Yale Researchers Discover Protein in the Immune System Can Help Suppress HIV
According to the Centers for Disease Control and Prevention data, there were an estimated 39,782 new HIV infections in the United States in 2016, the most recent year for which data is available.
Over the past year, the U.S. Food and Drug Administration (FDA) has approved a number of combination therapies for HIV, including approval for Gilead Sciences' Biktarvy, a triple combination treatment of bictegravir and emtricitabine/tenofovir alafenamide. Mylan also snagged approval for its HIV treatment Symfi. Last year, the FDA gave the go-ahead for Merck’s Delstrigo, a once-per-day triple combination treatment and Pifeltro, a new non-nucleoside reverse transcriptase inhibitor.
While three have been a number of new medications approved, there are also quite a few HIV treatments that are likely to be approved over the next year. A new report released by researchers at Yale University could change the way some HIV patients are treated. The study reveals the role a protein called Apobec3A (A3A) plays in blocking HIV gene expression once it has infected human cells.
According to a report in Yale News, the research team studied T cell lines infected with latent HIV. The team was led by Manabu Taura, a postdoctoral fellow in the laboratory of immunobiologist Akiko Iwasaki. The report notes that the researchers observed “the effect of modifying genes to either overexpress or knock out” A3A, a protein known to suppress HIV in the earlier stages of infection. Taura and his team found that “A3A blocks HIV reactivation by binding to a region of HIV DNA” that would “promote the virus.” Additionally, the researchers said that A3A is capable of recruiting a “complex of enzymes” that are capable of inhibiting HIV. The team confirmed the results through various experiments conducted on HIV-infected human T cells, Yale News said.
The researchers were quick to note that more study is required to fully grasp the implications. But, the research does suggest that the A3A protein could be a potential focus for drugmakers when designing new HIV treatments.
Iwasaki told Yale News that if researchers can find a way to “express A3A in latently infected cells,” it will be possible to block the reactivation of HIV.
“That’s a good thing because if infected cells in HIV patients can’t express viral genes, there’s no disease,” Iwasaki said.
In addition to the A3A discovery, Iwasaki’s team identified two genes that control the expression of a large body of endogenous retroviruses in a separate study with mice. The genes, Snerv-1 and Snerv-2, were discovered to have been deleted in mice that are prone to lupus, the research showed. With the absence of those genes, the endogenous retrovirus expression goes up in mice, which then creates proteins that are the target of antibody responses. That can cause an autoimmune condition known as lupus nephritis, Yale News said.