Scientists have discovered why a small minority of people are naturally resistant to the virus that causes AIDS, a finding that could be key to creating a vaccine.
Researchers from Simon Fraser University and their colleagues in the United States, Japan and Germany found the secret lies not in the number of infection-killing cells a person has, but in how well they work. In a small number of people, a strain of “killer” cells called cytotoxic T lymphocyte cells can detect and kill HIV-infected white blood cells.
Until now, it has been well known that people with HIV “have tons of these killer cells,” said Bruce Walker, an infectious diseases expert at the Ragon Institute in Massachusetts.
“We have been scratching our heads since then, asking how, with so many killer cells around, people are getting AIDS. It turns out there is a special quality that makes them [some cells] better at killing.”
SFU researchers Mark Brockman and Zabrina Brumme worked with doctors at the Ragon Institute to design the study comparing how people progressed from HIV to AIDS.
“We know different people will progress to AIDS in a varying amount of time. Some people progress very quickly and some very slowly,” said Brockman. “The Boston lab is interested in people progressing the slowest.”
About one in 300 patients is able to control HIV infection naturally, without drugs. “If we understand what that one in 300 is doing [differently], we could be developing vaccines and therapies.”
That tiny minority can be explained in part by “lucky” genetics, and whether their immune system assigns cytotoxic T lymphocyte (CTL) cells – known as “killer-T cells” – to attack the virus.
The study showed that the strain has molecules called receptors that are better able to identify HIV-infected white blood cells for attack.
The study, published in the Nature Immunology Journal, looked at 10 infected people, of whom five took antiretroviral drugs to keep HIV under control while five were so-called elite controllers who remained naturally healthy.
HIV kills a type of white blood cell called CD4, leaving people with AIDS wide open to other, opportunistic and potentially deadly infections.
“What we found was that the way the killer cells are able to see infected cells and engage them was different,” said Walker, adding attempts at creating vaccines had so far failed because the T-cell receptors they generated were not the efficient type.
But while the research has showed scientists how to find and measure the good cells, they still do not yet know how to generate them.
“We now think, in the lab, we can identify the cells that are more functionally associated with slow progression,” said SFU’s Brock-man. “The next big question will be to develop a vaccine. That will be a long time in coming, but this gives us a diagnostic test we think is useful,” to guide that research, Brockman said.