID-19 compared to those without pre-existing conditions who are otherwise well," he added.

"We're very worried about those patients getting a COVID-19 infection," he said. "Similar to the elderly population that we're very concerned about, I would consider these patients another high-risk group."

Heart may be 'directly' targeted by virus

One essential organ that may be at direct risk from the virus is the heart.

A cohort study found almost 20 per cent of 416 hospitalized COVID-19 patients in China had heart damage during hospitalization, putting them at a higher risk for death.

While recent research from the American College of Cardiology found arrhythmia, or irregular heartbeat, in 16 per cent of patients and acute cardiac injury in 7.2 per cent.

"There's the possibility and the likelihood that some of the virus might actually get taken directly up into the heart muscle cells and cause that heart injury," said Dr. Patrick Lawler, a cardiologist and clinician scientist at the Peter Munk Cardiac Centre in Toronto.

"We hear anecdotes from other people that have had a little bit more experience, unfortunately, with this that really are consistent with the heart suddenly starting to become weak."

An observational study of 187 patients hospitalized with COVID-19 published in the New England Journal of Medicine last month found high levels of troponin, which can indicate problems with the heart, in 28 per cent of hospitalized COVID-19 patients in Wuhan, China, which concluded they were at risk of "much higher mortality."

Emerging research shows the heart may be at direct risk from the virus. One study
found almost 20 per cent of 416 patients had cardiac issues.

Lawler said the outcomes for COVID-19 patients with cardiac issues are "dramatically worse," and even though the virus enters through the respiratory system, it can take root in other areas of the body.

"The heart is really a critical, critical part of what determines whether or not patients are going to recover from this or not," he said.

Can it help us find a cure?

Lawler is currently looking at the use of blood thinners as a possible treatment for COVID-19 patients, which may prevent the virus from binding to ACE2 receptors — enzymes found in cells throughout the human body that can act as an entryway for coronaviruses.

He said research suggests blood clots may play a role in organ failure in critically ill patients, so different doses of anticoagulants may prevent that from happening.

Fraser is also using his research on the "cytokine storm" immune response to COVID-19 to find "targets" to further efforts toward an effective treatment.

He said there could be multiple components to why different people are susceptible to the virus that range from genetics, to pre-existing conditions to age.

"Once we have an understanding of what's going on, we can develop therapies, we can develop vaccines," he said.

"Then we can get back to a normal life."

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mr peabody

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Scientists uncover how Zika virus spreads through sexual contact

by Experimental Biology | Medical Xpress | 27 April 2020

Zika virus is capable of replicating and spreading infectious particles within the outermost cells lining the vaginal tract, according to new research. The findings provide the first molecular-level insights into how the virus can move from person to person through sexual contact.

While Zika is primarily spread by mosquitoes, researchers have been aware of its potential for sexual transmission based on cases in which people became infected after having sex with a partner who had visited a Zika-affected area. Previous studies have also found Zika particles present in semen and vaginal fluid from infected individuals.

Having a more detailed understanding of how Zika infiltrates the body through sexual contact could help scientists identify new ways to prevent or treat Zika infections. The new study examined how Zika particles behaved in cultures of human vaginal epithelial cells and identified the virus's likely entry point as a protein on the surface of the cells called tyrosine-protein kinase receptor UFO, which is encoded by the AXL gene.

"The outcome of this research highlights how local replication of Zika in the vaginal epithelium plays an important role in mediating sexual transmission and subsequent systemic infection in the human host," said lead study author James Mungin Jr., a doctoral candidate at Meharry Medical College. "Additionally, our research findings confirming that the receptor UFO (AXL) promotes viral entry can be very instrumental in developing drugs and antibody-based therapies that target and block this receptor, therefore eliminating the pathology caused by this virus."

Mungin was scheduled to present the research at the American Society for Investigative Pathology annual meeting in San Diego this month. Though the meeting, to be held in conjunction with the 2020 Experimental Biology conference, was canceled in response to the COVID-19 outbreak, the research team's abstract was published in this month's issue of The FASEB Journal.

Zika spread rapidly around the world during a major 2015-2016 outbreak, causing about 42,000 infections in the United States and its territories. While the number of cases has since dropped precipitously, the virus is still considered a health threat in many places around the world. Babies born to mothers infected with Zika have a high risk of birth defects.

Mungin and colleagues found that Zika virus particles were able to successfully enter vaginal epithelial cells through the UFO receptor, replicate their RNA genome and steadily release infectious viral particles inside the cells. The research team plans to further study the factors that contribute to Zika replication for insights on how those factors might be interrupted.

Like Zika, many other viruses in the flavivirus family are spread by insects. However, research on those other viruses, such as dengue and yellow fever, does not always translate well to Zika because they are not sexually transmitted.

