Scientists Discover Why Some People May be Immune to HIV-1

HIV-1 rapidly sickens some individuals, but struggles to gain a foothold in others. Now, scientists may have an explanation as to why that is. A new study of genetic variation in HIV-1 and in the cells it infects reveals a chink in HIV-1's armor that may explain the puzzling difference.

HIV-1 infects people by invading immune system cells known as T lymphocytes, hijacking their molecular machinery to make more of themselves, and then destroys the host cells. This leaves an infected person more susceptible to other deadly diseases.

Yet T lymphocytes aren't completely undefended. Among their anti-virus mechanisms is a class of proteins known as APOBEC3s. These proteins have the ability to block HIV-1's ability to replicate. Yet HIV-1 has a counter: a protein called Vif. This protein cons the T lymphocytes into destroying their own APOBEC3s.

In this case, the researchers suspected that differential susceptibility to HIV-1 might be linked to genetic variations in this system. The scientists took a closer look and found that HIV-1 infection boosts the production of one kind of APOBEC2, called APOBEC3H. This suggests that this protein is a key player in fighting back. The researchers then used an experimental technique known as separation of function mutagenesis; this revealed that different people have different strengths and potencies of APOBEC3H. More specifically, the scientists found that the stable variations of this protein successfully limited HIV-1's ability to replicate.

"This work shows that the competition between the virus and the host is still ongoing," said Eric Refsland, one of the researchers, in a news release. "The virus hasn't completely perfected its ability to replicate in humans."

The findings reveal a bit more about HIV-1. More specifically, it shows why some people are better at coping with the virus than others. This, in turn, may lead to possible avenues of new research in the future.

The findings are published in the journal PLOS Genetics.