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Covid-19 Outbreak of new SARS-like coronavirus (Covid-19)

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6am-64-14m said:
Now, when ya put something before your own well being... can ya see how it would/could/maybe should (?) feel like a mf is under attack not only with the core threat but with other "influences" providing fuel to the threat helping create the stage for an all out war? Yeah, it is a mental thing at the moment. I pray to whoever that it does not go any further than my feeble mind. It wont. I feel confident of this.
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9xWdvjK.jpg

no vaccine yet. btw. what strain. would like to kno. 👽
 
atara said:
Photons are not "small" in space; in fact they may be arbitrarily large (resonant photons in a cavity may be considered to occupy the whole space, overlapping with each other). They are small in energy, though.
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Yep, you're right. I misspoke. I was more trying to say that the scales in which we talk about photons and other elementary particles are generally waaay smaller than that of even viruses. But yea I totally botched it. :D
 
A photon is a period of a light wave a particle. It ranges on a continuum from infinitesimally small to large.
 
JessFR said:
Yep, you're right. I misspoke. I was more trying to say that the scales in which we talk about photons and other elementary particles are generally waaay smaller than that of even viruses. But yea I totally botched it. :D
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i'd interpreted you as meaning the wavelength of visible light, as that's what our eyes detect, and is on the order of nanometers. i just looked up the size of SARS-COV2 and it is apparently 60-140nm so they are within the same order of magnitude of visible light. which actually means, colour etc is meaningless on that scale such things only pertain to objects that are large enough to reflect visible light. i guess you could create a visible light analogue of radio to transmit data on, but our eyes have no mechanism to receive that.

i really don't know why i'm continuing to pick apart this theory when not even its originator (in this thread at least) has bothered to defend it.

none of this matters, clearly viruses are not transmitted by eye contact and i'm at a complete loss as to why anyone would suggest they are except to try to distract from/obfuscate the truth.
 
JessFR said:
Fun little factoid children and to a lesser degree many adults can also see into infrared.
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The article I posted, which was pretty interesting to me, links to this article to explain how the eye can detect infrared.
www.pnas.org

Human infrared vision is triggered by two-photon chromophore isomerization

This study resolves a long-standing question about the ability of humans to perceive near infrared radiation (IR) and identifies a mechanism driving human IR vision. A few previous reports and our expanded psychophysical studies here reveal that humans can detect IR at wavelengths longer than...
www.pnas.org www.pnas.org
 
Chemists use infrared to study vibrational modes between atomic nuclei. I was way into UV/Vis to study electronic excitations of great interest to me was the d-pi* Metal to ligand charge transfer which was in the case of Ru(bpy)3 luminescent.

Luminescence is when an excited state electron radiatively decays and releases a photon of light.

UV light is used as an airplane disenfectant to quickly kill corona. And we're back.
 
Interesting concept, but missing the point perhaps? Photons are very probably not a transmission agent. But there is significantly more of the other 'gunk' and particulate matter we breath in on a day-to -day basis. Pollen, car exhaust fumes, et al which may be acting as transmission agents which are larger and heavier than the virus itself and some of which could/might pass through home-made or surgical masks.

Could it be then that the original virus, or its subsequent mutations, are indeed air-borne over short distances of 15-20 ft?
 
empeebee said:
Could it be then that the original virus, or its subsequent mutations, are indeed air-borne over short distances of 15-20 ft?
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yes that's the entire point, both the original virus and existing mutations are air borne over short distances. though its also believed that you need a relatively high viral load to get a severe infection, so you'd need to be breathing air from an infected person for a protracted period rather than just walking past them in the sttreet.
 
Well yeah, that's kinda my point.

I think, or would like to think anyway, that we appreciate that standing 3 ft away from another shopper in a supermarket checkout queue is hazardous in the current environment. I am going more along the lines of walking along the sidewalk where someone 15 ft in front of you, asymptomatic but carrying, coughs into the breeze. The virus attaches to pollen/NO2 exhaust particles which you then breathe in causing you to be infected.