"Interestingly, sexual transmission among flaviviruses is in fact unique in nature," said Mungin. "As of now, Hepatitis C and Zika virus have been identified as the only two flaviviruses known to establish infection via sexual contact with an infected partner."

According to the U.S. Centers for Disease Control and Prevention, using condoms can prevent sexual transmission of Zika.

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mr peabody

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Injectable drug more effective at blocking HIV than daily pills

by Lenny Bernstein | Washington Post | 7 Jul 2020

The pill Truvada is used to prevent HIV infection. Research shows that a new long-acting form of the drug injected every two months is even more effective at preventing HIV.

A long-acting drug injected every two months is more effective at preventing HIV than the pills most commonly used by people at risk of acquiring the infection, according to research released Tuesday at an international AIDS conference.

The drug cabotegravir was tested on more than 4,500 cisgender men who have sex with men and transgender women who have sex with men in 43 countries. While Truvada, the pill used most often to block the virus, is also highly effective, the injectable drug proved to be even better, the research shows.

Perhaps more importantly, an injection every two months may allow more people to remain on medication, known as "pre-exposure prophylaxis" or PrEP, that blocks the virus. People whose medical care is inconsistent, including homeless people, intravenous drug users and others in unstable situations, have trouble remaining on the daily pills. Others are reluctant to obtain them because of the stigma still associated with HIV.

"Giving individuals an option of an injection every eight weeks instead of taking a daily pill to prevent HIV provides choices and flexibility," Monica Gandhi, San Francisco co-chair of the AIDS 2020 conference, said in an email. The worldwide conference is taking place online this week.

Truvada and Descovy, both manufactured by Gilead Sciences, are the only PrEP drugs approved by the Food and Drug Administration on the market. A generic form of Truvada is expected soon, but Gilead has been the target of activist groups for setting high prices for its drugs.

The injectable drug tested in the new study is made by ViiV Healthcare.

Kimberly Smith, head of research and development for the company, said removing the problem of adhering to a daily drug regimen accounts for the injectable's superior performance. Adherence to pills starts off strong in many men, she said, but wanes over time.

Overall, 52 people in the study contracted HIV in a little less than three years - 39 who were on daily pills and 13 who received the experimental injections. Test subjects were enrolled at 43 sites in the United States, Africa, Asia and Latin America.

"I believe the result is primarily driven by the fact that you don't need to adhere to a regimen every day," Smith said.

About 1.7 million people throughout the world became infected with HIV last year - a figure experts say could be greatly reduced if more people had access to PrEP and stayed on it. Taken daily, the drug is more than 90% effective at preventing sexual transmission of the virus and more than 70% effective at blocking it among people who inject street drugs and share needles.

But in the United States, only about 10 to 20% of the 1.1 million people considered at risk of contracting HIV are on PrEP. A disproportionate number of those not on medication are black and Latino men who have sex with other men. The United States has launched a program that, in part, focuses on them in a bid to end transmission of HIV by 2030.

Smith said the company made a point of enrolling African American men who have sex with men in the hope that good results would persuade that group to adopt the medication. Half the U.S. subjects in the study, 844 men, were in that category, she said.

"Black men who have sex with men did extremely well" in the trial, Smith said. "This is a message we can carry to that population."

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A woman being taken from Elmhurst Hospital Center in Queens and placed in an ambulance in April.

Race, ethnicity, age and sex increase risk of dying from Covid-19

by Katherine Wu | New York Times | 8 Jul 2020

Analysis of more than 17 million people in England has pinpointed factors that can raise a person’s chances of dying from Covid-19, the disease caused by the coronavirus.

The paper, published Wednesday in Nature, echoes reports from other countries that identify older people, men, racial and ethnic minorities, and those with underlying health conditions among the more vulnerable populations.

“This highlights a lot of what we already know about Covid-19,” said Uchechi Mitchell, a public health expert at the University of Illinois at Chicago who was not involved in the study. “But a lot of science is about repetition. The size of the study alone is a strength, and there is a need to continue documenting disparities.”

The researchers mined health records of about 40 percent of England’s population, collected by the United Kingdom’s National Health Service. Of 17 million adults tracked over three months, 11,000 reportedly died of Covid-19 or Covid-19-related complications.

“A lot of previous work has focused on patients that present at hospital,” said Dr. Ben Goldacre of the University of Oxford, one of the authors on the study. “That’s useful and important, but we wanted to get a clear sense of the risks as an everyday person. Our starting pool is literally everybody.”

Dr. Goldacre’s team found that "patients older than 80 were at least 20 times more likely to die from Covid-19 than those in their 50s, and hundreds of times more likely to die than those below the age of 40." The scale of this relationship was “jaw-dropping,” Dr. Goldacre said.

