HIV persistence: chemokines and their signalling pathways

Cytokine Growth Factor Rev. 2012 Aug-Oct;23(4-5):151-7. doi: 10.1016/j.cytogfr.2012.05.002. Epub 2012 Jun 28.

Abstract

Latently infected resting CD4+ T cells are the major barrier to curing HIV. We have recently demonstrated that chemokines, which bind to the chemokine receptors CCR7, CXCR3 and CCR6, facilitate efficient HIV nuclear localisation and integration in resting CD4+ T cells, leading to latency. As latently infected cells are enriched in lymphoid tissues, where chemokines are highly concentrated, this may provide a mechanism for the generation of latently infected cells in vivo. Here we review the role of chemokines in HIV persistence; the main signalling pathways that are involved; and how these pathways may be exploited to develop novel strategies to reduce or eliminate latently infected cells.

Publication types

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

MeSH terms

  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / metabolism
  • CD4-Positive T-Lymphocytes / virology
  • Chemokines / immunology*
  • Chemokines / metabolism
  • HIV Infections / immunology*
  • HIV Infections / metabolism
  • HIV Infections / virology
  • HIV-1 / immunology*
  • HIV-1 / physiology
  • Host-Pathogen Interactions / immunology
  • Humans
  • Models, Immunological
  • Receptors, Chemokine / immunology
  • Receptors, Chemokine / metabolism
  • Signal Transduction / immunology*
  • Virus Latency / immunology*

Substances

  • Chemokines
  • Receptors, Chemokine