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Immune evasion

Overcoming host defences

Nature Reviews Immunology volume 3, page 849 (2003)Cite this article

Cells expressing endogenous APOBEC3G are 'non-permissive' for the production of fully infectious Vif-mutant virus, whereas cells deficient for APOBEC3G are 'permissive' for virus production. To elicit its anti-viral effect, APOBEC3G must be incorporated into Vif-mutant virion particles for transport to the virion's target cell. After entry into a new host cell, APOBEC3G deaminates cytidine residues in the viral DNA generated during reverse transcription, causing calamitous mutations to the viral DNA-replication intermediates.

In each of these new reports, APOBEC3G was found to be absent from virions that were generated in the presence of Vif and so its anti-viral potential was suppressed. Vif-mediated exclusion of APOBEC3G from virions was shown to occur independently of other viral proteins and to be associated with the depletion of APOBEC3G protein from the cell, although APOBEC3G messenger RNA levels were not reduced.

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ORIGINAL RESEARCH PAPERS

  1. Stopak, K. et al. HIV-1 Vif blocks the antiviral activity of APOBEC3G by impairing both its translation and intracellular stability. Mol. Cell 12, 591–601 (2003)

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  2. Sheehy, A. M. et al. The antiretroviral enzyme APOBEC3G is degraded by the proteasome in response to HIV-1 Vif. Nature Med. 5 October 2003 (DOI: 10.1038/nm945)

  3. Marin, M. et al. HIV-1 Vif protein binds the editing enzyme APOBEC3G and induces its degradation. Nature Med. 5 October 2003 (DOI: 10.1038/nm946)

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Authors
  1. Karen Honey
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Honey, K. Overcoming host defences. Nat Rev Immunol 3, 849 (2003). https://doi.org/10.1038/nri1236

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  • DOI: https://doi.org/10.1038/nri1236

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