Additionally, men stricken with the virus had a higher likelihood of dying than women of the same age. Medical conditions such as obesity, diabetes, severe asthma and compromised immunity were also linked to poor outcomes, in keeping with guidelines from the Centers for Disease Control and Prevention in the United States. And the researchers noted that a person’s chances of dying also tended to track with socioeconomic factors like poverty.

The data roughly mirror what has been observed around the world, said Avonne Connor, an epidemiologist at Johns Hopkins University who was not involved in the study. But seeing these patterns emerge in a staggeringly large data set “is astounding” and “adds another layer to depicting who is at risk” during this pandemic, Dr. Connor said.

Particularly compelling were the study’s findings on race and ethnicity, said Sharrelle Barber, an epidemiologist at Drexel University who was not involved in the study. Roughly 11 percent of the patients tracked by the analysis identified as nonwhite. The researchers found that these individuals — particularly Black and South Asian people — were at higher risk of dying from Covid-19 than white patients.

That trend persisted even after Dr. Goldacre and his colleagues made statistical adjustments to account for factors like age, sex and medical conditions, suggesting that other factors are playing a major role.

An increasing number of reports have pointed to the pervasive social and structural inequities that are disproportionately burdening racial and ethnic minority groups around the world with the coronavirus’s worst effects.

Some experts pointed out flaws in the researchers’ methodology that made it difficult to quantify the exact risks faced by members of the vulnerable groups identified in the study. For instance, certain medical conditions that can exacerbate Covid-19, like chronic heart disease, are more prevalent among Black people than white people.

The researchers removed such variables to focus solely on the effects of race and ethnicity. But because Black individuals are also more likely to experience stress and be denied access to medical care in many parts of the world, the disparity in rates of heart disease may itself be influenced by racism, said Usama Bilal, an epidemiologist at Drexel University who was not involved in the new analysis. Ignoring the contribution of heart disease, then, could end up inadvertently discounting part of the relationship between race and ethnicity and Covid-19-related deaths.

The study was also not set up to conclusively show cause-and-effect relationships between risk factors and Covid-19 deaths.

Regardless of the methodological drawbacks of this study, experts agree that “the causes of disparities, whether in Covid-19 or other aspects of health, are intricately linked to structural racism,” Dr. Mitchell said.

In the United States, Latino and African-American residents are three times as likely to become infected by the coronavirus as white residents, and nearly twice as likely to die.

Many of these individuals work as front-line employees, or are tasked with essential in-person jobs that prevent them from sheltering in place at home. Some live in multigenerational households that can compromise effective physical distancing. Others must cope with language barriers and implicit bias when they seek medical care.

"Any study publishing data on an ongoing and fast-shifting pandemic will inevitably be imperfect," said Julia Raifman, an epidemiologist at Boston University who was not involved in the study. But the new paper helps address “a real paucity of data on race,” Dr. Raifman added. “These disparities are not just happening in the United States.”

With regard to the racial inequities in this pandemic, Dr. Barber said, “I think what we’re seeing is real, and it’s not a surprise. We can learn from this study and improve on it. It gives us clues into what might be happening.”

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European arrival and The Great Dying in the Americas after 1492*

Alexander Kocha, Chris Brierley, Mark Maslina, Simon Lewis

Here we investigate the large-scale depopulation of the Americas after European arrival, and quantitatively review the evidence for (i) the pre-Columbian population size, and (ii) the post-1492 population loss. From 119 published regional population estimates we calculate a pre-1492 CE population of 60.5 million. European epidemics removed 90% of the indigenous population over the next century. The Great Dying of the indigenous Peoples of the Americas resulted in a human-driven global impact on the Earth System in the two centuries prior to the Industrial Revolution.

We therefore test the hypothesis that human actions impacted first, the existence of a sufficiently large indigenous population in the Americas 1492, and second, the population decline estimates following the arrival and spread of European diseases. These records are then cross-combined and sampled to obtain revised estimates of the 1492 population, and mortality from European-contact diseases.

The population of the Americas in 1492

The first population groups to arrive in North America between 20,000 and 15,000 years ago were of east Asian- and north Eurasian ancestry. The adoption of a sedentary, agricultural way of life in the Americas began 10,000–8000 BP. Large, complex civilizations emerged in North, Central and South America, further increasing population density, with abundant evidence for a large population living in the Americas prior to European arrival. However, as the epidemics spread, often ahead of the European explorers, pre-European population estimates were never formally documented in colonial censuses. Hence, Native American populations were only documented in the decades after European contact. Our estimate of the number of people living in the Americas in 1492 CE is 60.5 million.

