Inhibition of tRNA₃(Lys)-primed reverse transcription by human APOBEC3G during human immunodeficiency virus type 1 replication

J Virol. 2006 Dec;80(23):11710-22. doi: 10.1128/JVI.01038-06. Epub 2006 Sep 13.

Abstract

Cells are categorized as being permissive or nonpermissive according to their ability to produce infectious human immunodeficiency virus type 1 (HIV-1) lacking the viral protein Vif. Nonpermissive cells express the human cytidine deaminase APOBEC3G (hA3G), and Vif has been shown to bind to APOBEC3G and facilitate its degradation. Vif-negative HIV-1 virions produced in nonpermissive cells incorporate hA3G and have a severely reduced ability to produce viral DNA in newly infected cells. While it has been proposed that the reduction in DNA production is due to hA3G-facilitated deamination of cytidine, followed by DNA degradation, we provide evidence here that a decrease in the synthesis of the DNA by reverse transcriptase may account for a significant part of this reduction. During the infection of cells with Vif-negative HIV-1 produced from 293T cells transiently expressing hA3G, much of the inhibition of early (> or =50% reduction) and late (> or =95% reduction) viral DNA production, and of viral infectivity (> or =95% reduction), can occur independently of DNA deamination. The inhibition of the production of early minus-sense strong stop DNA is also correlated with a similar inability of tRNA(3)(Lys) to prime reverse transcription. A similar reduction in tRNA(3)(Lys) priming and viral infectivity is also seen in the naturally nonpermissive cell H9, albeit at significantly lower levels of hA3G expression.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • APOBEC-3G Deaminase
  • Cell Line
  • Cytidine Deaminase
  • Gene Expression Regulation
  • Gene Products, vif / genetics
  • Gene Products, vif / metabolism*
  • HIV-1 / genetics
  • HIV-1 / physiology*
  • Humans
  • Nucleoside Deaminases / chemistry
  • Nucleoside Deaminases / pharmacology*
  • Repressor Proteins / chemistry
  • Repressor Proteins / pharmacology*
  • Reverse Transcription / drug effects*
  • Virus Replication / drug effects*
  • Virus Replication / physiology
  • vif Gene Products, Human Immunodeficiency Virus

Substances

  • Gene Products, vif
  • Repressor Proteins
  • vif Gene Products, Human Immunodeficiency Virus
  • Nucleoside Deaminases
  • APOBEC-3G Deaminase
  • APOBEC3G protein, human
  • Cytidine Deaminase