HIV-1 subtype variability in vif derived from molecular clones affects APOBEC3G-mediated host restriction

Irene Lisovsky, Susan M. Schader, Richard D. Sloan, Maureen Oliveira, Dimitrios Coutsinos, Nicole F. Bernard, Mark A. Wainberg

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Background: The host protein APOBEC3G (A3G) can limit HIV-1 replication. Its protective effect is overcome by the HIV-1 'viral infectivity factor' (Vif), which targets A3G for proteosomal degradation. Although Vif is considered to be essential for HIV-1 replication, the effect of Vif variability among commonly used HIV-1 molecular clones of different genetic backgrounds on viral infectiousness and pathogenesis has not been fully determined. Methods: We cloned the intact Vif coding regions of available molecular clones of different subtypes into expression vectors. Δvif full-length HIV-1 clonal variants were generated from corresponding subtype-specific full-length molecular clones. Replication-competent viruses were produced in 293T cells in the presence or absence of A3G, with Vif being supplied by the full-length HIV-1 clone or in trans. The extent of A3G-mediated restriction was then determined in a viral replication assay using a reporter cell line. Results and Conclusions: In the absence of A3G, Vif subtype origin did not impact viral replication. In the presence of A3G the subtype origin of Vif had a differential effect on viral replication. Vif derived from a subtype C molecular clone was less effective at overcoming A3G-mediated inhibition than Vif derived from either subtype B or CRF02-AG molecular clones.

Original languageEnglish
Pages (from-to)258-264
Number of pages7
Issue number4
Early online date8 May 2013
Publication statusPublished - Jul 2013

Keywords / Materials (for Non-textual outputs)

  • HIV-1 subtype diversity
  • Vif
  • Viral infectivity


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