Antiviral Mechanism Of The Cytosine Deaminase APOBEC3F

APOBEC3F(A3F) and APOBEC3G(A3G) are both located on the samechromosome separated by24667bp. In the colorectal adenocarcinoma, chronicmyelogenous leukemia, and epithelial cells we can detecte the expression ofAPOBEC3G and APOBEC3F.Their share almost100%similarity in the N-terminal.APOBEC3F has seven exons, and APOBEC3G has eight exons. APOBEC3F couldhave a similar anti-virus activity as APOBEC3G. Epidemiologically, there are twosubtypes A3F naturally, its differences in the231th amino acid residues one is Valine(V), the other is Isoleucine (I).Vif(viral infectivity factor) is one of non-structural proteins that was encoded byall lentiviruses except Equine infectious anemia virus. During HIV infection, the Vifproteins through recruiting Cullin5, ElonginB, ElonginC E3ubiquitin ligase to inducetargeted protein ubiquitination and proteasome-mediated degradation to suppress thenative defensive factors APOBEC3proteins.On the basis of HIV-1,we study the regulatory mechanism of human A3Fprotein, the different subtypes of HIV and retrotransposon LINE-1.In this paper,we confirmed that two subtypes of A3F both have the ability to suppress thevirus infection, and when the Vif protein is absent the suppression ratio can reach80%.This paper also confirmed the two subtype A3F have the same inhibition ability for the most of subtypes of the virus, and have the different inhibiton for only three subtypes Vif proteins. the reason is：although the Vif proteins used in experiment come from the different HIV-1virus, the functional domain of Vif combined A3F may be conserved. This will provide theoretical basis for the mechanism of A3F protein antiviral ability and will help to the study of the relationship of A3F gene polymorphism and the distribution of different subtypes of the virus.