AIDS researchers found clues that help explain why an HIV vaccine worked better for some people than others in a study, advancing scientists’ understanding of the virus.
Researchers identified two genetic “signatures” in the virus among people who contracted HIV despite being vaccinated in a 2009 trial in Thailand. Those genetic features may have helped the virus to evade the vaccine, according to the U.S. Military HIV Research Program in Silver Spring, Maryland, which published the findings today in the journal Nature. The study is also being presented at an AIDS conference in Boston.
The new research shows that the vaccine, the only one that has shown any success fighting HIV, was more effective combating the virus when the signatures included one specific mutation and lacked another one, protecting in as much as 80 percent of the cases. The findings may help scientists design future vaccines, said Jerome Kim, who led the research.
“It’s as though you had 50 different kinds of fish that can potentially be caught, and you catch most of them, but by looking at the ones that escaped you can tell what the problems are with the net,” Kim said in a phone interview.
The 2009 trial on Sanofi’s Alvac and VaxGen Inc.’s Aidsvax surprised researchers by showing that the two vaccines, which had failed in tests on their own, reduced infections by 31 percent over three years when used in combination. Researchers have been scouring the blood of participants in the trial for clues to help improve on the result.
Kim and colleagues found the two genetic features in an area of the virus’s outer coat called the V2 loop, an area on HIV’s surface that is constantly changing, confounding vaccine hunters for more than three decades.
An analysis published in April showed that those who were protected against HIV in the trial developed antibodies against the V2 loop, suggesting the region plays a key role in the virus’s ability to infect, Kim said.
Today’s findings combined with the April study show that the antibodies generated by the vaccine forced the virus to mutate to escape it, Kim said.
Kim and colleagues are part of a consortium called the Pox Protein Public-Private Partnership that is planning follow-on trials to the Thai study, including one in South Africa where it’s hoping to generate a larger and longer-lasting response to V2.