A new study released today in the Journal of Virology gives insights into how the HIV-1 virus, which often persists in the body despite antiretroviral treatment, reemerges when treatment stops. More importantly, the study also gives clues on how to stop this reemergence from occurring.
We wanted to answer the question 'How does HIV, the virus that causes AIDS, bounce back when treatment is stopped, even when undetectable after many years of highly efficacious treatment?'" Dr. Florian Hladik, senior author
He is a research professor in the Department of Obstetrics and Gynecology at the University of Washington School of Medicine.
"In principle, we know how HIV persists by hiding in the genome of infected cells in the form of so-called latent provirus," added lead author Dr. German Gornalusse, who is also in the obstetrics and gynecology department of the UW School of Medicine. "During treatment, these latently infected cells are usually quiet, but when treatment is stopped some of them resume to make the infectious virus. If we know how these cells are triggered to produce virus and where in the body this happens, we will be better able to prevent reemergence of HIV."
Curing HIV faces some of the same hurdles as curing cancer, Hladik noted. Even with the best imaginable curative treatments, which notably all still remain experimental, some infected cells will likely remain.
This study looked at the mechanisms of how HIV-1 provirus containing cells may be triggered into producing HIV in female patients.
To mimic latency, the researchers used human T lymphocyte lines containing HIV provirus. Using primary epithelial cells, harvested from gynecological surgeries from nine donors, the researchers found that epithelial cells from the endocervical canal of the human uterus were particularly effective in triggering latent HIV to remerge. This capacity was enhanced when the epithelial cells were infected with herpes simplex virus or triggered with some other pathogen-derived factors. Related Stories
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