What would the viral load need to be over any given distance of 5ft, 10ft, 15ft, etc., for the virus to pass from person A to person B? I don't think I have seen any stats on that other than 6 ft is the recommended distance even though I have seen modelling that transmission can occur, at decreasing rates, at a distance of 15-17ft in enclosed air-circulated environments such as supermarkets where transmission could (note could) occur from aisle 1 to aisle 4 - aisle spacing dependant.
 
Some information about the COVID-19 variants.

4 Big Myths About COVID-19 Variants People Need To Stop Believing​

There's a lot of misinformation about the coronavirus strains from the U.K., South Africa and Brazil. Here's what you actually need to know.​

Over the past month, news of new SARS-CoV-2 variants has emerged from around the globe: first in the United Kingdom, then South Africa and Brazil. Now those strains are in the United States.

The reports are unsettling. Many of us were finally hoping for better days, thanks to the vaccine rollout and a slight dip in positivity rates in this country. Instead, infectious disease experts warn that the next six to 14 weeks may be the “darkest” period of the pandemic yet if we’re not careful.

We’ve been thrust back into a period of real scientific uncertainty, but it’s also not all bad news. Struggling to make sense of what’s going on? Here are four common myths about the COVID-19 variants — and some details on what we know (and don’t) so far:

Myth #1: The COVID-19 variants caught health experts by surprise.​

The recent explosion in COVID-19 variant-related news coverage may make it seem as though these strains popped up unexpectedly. But this type of situation isn’t new. As the Centers for Disease Control and Prevention explains: “Viruses constantly change through mutation, and new variants of a virus are expected to occur over time.”

Since the pandemic began, health officials have been ready for new strains to develop and spread.

“The variants are not unexpected,” said Priya Soni, a pediatric infectious disease specialist at Los Angeles’ Cedars-Sinai Medical Center. She added that COVID-19 appears to actually be mutating at a slower rate than other viruses, like the seasonal flu.

That said, the fact that some of these variants have spread widely at this point does suggest they were around before health officials really noticed. That is, in part, because genomic sequencing of the virus has not been happening nearly enough.

“Though the initial U.K. variant was detected in November, it appears that most of the circulating virus in the U.K. now is this predominant variant — up to 60%,” Soni said. “This tells us that the variants were present much longer before we discovered them.”

The CDC also notes that some variants, like the strain discovered in South Africa, emerged months before they began getting international news coverage.

Myth #2: The COVID-19 variants are more dangerous.​

Right now, no one really knows whether the new variants are more likely to cause severe illness or death.

Recently, officials in the U.K. suggested that variant could be more deadly than the original virus, which ran counter to their initial assessment that the variant was just simply more contagious. When providing this new-ish take, the U.K.’s chief scientific officer offered an example:If 1,000 men age 60 and up were infected, the original virus would likely kill around 10 of them, whereas the new variant might kill 13 or 14.

But that could just be because more people are getting infected since the variants are more transmissible, not because the strains themselves are causing the deaths. The new variants “spread more easily and quickly than other variants — which may lead to more cases of COVID-19,” according to the CDC. That could lead to more hospitalizations and possibly more deaths.

Experts do expect that more variants could emerge as the pandemic continues ― but they won’t necessarily be worse.

“In general, the way variants evolve over time is they become more infectious and less virulent,” said Eric Vail, director of the molecular pathology program with Cedars-Sinai. He added that viruses don’t want to kill their hosts, because they want to continue spreading.

“It’s less likely that a more deadly form would evolve,” he said.

Myth #3: Our current vaccines don’t work against the COVID-19 variants.​

At this point, both the Pfizer and Moderna vaccines (which are the only ones currently approved for use in the U.S.) appear to protect against the known COVID-19 variants to some degree.

