The human body has innate mechanisms to combat viral infection. One such defense mechanism, the enzyme APOBEC3G (A3G), fights off HIV. But HIV fights back with a countermeasure called virion infectivity factor (Vif) to try to deplete A3G from cells. The one known mechanism by which A3G blocks HIV does not impair virus production from infected cells. Instead, it makes the viral particles (virions) produced by an infected cell unable to infect the next target human cell.
Richard D’Aquila, professor of pathology, microbiology and immunology, graduate student Kenneth Martin and colleagues now find that A3G has an additional mechanism to stop HIV. They found that large aggregates of A3G and other cellular components (called A3G complexes) can decrease the number of virions produced from an infected cell.
The results, reported in the Sept. 1 Journal of Virology, suggest additional ways to boost anti-HIV effects of members of the APOBEC3 family for innovative therapeutic or preventive strategies against HIV.
