HIV-1 evolution: ‘Badder’ still isnt ‘Better’

I write about lots of things on ERV, but I didnt anticipate ever getting to the point where I can write new blog posts on new publications by cutting and pasting from old blog posts on old papers...

Lots of news outlets have been talking about this new paper:

Impact of HLA-driven HIV adaptation on virulence in populations of high HIV seroprevalence

Ive covered the themes of this paper several times in the past.

1-- Some people progress to AIDS after HIV infection, some dont, or do so slowly. One of the reasons why one person might not progress to AIDS would be their particular MHC Class I allele (what 'flavor' of MHC Class I you inherited from your parents).

2-- HIV-1 is adapting to this MHC Class I selective pressure. We would LOVE to have an HIV vaccine that protected people by training their immune systems to see bits and pieces of HIV in MHC Class I, but that window is closing.

3-- HIV-1 adapting to humans does not mean it is becoming more pathogenic. In fact, we would not expect HIV to follow that particular trajectory. That has happened in no other SIV-primate. In every other primate, co-evolution with SIV has led to a sort of mutual 'Meh.' And, studies specifically addressing the evolution of HIV fitness in humans have found that HIV is doing the same in humans.

This paper is more data to support some older ideas in HIV. While I dont quite understand the media frenzy, with HIV, you cant ever assume things or take old ideas for granted, so I am quite happy they performed this work.

 

More like this

For some reason, pop news became enamored with this paper last month (unfortunately while I was away at a conference): HIV infection en route to endogenization: two cases Inexplicable media frenzy-- Scientists find mechanism for spontaneous HIV cure French scientists find genetic mechanism by which…
HIV-- Its a terrible game of chance. Odds of HIV transmission are, superficially, rather low (its no measles). And, we can make the risk of transmission even lower various pro-active ways-- antiretroviral use to keep viral loads down in HIV+ people (especially in pregnant women about to give birth…
*sigh* *heaviersigh* One of the many problems we have when treating HIV patients is that HIV can hide (latent). So a cell can be infected with HIV, but not show any signs of being infected. The HIV provirus is just chillin in the host cell DNA, not making any viral proteins/babby viruses, so the…
This is a repost from the old ERV. A retrotransposed ERV :P I dont trust them staying up at Blogger, and the SEED overlords are letting me have 4 reposts a week, so Im gonna take advantage of that! I am going to try to add more comments to these posts for the old readers-- Think of these as '…

I've been kind of surprised that antivaccine crank Cynthia "CIA" Parker hasn't stapled this to her freak flag yet. I wish I had noticed Fig. S3D earlier.

I read somewhere( Peter Cresswell,December 23, 2014, The first step of peptide selection in antigen presentation by MHC classI molecules) that the MHC class I molecules select and present a limited set of antigen peptides from a vast that are provided. So MHC class I molecules technically go through rounds of considering and rejecting peptides until peptides with high affinity are acquired for presentation. This explains the effect on the progression of HIV.
15073883

By Nomaswazi Mase… (not verified) on 16 Apr 2015 #permalink

How do you get tested for which MHC molecule you have?

By Simangele Hlaza (not verified) on 16 Apr 2015 #permalink