Moderna and Pfizer have both said their vaccines are less potent against the South Africa strain. That is not, however, the same as saying those vaccines don’t work — or work well, even. Also, both drug manufacturers are working on boosters they hope will be even more effective at fighting against COVID-19 variants.
New data on Johnson & Johnson’s one-shot COVID-19 vaccine, which could be available for use in the coming weeks, does suggest it is not as effective against the South Africa variant. (But again, that doesn’t mean it doesn’t work at all.)

On the whole, physicians and researchers are really hopeful that drug manufacturers will be able to quickly pivot and adapt to new variants as they emerge, especially since mRNA vaccines are more programmable.

“Because these are mRNA vaccine platforms, the changes to the vaccine as mutations occur can be made quite quickly because of our ability to sequence out the specific mutations in real time,” Soni said.
So plan to get a vaccine whenever one is available to you, Vail urged. “Don’t wait. Don’t say, ‘Oh, I’ll wait for the booster,’” he said. “Get it when you can.”

Myth #4: We can’t keep these variants — or future ones — from spreading.​

Yes, the new COVID-19 variants are definitely spreading rapidly, both around the world and probably here in the U.S. The CDC has warned that the U.K. variant could be the predominant strain in this country by March.

That might sound pretty startling, but there are known ways to mitigate it. All of the protective strategies that have helped in the fight against the original strain of the virus can also help prevent the spread of variants.

“There is a real ability to prevent the spread of this virus,” Vail said, pointing to proven measures like mask-wearing, hand-washing and social distancing. Health officials like Dr. Anthony Fauci, the country’s top infectious disease expert, say now is a good time to double-mask, which can create a stronger shield against viral particles.

Our most potent tool is the vaccine. So again, be sure to get vaccinated as soon as you can. It’s possible that the general public will be vaccinated by this summer.

“We’re in a race with the COVID-19 variants, and our chariots are the vaccines,” Soni said. “Ultimately, if we can speed up the process of mass vaccination, we can win the race and thus limit the potential implications of these variants.”
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www.huffpost.com

4 Big Myths About COVID-19 Variants People Need To Stop Believing

There's a lot of misinformation about the coronavirus strains from the U.K., South Africa and Brazil. Here's what you actually need to know.
www.huffpost.com www.huffpost.com
 
An interesting piece that describes viral interference, which might explain why the flu infections are down with COVID.

A viral mystery: Can one infection prevent another?

In September 2009, the H1N1 swine flu had arrived in Portugal, Spain, and the UK, so France braced itself for cases of the infection.

Indeed, the number of people in France with respiratory symptoms soon increased. But they did not seem to have H1N1. France registered only sporadic positive tests for the new swine flu for most of that September and the first half of October. When H1N1 finally took hold in France, it was much later in the fall than expected. And that got scientists thinking: Why?

A flurry of papers since then have narrowed in on a beguiling hypothesis: The pandemic flu was deflected by the common cold.


For many people, Covid-19 has revealed, in terrifying detail, the bizarre nature of viruses. Beneath the surface of our daily lives is a constantly shifting ecology of pathogens that often behave in unexpected ways. In France in 2009, infections by rhinoviruses, which usually cause colds, were spiking when H1N1 was expected to arrive, and when they petered out, the pandemic flu took off. Since then, studies have found that instances in which people have two viruses at once are rarer than chance alone would predict. That suggests that having one protects you from the other, at least for a while — somehow.

During the Covid-19 pandemic, cases of many other respiratory infections have plummeted. This is likely a result of social distancing protocols, but it’s also possible that viral interference, the phenomenon of viruses affecting each other, may be involved. This insight could offer a head start on fighting future pandemics. With a deeper understanding of our viral ecology, what if, someday, we could use viruses against each other?

In recent years scientists have developed a much more sophisticated picture of what bacteria do to us and for us. They’ve been exploring how our health is shaped by the mix of beneficial and dangerous bacteria in our microbiomes. Now viruses may merit a reexamination as well.

