1. HIV-1 Vif: Counteracting Innate Antiretroviral Defenses
Bryan R. Cullen 
Molecular Therapy 
Volume 8, Issue 4, Pages (October 2003)
DOI: /j.ymthe
Copyright © 2003 The American Society of Gene Therapy Terms and Conditions

2. FIG. 1
Proposed mechanism of action of APOBEC3G and HIV-1 Vif. In the absence of functional Vif (lower half of figure), the human APOBEC3G protein is incorporated into virions released from APOBEC3G-expressing (nonpermissive) cells. Once these virions infect new cells, APOBEC3G attacks newly generated reverse transcripts by editing dC residues in the DNA minus strand to dU. Some of these dU residues are then believed to be targeted by uracil DNA glycosylase (UNG), which excises the deoxyuridine residues and leaves an abasic site that is cleaved by a cellular endonuclease. In the presence of Vif (upper panel), the APOBEC3G protein is bound by Vif and sequestered away from virion incorporation. Vif may also induce the degradation of the bound APOBEC3G protein. This allows virus reverse transcription and infection to proceed normally. Vif is also incorporated into HIV-1 virions, but as Vif has no evident effect on viral replication in permissive cells (cells that do not express APOBEC3G), the significance of this incorporation remains unclear.
Molecular Therapy 2003 8, DOI: ( /j.ymthe )
Copyright © 2003 The American Society of Gene Therapy Terms and Conditions