This week, researchers from Yerkes and Emory Vaccine Center led by Cindy Derdeyn published a paper that I first thought was disturbing. It describes how monkeys vaccinated against HIV’s relative SIV (simian immunodeficiency virus) still become infected when challenged with the virus. Moreover, it’s not clear whetherÂ the vaccine-induced antibodies are exerting any selective pressure on the virus that gets through.
But then I realized that this might beÂ an example of “burying the lead,” since we haven’t made a big hoopla about the underlying vaccineÂ studies, conducted by Rama Amara. Some of these studiesÂ showed that a majority of monkeys can beÂ protected from repeated viral challenge.Â TheÂ more effective vaccine regimens include adjuvants such asÂ the immune-stimulating molecules GM-CSF or CD40LÂ (links are the papers on the protective effects).
This was some helpfulÂ perspective. News has come this year about apparently very effective vaccines (Ebola) and lessÂ effective ones (malaria). The HIV vaccine field is gearing up for a follow-up in South Africa to the RV144 Thai trial, the first to show any protectiveÂ effect at all.
Taken together, the non-human primate resultsÂ mean HIV vaccine researchers have made some progress onÂ one puzzle: how to cajole the immune system to make neutralizing antibodies, at least against SIV. However, aÂ second puzzle remains –Â how to get those antibodies to the right places in the body, on the mucosal surfaces where the virusÂ is transmitted, such as the rectum and vagina.
A thirdÂ puzzle, how to deal with the varietyÂ of HIV strainsÂ that are out there, is addressed by a Journal of Virology paper, whichÂ Derdeyn and colleagues recently published. The bottom line:Â tuning theÂ viral part of aÂ vaccine, butÂ not adjuvants,Â will beÂ key for tacklingÂ virus diversity.