The Great Dying

Accounts from eyewitnesses and documentary evidence from census data report a widespread collapse of the indigenous population over the decades after European contact. Such a large population decline meant that the indigenous population would not have been able to manage their existing agricultural systems over such large areas. While other factors such as warfare, the enslavement of indigenous people, and hunger following social disintegration, resulting from the loss of such a large fraction of societies, meant even larger population losses, we focus on the epidemics as the main driver behind the majority of the deaths in the Great Dying.

Unprecedented mortality after European arrival

Existing evidence suggests that the indigenous population collapse was primarily caused by the introduction of pathogens unknown to the American continent together with warfare and slavery. Part of a wider Columbian Exchange of once-separate continental fauna and flora, these epidemics were introduced by European settlers and African slaves and were passed on to an indigenous population that had not been previously exposed to these pathogens and therefore did not initially possess suitable antibodies. Such diseases included smallpox, measles, influenza, the bubonic plague, and later malaria, diphtheria, typhus and cholera. Most of these diseases originated from domesticated farm animals from Europe to which Native Americans had no prior exposure. The relative absence of American diseases arriving in Europe can therefore be explained by the low number of domesticated animals in the pre-contact Americas. Thus, influenza, smallpox, bubonic plague and other diseases ravaged the Americas, and not vice versa. Such diseases typically individually killed ~30% or more of the initial population. Hence a series of epidemics in rapid succession could have led to the loss of whole societies.

Overall, hemisphere wide post-epidemics population estimates range between 4.5 million and 14.4 million for 1600–1700 CE. These studies are less clear on their assumptions than their reports of pre-contact population estimates. Furthermore, the rate of loss is strongly influenced by the chosen dates used to calculate it. Loss rates ranging from 40% to 95%, with Denevan’s more recent update producing a robust initial population estimate of 54 million (similar to our 60.5 million) that results in a 90% decline to 5.6 million in 1600 CE.

For indigenous people that survived, immunity to most of the European diseases would be acquired during childhood of future generations. Two main hypothesis, not mutually exclusive, have been proposed to explain why the depopulation continued until centuries after initial contact. The first is that the low genetic diversity between the indigenous hosts has facilitated the spread of potent pathogens. The ancestors of the modern Native Americans migrated most likely from East Asia into North America. Due to their small initial group size, the newly established population of the Americas had a lower level of genetic diversity compared to the original Asian population (“founder effect”) which would have lowered resistance against diseases from certain pathogens. However, despite this there is no evidence for a causal relationship between genetic differences and the increased severity of the impacts of diseases.


We estimate that 55 million indigenous people died from European-contact diseases following the European conquest of the Americas beginning in 1492.

*From the study here :
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Nancy and Dave Nathan of Bethesda, Md., worry about whether to proceed with a family trip.

How should older adults calculate coronavirus risk right now?*

by Paula Span | New York Times | 17 Jul 2020

For weeks, Dave and Nancy Nathan have been debating whether to proceed with a family trip to a lodge in upstate New York next month, marking his 80th birthday.

“It looks dreamy..., mountains and lakes,” says Nancy, 74. Besides, they haven't gathered their clan — three daughters and their families, a dozen people in all — for a year. She thinks she and Dave could manage the drive from their home in Bethesda, Md., to upstate New York.

He's not so sure.

Both retirees, they have been cautious through the pandemic, mindful that while neither have health conditions that would make Covid-19 especially dangerous, age alone puts them at higher risk. They avoid supermarkets, and relied on grocery delivery services and take out food. Dave wears gloves on the tennis court.

“I’ve been dubious about travel,” he says. “I have no need to be more daring.” Worried, too, about the family members flying from Oregon and Florida for his birthday, he calls himself Dr. No.

“It’s not fun for him, or anyone, if he’s always looking over his shoulder,” Nancy says, sympathizing. Still, she hopes they can go.

Early on in the pandemic, public health officials warned older adults to simply stay at home, except to buy food or medicine or exercise outdoors apart from others. Now, with states and cities reopening (and some re-closing) at varying paces, the calculations grow steadily more complicated.

“Lots of people are really agonizing about what to do and whom to have faith in,” said Dr. William Schaffner, an infectious disease specialist at Vanderbilt University.

The Centers for Disease Control and Prevention has reported that Covid-19 hospitalizations rise with age, from about 12 per 100,000 people among those 65 to 74 years old to 17 per 100,000 for those over 85. And a large study from England has reported that patients over 80 are at least 20 times more likely to die than those in their 50s.

"While the risk of contracting the new coronavirus appears no higher for people over 65, once infected, the virus is much nastier,” said Dr. Schaffner, an older adult himself.