The idea that viruses might interfere with each other is old — as old as vaccination. Edward Jenner, the English doctor who helped develop the practice of inoculating against smallpox in the 18th century, noticed it. Inoculation involved infecting a person with the milder cowpox virus. But if the patient had herpes, then it did not work as well. It was as if having two active infections at once altered how the immune system responded.

Over the next two centuries, scientists reported more and more situations in which it was clear that infections didn’t operate in a vacuum. One 1950 review article even called it a “well-known fact” that having one virus could inhibit the growth of another.

The topic is not frequently discussed these days, though. Viral interference that protects people can be difficult to study and is generally overlooked, says Stacey Schultz-Cherry, an infectious disease researcher at St. Jude’s Hospital in Memphis, Tenn. That’s because, she explains, situations in which simultaneous infections cause a worse prognosis are so much better known. The flu, for instance, is notorious for opening the door to bacterial pneumonia. Small studies from the beginning of the pandemic suggest having both the flu and Covid-19 is worse than having either alone.

But the worst-case scenarios might mask something profound about what often happens as our immune systems encounter viruses all day, every day, says Michael Mina, an epidemiologist at Harvard Medical School and Brigham and Women’s Hospital. “Viral infections may actually protect people from other viral infections — or bacterial infections — by stimulating immune responses, by keeping our innate immune system on its toes all the time, with these constant little pushes and nudges,” he says. “They are like training for us,” he suggests.

Adaptive immune defenses target specific pathogens, and these are what protect us after we’ve been vaccinated. But innate immunity is more all-purpose. After studying the H1N1 flu, Ellen Foxman, an immunologist at the Yale School of Medicine, and colleagues released a paper in October suggesting that once the innate immune system is activated by one pathogen, the body can repel another invader.

To model what might have been happening during the swine flu pandemic, the researchers grew human airway tissue in the lab and infected it with rhinovirus. Then, three days later, they gave it the H1N1 flu. They were intrigued to see that the flu virus just fizzled out, and they determined that the rhinovirus had switched on a number of genes that produce innate immune proteins. Suspecting that molecular messengers called interferons had flipped those switches, they treated the tissues with a drug that blocked interferons and ran the experiment again. “Lo and behold, the influenza grows just fine,” says Foxman. Interferons produced to fight the rhinovirus had been beating back the flu.

A number of viruses trigger the interferon response, and it’s possible that any of them could make the body put up stiff resistance to a new infection for some period of time. For instance, the team didn’t test whether having the flu first would stop a rhinovirus in its tracks, but it’s plausible, says Foxman. That might explain why flus and colds have alternating peaks every year. There are a lot of reasons why one virus might take center stage over others, including human behavior, school schedules, and climate. “But you really wonder if viral interference is one missing piece of that equation,” Foxman says.

In the current pandemic, the same questions are at play. While social distancing and masks are reducing the incidence of seasonal flu, perhaps the prevalence of Covid-19 is cutting it down further. Or, says Schultz-Cherry, maybe the flu would have slowed down Covid-19. They’re questions that can only be answered with further research, but they are worth asking.

Because the new research demonstrates how one infection can stop another, it hints at the possibility of unusual new therapies somewhere down the road. One can imagine viruses engineered to provoke just enough of a response to protect us against more dangerous things for, say, the next week — a benign infection to block an immediate threat. On a more practical level, says Schultz-Cherry, a protective interferon response might someday be generated in just the right places in the body by something like a nasal mist. For people at high risk, interference might provide a shield.

On the larger scale, these immune responses are the result of eons of coevolution between humans and viruses. Is it possible that after our long dance with these self-replicating snippets of genetic code, there are viruses that do us more good than harm? Mina suspects that medical research’s focus on the negative outcomes of viral infections may have blinded us to that reality.

