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Early- and intermediate-stage variants of simian immunodeficiency virus replicate efficiently in cells lacking CCR5

Serene Forte1, Mary-Elizabeth Harmon, Mario J Pineda

  • 1Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.

Journal of Virology
|August 14, 2003
PubMed

Insights

Some simian immunodeficiency virus (SIV) variants can infect cells without the typical CCR5 coreceptor. Early-stage SIV evolved to use an uncharacterized receptor, crucial for viral entry into host cells.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Primate lentiviruses, including simian immunodeficiency virus (SIV), primarily utilize the chemokine receptor CCR5 for cellular entry.
  • Understanding viral coreceptor usage is critical for deciphering host-pathogen interactions and viral pathogenesis.

Purpose of the Study:

  • To investigate the coreceptor usage of different simian immunodeficiency virus (SIV) variants during infection.
  • To identify potential novel cellular receptors involved in SIV replication in peripheral blood mononuclear cells (PBMCs).

Main Methods:

  • Comparative replication assays of sequential SIV variants in PBMCs with and without functional CCR5.
  • Coreceptor specificity analysis using indicator cell lines expressing known SIV coreceptors.

Main Results:

  • Certain SIV variants demonstrated efficient replication in PBMCs lacking functional CCR5.
  • Early- and intermediate-stage SIV variants replicated effectively in CCR5-negative PBMCs, unlike late-stage pathogenic variants.
  • No known SIV coreceptors fully explained the differential replication patterns observed.

Conclusions:

  • SIV replication in PBMCs can occur independently of CCR5, suggesting the involvement of alternative coreceptors.
  • An uncharacterized cellular receptor may mediate the entry of specific SIV variants into target cells.
  • This novel coreceptor could play a significant role in SIV pathogenesis and viral spread within host populations.

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