Wild type and H43Y variant of human TRIM5alpha show similar anti-human immunodeficiency virus type 1 activity both in vivo and in vitro

Immunogenetics. 2007 Jun;59(6):511-5. doi: 10.1007/s00251-007-0217-7. Epub 2007 Apr 4.

Abstract

Polymorphisms in human genes have been shown to affect the rate of disease progression to acquired immune deficiency syndrome in human immunodeficiency virus type 1 (HIV-1)-infected individuals. Recently, tripartite motif 5alpha (TRIM5alpha) was identified as a factor that confers resistance to HIV-1 infection in Old World monkey cells. Subsequently, Sawyer et al. (Curr Biol 16:95-100, 2006) reported a single nucleotide polymorphism (H43Y) in the human TRIM5alpha gene and TRIM5alpha protein with 43Y was found to lose its ability to restrict HIV-1. In the present study, we reevaluated effects of this allele on in vitro anti-HIV-1 activity as well as on HIV-1 disease progression in European and Asian cohorts of HIV-1-infected individuals. Our epidemiological and molecular biological findings clearly indicate H43Y has a very minor effect on anti-HIV-1 activity of TRIM5alpha, suggesting that this allele is immaterial, at least in HIV-1-infected Europeans and Asians.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acquired Immunodeficiency Syndrome / genetics*
  • Acquired Immunodeficiency Syndrome / metabolism
  • Animals
  • Antiviral Restriction Factors
  • Asian People
  • Carrier Proteins / biosynthesis
  • Carrier Proteins / genetics*
  • Cell Line
  • Cricetinae
  • Genetic Predisposition to Disease*
  • HIV-1 / physiology*
  • Humans
  • Mutation
  • Sendai virus / genetics
  • Tripartite Motif Proteins
  • Ubiquitin-Protein Ligases
  • Virus Replication
  • White People

Substances

  • Antiviral Restriction Factors
  • Carrier Proteins
  • Tripartite Motif Proteins
  • TRIM5 protein, human
  • Ubiquitin-Protein Ligases