Chemokine coreceptor signaling in HIV-1 infection and pathogenesis

Yuntao Wu1, Alyson Yoder

  • 1Department of Molecular and Microbiology, George Mason University, Manassas, Virginia, USA. ywu8@gmu.edu

Plos Pathogens
|December 31, 2009
PubMed

Insights

Human immunodeficiency virus type 1 (HIV-1) exploits chemokine coreceptor signaling to infect resting CD4 T cells. This hijacked signaling pathway is crucial for viral entry and may contribute to HIV pathogenesis.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Chemokine coreceptors are critical for HIV-1 entry into host cells.
  • While HIV-1 fusion is understood, the role of coreceptor signaling in infection remains unclear.
  • Recent findings highlight signaling's necessity for latent HIV-1 infection in CD4 T cells.

Purpose of the Study:

  • To revisit the role of chemokine coreceptor signaling in HIV-1 infection.
  • To explore how HIV-1 may exploit host cell signaling pathways.
  • To discuss the implications of coreceptor signaling in viral pathogenesis.

Main Methods:

  • Review of existing literature on HIV-1 coreceptor signaling.
  • Analysis of studies demonstrating signaling requirements for infection.
  • Discussion of proposed mechanisms of viral exploitation of signaling networks.

Main Results:

  • HIV-1 envelope binding to coreceptors triggers both fusion and signaling.
  • Chemokine coreceptor signaling is essential for latent HIV-1 infection of resting CD4 T cells.
  • Virus-hijacked signaling may facilitate HIV-1 entry and pathogenesis.

Conclusions:

  • Chemokine coreceptor signaling is a key, yet underappreciated, factor in HIV-1 infection.
  • HIV-1 likely exploits host chemokine signaling pathways to enhance infectivity.
  • Understanding this aberrant signaling is vital for developing new therapeutic strategies against HIV-1.

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