“Even if we recover, there’s the possibility that we will never get back to the same level of physical and mental competence,” he added.

Given that prospect, do you get a haircut? Dr. Schaffner has decided he will, wearing a surgical mask and knowing his longtime stylist will take “meticulous” precautions.

The Nathans’ book group has been meeting on Zoom. Can the four couples now meet in a back yard? The members agreed, as long as everyone distanced.

“The least risky thing is to stay home and lock the door,” Dr. Schaffner said.

Economists at M.I.T. came close to endorsing that strategy in a recent paper suggesting age-targeted lockdowns. They proposed protecting people over 65 by having them isolate for an estimated 18 months until a vaccine becomes available; younger people, facing less health risk, would return to work.

“We could have both way fewer deaths and way less economic pain,” said Michael Whinston, a co-author. In March, when he and three colleagues developed their model, they wanted to avert two extreme prospects: a projected 2 million American deaths if the country didn’t shut down; economic devastation, if it did.

But their approach also assumes that older adults’ only interest lies in not dying.

“We have to find a balance between preserving safety and living,” said Dr. Linda Fried, a geriatrician and the dean of the Mailman School of Public Health at Columbia University. “We all need to do some things to maintain our mental health and well-being.”

Normally, Dr. Fried pointed out, seniors would find decision-making less knotty because the C.D.C. would be providing detailed, science-based guidance for at-risk groups, updated weekly.

“It’s immensely atypical, I believe unprecedented, that we’re not seeing this,” she said. Without that leadership, seniors confront a crazy quilt of changing state and local policies, and “everyone’s on their own.”

That means older people need to consider their individual health status when deciding which risks to take. Their less robust immune systems make it harder to bounce back from serious infection. They’re also more apt to have the underlying conditions — diabetes, serious heart, lung or kidney disease — shown to increase severe illness and hospitalizations. People of color, obese people and men face higher risk.

“If you’re a vibrant older person without chronic illnesses, you’re probably a little more resilient,” said Dr. Fried, quickly adding that “there are no guarantees.”

A calculator developed by researchers at the Cleveland Clinic may provide a clearer sense of individual risk.

Geography matters too. Older people in New Hampshire or Maine — where new cases were falling last week — may reasonably opt for less restrictive behavior than those in Florida and Arizona, where Covid has been surging. (Pay attention to which counties are seeing cases rise and which are doing a good job at observing guidelines.)

“You base what you do on where you are,” said Dr. Nathaniel Hupert, the co-director of the Institute for Disease and Disaster Preparedness at Weill Cornell Medicine, who advises New York State’s Covid task force.

Personal calculations also include what seems most important. Dr. Schaffner and his wife visited her son, daughter-in-law and two grandchildren recently for the first time in months. They sat indoors for two hours — Nashville was too hot for outside socializing — wearing masks, sitting apart, not eating or drinking. But they’re nixing restaurants for now, along with their annual summer trip to Florida.

Even with individual decisions, the basic precautions that public health leaders have urged on everyone, old and young, still apply. Wearing masks in public, maintaining at least six feet of distance from others, avoiding crowds, washing hands — all help protect oneself and others.

Outdoor activities are safer, but “if you have to be indoors, open a window or crack a door,” Dr. Hupert said. “Even a small change in the seal of a room dramatically changes the way aerosols travel and land.”

He also urges his older patients to stay up-to-date on recommended vaccinations, which appear to boost immune responses against illnesses beyond those for which they’re intended. “A whole host of changes in the body potentially can benefit you for months by ramping up the body’s response to viral diseases,” Dr. Hupert said.

Older people I spoke with talked about developing individual strategies. Going places early, before crowds develop. Reserving an establishment’s first appointment of the day. Bringing their own plates, cutlery and drinks to distanced outdoor dinners.

Dr. Schaffner advocates discussing ground rules before issuing or accepting invitations, “so you don’t have to make a decision on the fly.” Call beforehand to ask about a funeral/barbecue/birthday party. Will it be indoor or outdoors? Is there room to distance? Will participants wear masks? If you don’t like the answers, you may elect to meet more safely another time.

In the end, the Nathans abandoned their Lake Placid plans. "Why push it," Nancy says, “if the birthday boy doesn’t want to go.”

But she’s holding onto airline and hotel reservations for a September trip to London. It may not come off — two of three shows she booked have already canceled performances — but “I have two months to daydream about it.”

*From the article here :
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New drug could stop deadly superbug, save tens of thousands of lives

by Chris Adam | Purdue University | Medical Xpress | 10 Sep 2020

Vancomycin-resistant enterococcus (VRE) is among the leading causes of hospital-acquired infections in the United States. An estimated 20,000 people in the U.S. become infected with it each year, and nearly 10% of people who get it die from it.

