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