drug interactions with HIV (not interactions with HIV drugs)

[hollywood_cole]

well, not directly with HIV, but with a protein present in HIV+ individuals:
http://www.the-scientist.com/?artic...70/title/HIV-Protein-Boosts-Cocaine-s-Effect/

this was forwarded to me by a biologist friend of mine who thought i'd find the pharmacology part of it interesting (which i did). however, since i have no actual training in that stuff (and since the article's a pretty summary look at a pretty new finding), i didn't feel like my speculation on it was all that well founded. so i wanted to see what people here made of it (also figured this crowd would probably find it interesting regardless of any speculating).

one thought i had: if this phenomenon is occurring via something dopamine related (i'll stay vague rather than try to use more specific language and maybe get it wrong), would other disorders that likely have to do with dopamine imbalance (e.g. gambling addiction or RLS) get affected by this protein?

 

[endotropic]

Here's the journal article discussed in the press release:

Effects of Conditional Central Expression of HIV-1 Tat Protein to Potentiate Cocaine-Mediated Psychostimulation and Reward among Male Mice.

Abstract
As a major neuropathogenic factor associated with human immunodeficiency virus (HIV) infection, HIV-1 Tat protein is known to synergize with psychostimulant drugs of abuse to cause neurotoxicity and exacerbate the progression of central nervous system pathology. However, the functional consequences of the interaction between HIV-1 Tat and abused drugs on behavior are little known. We tested the hypothesis that HIV-1 Tat expression in brain would modulate the psychostimulant effects of cocaine. Using the GT-tg bigenic mouse model, where brain-selective Tat expression is induced by activation of a doxycycline (Dox) promotor, we tested the effects of Tat on cocaine (10 mg/kg, s.c.) induced locomotion and conditioned place preference (CPP). Compared to uninduced littermates or C57BL/6 J controls, cocaine-induced hyperlocomotion was sustained for a significantly longer duration among Tat-induced mice. Moreover, although all groups displayed similar saline-CPP, Tat-induced GT-tg mice demonstrated a 3-fold increase in cocaine-CPP over the response of either uninduced littermates or Dox-treated C57BL/6 J control mice. Induction of Tat also increased the magnitude of a previously-established cocaine-CPP after an additional cycle of cocaine place conditioning. Despite Tat-induced potentiation, extinction of place preference occurred within 21 days, commensurate with cocaine-extinction among saline-treated littermates and C57BL/6 J controls. Re-exposure to cocaine produced reinstatement of an equivalent place preference in Tat-induced GT-tg, or C57BL/6 J, mice; however, induction of Tat protein after the extinction of CPP also produced reinstatement without additional exposure to cocaine. Together, these data suggest that central HIV-1 Tat expression can potentiate the psychostimulant behavioral effects of cocaine in mice.

I think your speculation is as good as anyone's at this point. I think there's (at least) a couple of points that need to be addressed before we can tell if this is a relevant interaction or just a flaming pile:

1) How do the expression levels in the mice relate to the expression levels in infected patients?

2) How does the expression pattern in the mice (astrocytes only) relate to the expression pattern in infected patients?