These superbugs typically develop from infections in the intestinal tract, where the bacteria become resistant to the antibiotic vancomycin. People who stay in a hospital have the highest odds of getting VRE.

A pair of Purdue University researchers from the College of Pharmacy and the College of Veterinary Medicine developed small molecules to combat deadly, drug-resistant enterococcus.

They created their molecules by repurposing a drug that has been used for more than 80 years to treat glaucoma, congestive heart failure and some other health issues. Their work is published in the Journal of Medicinal Chemistry.

"The potency of these molecules and the ability to tune the molecules' properties to target VRE in different compartments of the body make this an exciting project," said Daniel Flaherty, an assistant professor of medicinal chemistry and molecular pharmacology. "I believe our discovery may help to change the way people treat VRE in the future."

"We can have molecules that can be used to treat deadly systemic VRE infections, or through manipulation of the properties of the molecule, design a compound that will reside solely in the gastrointestinal tract to reduce VRE colonization. By working across disciplines at Purdue, we have been able to improve the effectiveness of this drug 600 times better than where we started in treating VRE."

Mohamed Seleem, a professor of microbiology, who co-created the molecules with Flaherty, said the problem with antibiotics on the market is that they are used for a wide variety of illnesses.

"These antibiotics can really rip apart the guts and destroy good bacteria," Seleem said. "Then someone can develop Clostridium difficile, also known as C. diff, which kills about 30,000 people each year in the United States. Scientists across the globe are working on better solutions, but I think we are far away from seeing narrow-spectrum antibiotics proliferate the market."

The Purdue team's small molecules have been shown to target VRE and have the properties necessary to treat VRE in both systemic circulation or in the GI tract, where all VRE infections originate.

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Vials of blood samples are seen on a rack at San Francisco General Hospital.

Those with type A blood at almost twice the risk of getting severely ill from Covid-19

by Peter Fimrite | San Francisco Chronicle | 9 Jul 2020

The roulette wheel that decides who lives and dies from the coronavirus is weighted by the type of blood coursing through the veins of victims, gifting some with innate resistance and dooming others to misery and torment.

Infectious disease specialists say the worldwide pandemic is especially cruel to people with type A blood, which apparently lacks certain compounds that help fight off the disease.

A study published June 17 in the New England Journal of Medicine found that people with type A blood have a higher risk of contracting the disease and suffering complications. The analysis, conducted by an international team of scientists, also showed that people with type O blood were at least partially protected from the virus.

It was one of several recent reports on the phenomenon, which epidemiologists say is not unique to COVID-19.

“People with Type A blood... are more likely to have severe disease and death than people with other types,” said John Swartzberg, an infectious-disease specialist at UC Berkeley. “It doesn't surprise me because we know that blood types are associated with other infectious diseases.”

Blood type is determined by a gene that tells the body what blood cell proteins to make. The different types have different antigens, which determine their properties, including weaknesses and strengths. A blood type that is positive means a person’s red blood cells carry a protein called Rh, also known as the RhD antigen. Negative blood type does not.

Epidemiologists have long known that blood type plays a role in how people’s bodies react to infectious diseases, and type A — positive and negative — appears to be among the most problematic.

For example, people with type A blood have a higher chance of developing certain cancers, particularly stomach cancer. All the different types of blood have agreeable and disagreeable qualities, but type A is associated with higher levels of the stress hormone cortisol, according the National Institutes of Health.

Swartzberg said people with type A blood are also more likely to contract the most virulent form of malaria, known as plasmodium falciparum. The protozoan parasite is transmitted through the bite of a female mosquito.

On the other hand, people with type O blood are less likely to develop inflammation during infections, suffer from heart disease, pancreatic cancer or contract parasitic diseases like falciparum.

The Journal of Medicine study sequenced the genomes of 1,980 COVID-19 patients in Spain and Italy who had suffered respiratory failure and compared their results with an approximately equal number of people who were not sick. The researchers concluded that people with type A blood had as much as a 45 percent higher risk of getting severely ill from the coronavirus.

Another study, of more than 2,000 people in China last March, also found that blood group A had a significantly higher risk of coronavirus infection. That information aligns with other studies, most of them not yet peer reviewed.

In each case, type O blood was linked to lower risk and less severe illness. A study by the genomics site 23andMe calculated that people with blood type O were 9% to 18% less likely to contract COVID-19 than people with other types of blood.

Type O blood is handy in other ways. O positive is the most common blood type, and O negative is compatible with all other types of blood. Because O negative blood can be given to anybody, it is commonly used for transfusions. Studies have shown that people with type O blood also get fewer blood clots, a serious problem among COVID-19 patients.

