Counteracts
the innate antiviral activity of human APOBEC3F and APOBEC3G. Forms a
complex with host APOBEC3F and APOBEC3G thus preventing the entry of
these lethally hypermutating enzymes into progeny virions
Enhances infectivity of virus particles
Inhibits T cell intracellular antiviral defences
Prevents T cell intracellular antiviral proteins from being incorporated in viral particles
Functions during virus particle assembly
Binds to viral genomic RNA in the cytoplasm to form a 40 S messenger ribonucleoprotein (mRNP) complex
Regulates protease activity
Additional
Information:
7 to 20 Vif molecules are incorporated into each virion (Ref. #8)
Vif requires phosphorylation in order to function
essential for replication of HIV in lymphocytes and macrophages (Ref. #3)
Vif mutants result in improperly packed nucleoprotein cores (Ref. #5)
Vif interacts with viral genomic RNA, and is package into the nucleoprotein complex (Ref. #6)
Vif activity is influenced by multimerization (Ref. #7)
When
involved in mRNP complexes, Vif may mediate viral RNA interactions with
HIV-1 Gag precursors during the formation of the viral particle
CEM15
is a human cytoplasmic protein that provides an intracellular defence
against HIV replication in T cells by binding to viral RNA
CEM15 expression is sufficient to prevent HIV infection
Viruses lacking Vif are only able to replicate in cells lacking CEM15
CEM15 is homologous to cytidine deaminase, an enzyme that edits RNA
Viruses lacking Vif are only able to replicate in cells lacking CEM15 (also known as apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G, APOBEC3G).
Vif prevents CEM15/APOBEC3G from being incorporated into viral particles. If CEM15/APOBEC3G
is incorporated with the HIV core, it will induce G-to-A hypermutation
of nascent viral DNA. Many viral mRNA transcripts would get degradated
by host factors, while remaining viral mRNA will result in proteins
with excessive polymorphisms
Vif interacts with HIV-1 Protease to prevent it from cleaving Gag and Gag-Pol polyproteins at the wrong stage of the replication cycle
