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Hostile communication of measles virus with host innate immunity and dendritic cells

B Hahm1

  • 1Department of Surgery, Center for Cellular and Molecular Immunology, University of Missouri-Columbia School of Medicine, One Hospital Dr., Columbia, MO 65212, USA. hahmb@health.missouri.edu

Current Topics in Microbiology and Immunology
|February 11, 2009
PubMed

Insights

Measles virus (MV) infection triggers innate immunity, including type I interferon (IFN) production. This review explores how MV interacts with dendritic cells (DCs) and manipulates immune responses.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Measles virus (MV) infection elicits prompt host innate immune responses.
  • Pattern recognition receptors like Toll-like receptors and RNA helicases detect viral components, initiating antiviral signaling.
  • Type I interferons (IFNs) are key antiviral and immunoregulatory molecules synthesized during infection.

Purpose of the Study:

  • To review the multifaceted roles of MV-induced type I IFNs in host immunity.
  • To examine the complex interplay between measles virus and diverse dendritic cell (DC) subtypes.
  • To understand MV's strategies for evading, suppressing, or utilizing host innate immunity and DC functions.

Main Methods:

  • Literature review focusing on molecular mechanisms of innate immunity.
  • Analysis of host-pathogen interactions between measles virus and dendritic cells.
  • Examination of type I interferon signaling pathways and their impact on immune responses.

Main Results:

  • MV employs sophisticated strategies to counteract host innate immunity and dendritic cell surveillance.
  • Type I IFNs exhibit dual roles, exerting both beneficial and detrimental effects on host defense against MV.
  • Heterogeneous dendritic cell populations at different anatomical sites display distinct responses to MV infection.

Conclusions:

  • Understanding the intricate interactions between MV, type I IFNs, and DCs is crucial for developing effective antiviral strategies.
  • MV's ability to manipulate innate immunity highlights the complex co-evolutionary relationship between viruses and their hosts.
  • Further research into DC subsets and IFN functions could reveal new therapeutic targets for measles and related viral infections.

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