PITTSBURGH — A study out of the University of Pittsburgh outlines a new technology for targeting Human Immunodeficiency Virus, or HIV.

Published Tuesday in the journal Cell Chemical Biology and funded by a grant from the National Institutes of Allergy and Infectious Diseases, it paves the way for a slice of medicine focused not just on allowing people with HIV to live long and happy lives, but ultimately working to clear the virus from their bodies.

More than 1.2 million people live with HIV in the U.S., according to the Centers for Disease Control and Prevention, and nearly 1 in 8 is unaware of their infection. While antiretrovirals have been approved in this country to treat HIV for decades, they do not destroy the virus, only quell viral load so long as a person takes them.

"The field now as a whole is looking at curative research," said Lori Emert-Sedlak, a research associate professor of microbiology and molecular genetics at Pitt and first author on the paper. "There are many drugs that suppress the virus," she said. "We need to get rid of the virus entirely."

One of those approaches involves targeting a key HIV protein — nef — and Pitt researchers were able to destroy it.

The nef protein is made by a gene in the HIV virus. Related viruses, like Simian Immunodeficiency Virus (SIV), the primate version of HIV, also have nef proteins. The protein shows up shortly after a person is infected and helps the virus replicate in the body. It evades immune responses — and allows the virus to slink by undetected — by removing key cell surface structures that would otherwise alert the immune system of their foreign presence.

"You can't cure something the immune system can't see," said Emert-Sedlak.

Studies have shown that certain people with HIV who have nef-defective genes often do not progress to developing AIDs, pointing to the potential that nef may be a good target.

While past research has focused on inhibiting nef and thus stopping replication of HIV in the body, there's a risk of viral rebound if the person stops taking the drug.

"Although (previous technologies) were effective in blocking some functions of nef, it was difficult to shut everything down, because it has multiple functions" said Thomas Smithgall, senior author on the paper and a professor in the Department of Microbiology and Genetics at the University of Pittsburgh School of Medicine. "(Our complex) is not just a blocker, but a destroyer."

...continued

©2024 PG Publishing Co. Visit at post-gazette.com. Distributed by Tribune Content Agency, LLC.