Treatment for HIV patients may soon be expanded due to research determining a new way to cripple the virus’s drug resistance, according to a report published last week by scientists from UC Berkeley and the National Institutes of Health.

The researchers determined the importance of a viral protein produced by HIV that plays a critical role in its ability to spread and take over a patient’s cells. The enzyme, Nef, must bind to a protein on cells in the victim’s body in order to fulfill its duty in HIV infection.

This particular binding spot for Nef could be the next hot spot for future HIV treatment that will focus on cell proteins instead of viral proteins, according to the paper, published in the online journal eLife.

“The HIV virus only has 15 proteins, yet it can do really complicated things to cells,” said James Hurley, co-author of the study and campus professor of biology. “Most of what it does, it does by hijacking our cells’ proteins and turning those proteins against us.”

Current treatments for HIV focus on three main proteins – protease, reverse transcriptase and integrase – that are found in the virus. Such treatments are able to mitigate further, more intensified infection by inhibiting the enzymes’ functions and preventing them from latching onto and overcoming more host cells.

Such medication, however, has led to the development of dangerous viral strains that are able to resist the treatment, causing scientists to seek alternate avenues for drug creation.

“The HIV virus rapidly acquires drug resistance, which is very dangerous,” Hurley said. “Its proteins can evolve very quickly. But if you target cellular proteins instead of viral proteins, that (drug resistance) is not gonna happen. Our own cells simply are not adapting that fast.”

This understanding of Nef could kick-start the creation of a new set of drugs that will be able to avoid the development of virulent, drug-resistant viral strains.

New types of drug cocktails for patients would still not fully eliminate the virus, though. By the time symptoms appear and the virus is detected, viral DNA will have already been incorporated into the victim’s genome. The only way to completely remove the virus is to kill all infected bodily cells – an extremely dangerous process, Hurley said.

Instead, the scientists hope an improved understanding of Nef’s functionality will simply reduce drug resistance in HIV and allow treatment to be more effective in the future.

“We’ve seen the possibility to develop a new HIV-specific drug,” said Sang Yoon Park, co-author of the study and visiting fellow at the NIH. “It might be possible to eliminate the Nef function, and if we can interrupt that process, it will be very helpful to prevent HIV propagation.”