SARS-CoV-2, the specific coronavirus that causes COVID-19, is essentially a tiny parasite that uses its tell-tale spike proteins to latch onto the much larger human cells, like pepper on an egg. The virus uses the cell’s receptors to worm its way inside, where it replicates itself billions of times and spreads throughout the body.

There are a variety of factors that influence vulnerability to COVID-19, including old age, underlying medical conditions and possibly race, although the high mortality rate among minorities is more likely related to poverty and a lack of medical care. A study, published Wednesday in Nature, said Latino and African Americans are three times more likely than white people to be infected by the coronavirus and nearly twice as likely to die.

Men are hospitalized and die from the virus more often than women, a disparity that researchers have linked to testosterone, the male sex hormone.

Researchers know that the coronavirus targets ACE2 receptors, a protein on the surface of human cells that normally helps regulate blood pressure. Peter Chin-Hong, a professor of medicine and infectious diseases at UCSF, said the genes that make the ACE2 receptors are next to the genes that provide the blood type codes.

“Because they are so close to each other they influence each other in ways we don't understand,” Chin-Hong said. “Things are next to each other for a reason.”

Nobody knows exactly how the coronavirus operates, but some scientists believe the virus, when it infects a new host, carries with it genetic coding — blood type antigens — from its last victim. Apparently, type O blood adapts better to the coronavirus’ coding.

Swartzberg said this may have something to do with the types of carbohydrates, or sugars, on the surface of red blood cells.

“The type A carbohydrate may facilitate the entrance of the protozoan into the red blood cell, causing more severe infection,” Swartzberg said. “People with type O blood, which doesn’t have any of those carbohydrates, may be somewhat protected.”

George Rutherford, a UCSF infectious disease specialist, said caucasians of Mediterranean descent have the highest percentage of type A blood.

“Most of these blood type observations are from Italy and Spain, which have had horrendous COVID outbreaks,” Rutherford said.

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CBD is a powerful antibiotic

University of Queensland | Neuroscience News | 28 Jun 2019

New research has found that CBD is active against Gram-positive bacteria, including those responsible for many serious infections such as Staph aureus and Streptococcus pneumoniae, with a potency similar to that of established antibiotics such as Vancomycin.

CBD, the main non-psychoactive chemical compound extracted from cannabis and hemp plants, has been approved by FDA for the treatment of a form of epilepsy and is being investigated for a number of other medical conditions, including, anxiety, pain and inflammation. While there is limited data to suggest CBD can kill bacteria, the drug has not been thoroughly investigated for its potential as an antibiotic.

Work led by Dr Mark Blaskovich at The University of Queensland’s Institute for Molecular Bioscience’s Centre for Superbug Solutions, in collaboration with Botanix Pharmaceuticals Ltd, an early stage drug discovery company investigating topical uses of synthetic CBD for a range of skin conditions, found that CBD was remarkably effective at killing a wide range of Gram-positive bacteria, including bacteria that have become resistant to other antibiotics, and did not lose effectiveness after extended treatment.

“Given CBD’s documented anti-inflammatory effects, existing safety data in humans, and potential for varied delivery routes, it is a promising new antibiotic worth further investigation,” said Dr. Blaskovich.

Importantly, the drug retained its activity against bacteria that have become highly resistant to other common antibiotics. Under extended exposure conditions that lead to resistance against vancomycin or daptomycin, CBD did not lose effectiveness. CBD was also effective at disrupting biofilms, a physical form of bacteria growth that leads to difficult-to-treat infections.

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Pilot study of psilocybin-assisted group therapy in older AIDS survivors

by Michael Haichin, PharmD | Psychedelic Science Review | 19 Nov 2020

Feasibility, safety, and potential efficacy of psilocybin-assisted group therapy was demonstrated in treating demoralization in this marginalized population.

Evidence for psilocybin-assisted psychotherapy (PcbAP) continues to accumulate for treating a number of psychiatric conditions. However, the majority of modern trials studying this treatment have been time-, staff-, and resource-intensive. A significant amount of two therapists’ time is required as part of pre-drug preparatory sessions, supervision during, and post-drug integration sessions. As a result, concerns about high costs and limited access have loomed over the potential translation to real-world clinical practice settings if it is approved. PcbAP administered in a group setting is regarded as a potential solution, though until recently, no modern trials examined whether it is feasible, safe, or effective.

Why psychedelic group therapy?

Traditionally, plant-based psychedelics like psilocybin, ayahuasca, and peyote were used in group settings by various Indigenous groups for healing and religious purposes. This group framework was replicated in earlier clinical studies of psychedelics in the 1960s-70s, which found promising evidence in treating alcohol use disorder and neuroses, predominantly with LSD. However, those studies were not up to present-day clinical trial standards, thus limiting what conclusions could be drawn about the safety and efficacy of psychedelic group therapy.

