Scientists have discovered how HIV evades detection by the immune system protein ZAP, a finding that could lead to improved therapies against the virus that causes AIDS.

ZAP (zinc finger antiviral protein) is a natural barrier to infection by viruses and serves as the first line of defence for the immune system. When a virus enters the body, ZAP binds to the viral RNA and prevents it from replicating.

However, HIV has evolved a way to outsmart ZAP. The virus produces a protein called Nef (Negative factor) that binds to ZAP and blocks its ability to bind to HIV RNA. This allows the virus to replicate freely and spread throughout the body.

"Our study reveals the molecular mechanism by which HIV Nef protein interferes with ZAP function," said Dr. Zixin Deng, lead author of the study and a researcher at the University of California, San Francisco (UCSF). "This finding provides a potential target for developing new drugs against HIV."

The research, published in the journal Cell Reports, could also help explain the varying susceptibility of different individuals to HIV infection. ZAP levels vary between individuals, and people with higher ZAP levels may be less likely to contract HIV.

"Understanding the interplay between HIV Nef and ZAP could lead to the development of novel therapeutic strategies to enhance ZAP activity and block HIV replication," said Dr. Robert J. Gorelick, professor of medicine at UCSF and senior author of the study.

Current HIV therapies work by targeting the virus itself or by blocking the enzymes that it needs to replicate. These drugs can be effective in suppressing the virus, but they can also have side effects and can lead to drug resistance.

The development of new drugs that target the interaction between HIV Nef and ZAP could provide a more effective and less toxic treatment option for people with HIV.