Differential anti-APOBEC3G activity of HIV-1 Vif proteins derived from different subtypes

Yukie Iwabu, Masanobu Kinomoto, Masashi Tatsumi, Hideaki Fujita, Mari Shimura, Yoshitaka Tanaka, Yukihito Ishizaka, David Nolan, Simon Mallal, Tetsutaro Sata, Kenzo Tokunaga

Research output: Contribution to journalArticlepeer-review

44 Citations (Scopus)


Antiretroviral cytidine deaminase APOBEC3G, which is abundantly expressed in peripheral blood lymphocytes and macrophages, strongly protects these cells against HIV-1 infection. The HIV-1 Vif protein overcomes this antiviral effect by enhancing proteasome-mediated APOBEC3G degradation and is key for maintaining viral infectivity. The 579-bp-long vif gene displays high genetic diversity among HIV-1 subtypes. Therefore, it is intriguing to address whether Vif proteins derived from different subtypes differ in their viral defense activity against APOBEC3G. Expression plasmids encoding Vif proteins derived from subtypes A, B, C, CRF01-AE, and CRF02-AG isolates were created, and their anti-APOBEC3G activities were compared. Viruses produced from cells expressing APOBEC3G and Vif proteins from different subtypes showed relatively different viral infectivities. Notably, subtype C-derived Vif proteins tested had the highest activity against APOBEC3G that was ascribed to its increased binding activity, for which the N-terminal domain of the Vif protein sequences was responsible. These results suggest that the biological differences of Vif proteins belonging to different subtypes might affect viral fitness and quasispecies in vivo.

Original languageEnglish
Pages (from-to)35350-35358
Number of pages9
JournalJournal of Biological Chemistry
Issue number46
Publication statusPublished - Nov 12 2010

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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