In an open-label trial of individual PcbAP for treatment-resistant depression, social connectedness was identified as a possible underlying mechanism of therapeutic change.4 Other contemporary trials’ participants have requested to meet other trial subjects, as well as corroborating the importance of connecting with those who have undergone the challenging-to-describe psychedelic experience. These results suggested that psychedelic group therapy may improve therapeutic outcomes and participant satisfaction.

The historical use, previous research, and more recent findings, combined with the cost-saving potential, pointed to the need to explore the psychedelic group therapy model more rigorously. A research team led by Brian Anderson, MD from the University of California San Francisco, therefore, conducted a pilot study to explore the feasibility, safety, and potential efficacy of psilocybin-assisted group therapy.

Older, long-term AIDS survivors and demoralization

This trial examined a marginalized population unique to psychedelic therapy: older, long-term AIDS survivors (OTLAS) suffering from demoralization. Demoralization, a prevalent response to serious medical illness, is a form of existential distress characterized by poor coping and feeling hopeless, helpless, and without meaning or purpose.5 These individuals were diagnosed with HIV/AIDS when it was considered a terminal diagnosis and lived through the overwhelming loss of loved ones, resulting in demoralization. The average age of participants included in the study was 59 years. This population also has complex past medical and psychiatric histories, reflected in 50% of the trial participants meeting criteria for a comorbid mental health condition (e.g., anxiety disorder, panic disorder, and borderline personality disorder).

Study design

In this single-arm, open-label trial, 18 self-identified gay men suffering from moderate to severe demoralization were enrolled into three cohorts of six. Participants met as a group on four occasions led by two therapists, before receiving a single, individual psilocybin (0.3-0.36 mg/kg) session. Four to six more group therapy sessions occurred after the psilocybin administration to integrate their experiences.

The feasibility was determined by rates of recruitment and retention of enrolled participants. Safety was evaluated with multiple measures and categorized by the severity and rate of any adverse events. The primary clinical outcome was the change in demoralization, assessed by the self-reported Demoralization Scale-II (DS-II), from baseline to end-of-treatment and at a 3-month follow-up. Various secondary clinical outcomes were measured due to the complex psychiatric needs of OLTAS, most notably related to trauma and unresolved grief.

Study findings

Rates of recruitment were high, and attendance to group therapy was 95%, attesting to the feasibility. It is important to note the participants were highly motivated, either on disability or retired, and had flexible schedules to attend group meetings. If the 18 participants received their therapy in the standard 1:2 subject to therapist ratio used in other psilocybin studies, a total of 954 therapist hours would be required. Because of the group therapy format, that time was reduced almost in half, down to 472 hours.

Despite a study population with greater psychiatric comorbidity than any other modern psilocybin trial, the treatment was found to be relatively safe. No psilocybin-related serious adverse events occurred, and two unexpected adverse reactions were detected during post-medication visits (post-traumatic stress flashback and methamphetamine relapse). Fourteen of 18 participants experienced moderate-to-severe expected psilocybin-related adverse reactions that resolved by the end of the administration session. While this is a relatively high adverse event rate, the researchers suspect it is partly related to the clinical complexity of the study population. The most common of those were high blood pressure (67 percent), anxiety (44 percent), and nausea (33 percent).

Demoralization scores were reduced from baseline at both end-of-treatment and at the 3-month follow-up, by an average of 6.67 (SD=6.51) and 5.78 points (SD=6.01), respectively. To put those results in context, the demoralization scale totals 32 points and a 2-point improvement is considered clinically meaningful. A >50% reduction in demoralization compared to baseline was found in 50% of participants at end-of-treatment and 33.3% at 3-month follow-up. Secondary measures related to trauma and grief also showed significant reductions over that time period.

Future research directions

While this pilot study demonstrated the feasibility, safety, and potential efficacy of psilocybin-assisted group therapy in treating demoralization among OTLAS, the results cannot be considered conclusive due to its small sample size and single arm, unblinded design. Larger, randomized, placebo-controlled trials are needed to confirm these promising results. An accompanying qualitative paper with the patients’ perspectives on the group therapy process is expected and can potentially corroborate the value of a group framework.

The results open the door to future studies assessing psilocybin-assisted group therapy in other populations where demoralization is present, such as those with substance use disorders, chronic pain, obesity, and the elderly. The social isolation, shame, and stigma associated with a variety of mental health conditions can be uniquely addressed with group therapy. The trailblazing pilot trial by Brian Anderson and colleagues lays the groundwork for combining that unique capability and the social connectedness brought on by psilocybin and may prove useful to improve access and lower costs should it become an approved treatment.

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