Human Antiviral Factor A3g And A3f

Vif (viral infectivity factor), a minor protein encoded by human immunodeficiency virus type-1(HIV-1), often plays an important role in viral replication of HIV-1. Recently, the research on Vif has revealed a novel component of innate immune system——APOBEC3G(A3G), and now APOBEC3F (A3F)becomes another one. A3G which is a cytidine deaminase and lethally hypermutates retroviruses and retro-elements, is a cellular protein required for resistance to infection by HIV-1, and has been shown to be a cytidine deaminase which is incorporated into virions and subsequently triggers massive deamination of deoxycytidine to deoxyuridine within the retroviral minus strand cDNA.A3G, which locates in human chromosome 22q13.1-q13.2, is one member of APOBEC family to which A3F belongs . A3G and A3F also can mediate the innate immunity. In fact, they are able to defense a wide spectrum of distantly related retroviruses, especially A3G interferes with HBV fiercely through a different mechanism from HIV. It is established that A3G acts better than 3TC, the antiviral drug. A3G not only can remarkably inhibite the HBV replication (at least 50 times less HBV DNA), but also can induce a decrease in the infectivity of MLV (Murine Leukemia Virus). A3F that can function as DNA editing enzyme co-expresses with A3G and defenses viruses together. In recent studies, A3G and A3F, the cytosine deaminases which are expressed in human cells, can defense the viral protein Vif. Vif, that is, viral infectivity factor encoded by HIV genome, is essential for replication. A3G and A3F overexpression can neutralize the Vif, which is shown in the test that△vif HIV is non-infective. The competition between them might be taken advantage of to lead a new way for AIDS in therapeutics. It may be definitely important to make A3G and A3F the new target and approach in the future drug design.Only in the virus-producing cell Vif expression is necessary;in its absence, infection of a subsequent target cell terminates at a postentry step through the action of the human A3G antiviral mechanism. Vif protein has two domains: one binds to A3G and the other...