Inhibition of HIV-1 replication in human lymphoid tissues ex vivo by measles virus

J Infect Dis. 2005 Jul 1;192(1):71-8. doi: 10.1086/430743. Epub 2005 May 31.


Human immunodeficiency virus (HIV) type 1 replication and disease progression are enhanced by various pathogens in coinfected individuals. However, acute infection with measles virus (MV) has been found to suppress HIV-1 replication in coinfected children. We investigated the mechanisms of this phenomenon using human lymphoid tissues coinfected ex vivo with HIV-1 and MV. MV inhibited both CXCR4-tropic (X4) and CCR5-tropic (R5) HIV-1, but the inhibitory effect was particularly profound for R5 virus, which transmits infection and dominates the early stages of HIV-1 disease. MV inhibits the replication of R5 HIV-1 in coinfected tissues by up-regulation of the CC chemokine RANTES, a well-known inhibitor of R5 HIV-1 infection, and this up-regulation is augmented in tissues coinfected with R5 HIV-1. Deciphering the molecular mechanisms by which MV and other pathogens alter local cytokine/chemokine networks and cause tissue microenvironments to become detrimental to HIV-1 may significantly contribute to the development of effective anti-HIV therapies.

Publication types

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

MeSH terms

  • Chemokine CCL4
  • Chemokine CCL5 / metabolism
  • Chemokine CXCL12
  • Chemokines, CXC / metabolism
  • HIV-1 / physiology*
  • Humans
  • Macrophage Inflammatory Proteins / metabolism
  • Measles virus / physiology*
  • Palatine Tonsil / virology*
  • Tissue Culture Techniques
  • Up-Regulation
  • Virus Replication / physiology*


  • CXCL12 protein, human
  • Chemokine CCL4
  • Chemokine CCL5
  • Chemokine CXCL12
  • Chemokines, CXC
  • Macrophage Inflammatory Proteins