“We miss these beautiful interactions that probably, evolutionarily, are completely working for and with us as humans, and not against us,” he continued. “The microbiome is a great example. . . . We saw bacteria everywhere and thought, maybe they’re good. Turns out they’re essential.”
Click to expand...
www.statnews.com

A viral mystery: Can one infection prevent another?

Our immune responses are the result of eons of coevolution between humans and viruses. Is it possible that after our long dance with these self-replicating snippets of genetic code, there are viruses that do us more good than harm? via @BostonGlobe
www.statnews.com www.statnews.com
 
cduggles said:
An interesting piece that describes viral interference, which might explain why the flu infections are down with COVID.


www.statnews.com

A viral mystery: Can one infection prevent another?

Our immune responses are the result of eons of coevolution between humans and viruses. Is it possible that after our long dance with these self-replicating snippets of genetic code, there are viruses that do us more good than harm? via @BostonGlobe
www.statnews.com www.statnews.com
Click to expand...
Up regulated innate immunity would do that. It is energetically and metabolically costly and gets wound down pretty quickly because epithelial cells that are running in safe mode don't work very efficiently.
Recent active infection with vaccine flu has been shown to protect to a degree against other different respiratory infections, this effect is only with live infections and has been seen in flumist live infuenza vaccine but not with inactivated vaccines. The bad news is that a lot the people who do badly with covid have auto-antibodies to interferon so the upregulation of the innate immunity is screwed up. So the people who do badly with COVID would gain limited or no protection from other previous infections because the mechanism needs B interferon to work which is screwed by the autoantibodies. The mystery is how do a lot of people clear coronavirus without generating detectable antibodies? it looks like innate immunity and IgA is key IgM may also be useful. Circulating IgG can help reduce severity once the virus gets beyond the epithelial barrier but that is like shutting the barn door once the horse has bolted. The data is mixed people with the highest IgG antispike titers (highest amount of antibodies) also had the most severe ilness (which way round the causal relationship is unclear, are high IgG antibodies caused by severe infection or do they lead to more severe infection because other systems don't work?) . Needless to say current vaccines mostly produce IgG antibodies and some T cells, they are barn door closers and appear to reduce serious illness.

This general non specific up-regulated innate immunity is why you don't read out vaccine efficacy 7 or 14 days after dosing...wait a minute NuScience (TM) did exactly that. Because the uprated innate immunity caused by the reactive vaccine gives a short lasting boost to general immunity. FWIW Pfizer BioNtech or Moderna efficacy against symptomatic disease is not 90% or even 80% after longer periods. instead roughly 80% after months based on the numbers that are around, with a constant rate of decline, Wild guess is 60% efficacy for symptomatic infection after 6 months. no real effect on infection and 30% decline in transmission because asymptomatic people are 2x worse transmitters, but asymptomatic people are not in bed feeling shit instead they are out there sharing their respiratory droplets perhaps twice as generously.

The more prosaic explanation for lack of influenza is the lack of people traveling from China where new flus are created by backyard recombination using ducks and pigs and stuff, so the influenzas that are still around are at least a year old and therefore not new to the immune systems of most people. On the other hand 2020-21 or perhaps 21-22 flu season could be big because the pigs and the ducks have been brewing stuff for at least a year which would make the distance from current immunity rather larger than normal. As demographics mean populations age and become less healthy overall novel epidemics are going to be more frequent. If that is the case then this future feature is pretty much baked in. Which sucks.
 
the russians were always telling the truth there spunik v 91.6% effecive

www.bbc.com

Russia's Sputnik V vaccine has 92% efficacy in trial

Trials with 20,000 volunteers show the vaccine gives a high level of protection against Covid-19.
www.bbc.com

germany might buy spunik v now.

I want spunik v i dont want the fucking ofxord trash which is 62% effecticve. pzfier will probably not get here for ages since the Eu are a bunch of stingy cunts stopping exports
 
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