If youll recall one of my first posts on SciBlogs, I urged everyone not to give up on an HIV-1 vaccine. Ya, we are sucking right now, but if we can get over our ‘AAAAAAAAAAAAHHHHH!!!!!’ response to HIV-1, refocus on the basic virology of HIV-1, we can get this mo-fo.
The first step in the right direction was a paper published a couple days ago in PNAS:
If youre wondering about who the gawds are in HIV-1 research, just look at the last three names on this paper: Bette Korber, Beatrice Hahn, George Shaw.
Heh. What they focused on was a really hard thing to study in the lab– what happens right after someone is infected with HIV-1. What happens right then? Are you infected with one virus? Is there a huge breech of a mucosal barrier, and lots of viruses get through? What are the molecular characteristics of the viruses that get through? Those first few moments are The Key for making an effective HIV-1 vaccine.
But these questions are nearly impossible to answer, because who the hell just happens to be collecting their own blood right before and right after they get infected with HIV?
Well, the gawds of HIV research know where to look for such samples– plasma donation banks. They got samples from 102 people who donated plasma often enough that they caught a donation right after infection. They isolated and sequenced lots of envelope genes (next ‘Intro to ERVs’ entry!), and tried to elucidate the relationship between the envelope sequences. If there was lots of diversity, that means that there were lots of different kinds of HIV-1 that established infection. Not a lot of diversity, fewer kinds of viruses got through. So what did they see?
What they found–
Of the 102 patients, 78 were initially infected by one genotype of virus. This is a point I was annoyed with the authors– they write ‘evidence of productive clinical infection by a single virus’– thats not what their data says. Their data says that these patients were infected with one type of envelope sequence. Not that it was ‘one virus’. There could be more diversity in other areas of the genome that they arent seeing, but because infection (viral entry) is mediated by the envelope proteins, that is the important sequence. Just want to clarify that point for ERV readers, since the paper is open for everyone to read ?
What this means–
There might be molecular determinants of HIV-1 transmission. Only one ‘kind’ of virus gets through. Is this random? Or is it a predictable, biochemical process that only certain variants of HIV-1 are good at? If its the former, were screwed. If its the latter, we can make vaccines that prevent transmission.
Im crossing my fingers for the latter, and hoping this cherub can get her act together to help out the gawds ?