The APOBEC3 proteins, A3G and A3F, may function as host defense factors in HIV infection. In vitro, they reduce HIV-1 replication and cause lethal mutations in the viral genome. The HIV-1 Viral infectivity factor (Vif), which is found in clinical samples, can counter the anti-HIV effects of A3G and A3F.
Now, MariaPia De Pasquale, Ph.D., Jordanka Kourteva, Ph.D., and colleagues provide evidence that A3G reduces Vif-positive HIV-1 replication in vivo. The investigators studied peripheral blood cells from 19 untreated HIV-infected adults: 12 long-term non-progressors (HIV-infected subjects who have stable CD4+ cells and low levels of virus without antiretroviral therapy) and 7 non-controllers (HIV-infected subjects with a typical pace of progression). They report that cells from non-progressors had higher levels of A3G and A3F, lower provirus levels, and more A3G-induced mutations in the viral genome than cells from non-controllers.
The findings in the Aug. 15 issue of Virology suggest that increased activity of A3G is a factor that can contribute to spontaneous control of HIV-1 in vivo. Increasing A3G/F levels and activity may provide therapeutic benefit for Vif-positive HIV-1.
This research was supported by the Vanderbilt-Meharry Center for AIDS Research, which is funded by the National Institute of Allergy and Infectious Diseases (AI054999) of the National Institutes of Health.
