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Retrovirus restriction by TRIM5alpha variants from Old World and New World primates

Byeongwoon Song1, Hassan Javanbakht, Michel Perron

  • 1Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Division of AIDS, Harvard Medical School, Boston, MA, USA.

Journal of Virology
|March 16, 2005
PubMed

Insights

Primate TRIM5alpha proteins vary, influencing retroviral restriction. Differences in TRIM5alpha, particularly in its B30.2 domain, explain why some monkey cells block infections like simian immunodeficiency virus (SIV) and human immunodeficiency virus (HIV).

Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • The TRIM5alpha protein acts as a post-entry restriction factor against retroviral infections in certain primate cells.
  • Human and Old World monkey TRIM5alpha proteins inhibit specific retroviruses after cellular entry.
  • New World monkey cells typically restrict simian immunodeficiency virus of macaques (SIVmac) infection post-entry.

Purpose of the Study:

  • To investigate the antiretroviral activities of TRIM5alpha orthologs across various primate species.
  • To correlate variations in TRIM5alpha protein structure, particularly the B30.2 domain, with observed retroviral restriction patterns.
  • To understand how primate-specific TRIM5alpha evolution contributes to differential susceptibility to retroviruses.

Main Methods:

  • Comparative analysis of TRIM5alpha protein sequences from humans, apes, Old World monkeys, and New World monkeys.
  • Functional assays to assess the ability of different TRIM5alpha orthologs to restrict infection by various retroviruses (e.g., N-MLV, HIV-1, SIVmac, SIVagm).
  • Examination of structural variations, such as tandem duplications in the B30.2 domain, and their impact on antiretroviral activity.

Main Results:

  • Chimpanzee and orangutan TRIM5alpha proteins showed functional similarity to human TRIM5alpha, restricting N-MLV and HIV-1.
  • New World monkey TRIM5alpha proteins effectively restricted SIVmac and SIVagm.
  • Spider monkey and African green monkey TRIM5alpha, featuring expanded B30.2 domain regions (v3 and v1, respectively), exhibited potent and broad-spectrum antiretroviral activity against multiple retroviruses.

Conclusions:

  • Variations in primate TRIM5alpha proteins, especially structural changes in the B30.2 domain, are responsible for species-specific post-entry restrictions of retroviral infections.
  • Specific structural modifications, like tandem duplications in the B30.2 domain, can significantly enhance the range of retroviruses inhibited by TRIM5alpha.
  • Understanding TRIM5alpha diversity provides insight into the evolutionary arms race between host defense mechanisms and viral pathogens.

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