HIV-1 Vif (viral infectivity factor) protein overcomes the antiviral activity of the DNA deaminase APOBEC3G by targeting it for proteasomal degradation. We report here that Vif targets APOBEC3G for degradation by forming an SCF-like E3 ubiquitin ligase containing Cullin 5 and Elongins B and C (Cul5-EloB-EloC) through a novel SOCS (suppressor of cytokine signaling)-box that binds EloC. Vif bindi...

Obtaining structural information about Vif is of interest for several reasons that include the study of the interaction of Vif with APOBEC3G, a resistance factor. Vif is a potential drug target and its function is essential for the HIV-1 infectivity process. To study Vif mechanism of action, we need to decipher its structure. Pivotal in this approach is the painstaking prediction of its protein...

We examined a series of site-directed point mutants of human immunodeficiency virus type 1 (HIV-1) Vif for their interaction with cellular anti-viral factors APOBEC3G/APOBEC3F. Mutant viruses that display growth-defect in H9 cells did not counteract effectively APOBEC3G and/or APOBEC3F without exception, as monitored by single-cycle infectivity assays. While growth-defective mutants of Vif C-te...

The vif gene of human immunodeficiency virus type 1 (HIV-1) greatly enhances the infectivity of HIV-1 virions that are released from cells classified as nonpermissive (e.g., lymphocytes, macrophages, and H9 leukemic T cells) but is irrelevant in permissive cells (e.g., HeLa or COS cells). Recently, it was reported that vif expression in nonpermissive cells dramatically increases infectivity not...

Viral infectivity factor (Vif) is one of the human immunodeficiency virus (HIV) accessory proteins and is conserved in the primate lentivirus group. This protein is essential for viral replication in vivo and for productive infection of nonpermissive cells, such as peripheral blood mononuclear cells (PBMC). Vif counteracts an antiretroviral cellular factor in nonpermissive cells named CEM15/APO...

The Vif protein of human immunodeficiency virus type 1 is required for productive replication in peripheral blood lymphocytes. Previous reports suggest that vif-deleted viruses are limited in replication because of a defect in the late steps of the virus life cycle. One of the remaining questions is to determine whether the functional role of Vif involves a specific interaction with virus core ...

Human immunodeficiency virus-1 (HIV-1) Vif overcomes the anti-viral activity of APOBEC3G by targeting it for ubiquitination via a Cullin 5-ElonginB-ElonginC (Cul5-EloBC) E3 ligase. Vif associates with Cul5-EloBC through a BC-box motif that binds EloC, but the mechanism by which Vif selectively recruits Cul5 is poorly understood. Here we report that a region of Vif (residues 100-142) upstream of...

One of the longest-standing mysteries in HIV research has been the function of the viral-encoded VIF protein. VIF is required for efficient viral infection in vivo [1–4], apparently because it overcomes the action of a host-encoded antiviral system [5,6]. A recent report in Nature describes a major breakthrough in understanding the cellular defense machinery that is overcome by HIV VIF [7]. In ...

The research on virion infectivity factor (Vif) protein had started in late 1980s right after HIV-1 was cloned, and the function of Vif had been a mystery for a long time. However, the research on Vif has finally lead to the identification of APOBEC3G, which opens up a new era in the research field of host restriction factors in HIV-1 infection followed by TRIM5α, Tetherin/BST-2, and SAMHD1. Th...