Measles virus-induced suppression of immune responses

Diane E Griffin1

  • 1W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. dgriffin@jhsph.edu

Immunological Reviews
|July 20, 2010
PubMed

Insights

Measles virus (MV) infection causes temporary immune suppression and increased susceptibility to secondary infections, despite eventually establishing lifelong immunity. This immune modulation involves shifts in T-cell responses and dendritic cell dysfunction.

Area of Science:

  • Immunology
  • Virology
  • Pediatrics

Background:

  • Measles virus (MV) is a significant cause of childhood mortality.
  • MV infection presents a complex interaction with the immune system, leading to both clearance and immune suppression.
  • Understanding MV's immunomodulatory effects is crucial for public health.

Purpose of the Study:

  • To elucidate the mechanisms behind measles-induced immune suppression.
  • To investigate the role of T-cell responses and dendritic cells in MV pathogenesis.
  • To explain the paradoxical outcomes of MV infection, including durable immunity and temporary immune deficits.

Main Methods:

  • Analysis of T-cell responses (CD8+, T-helper 1, T-helper 2) during MV infection.
  • Investigation of lymphocyte proliferation assays following MV exposure.
  • Assessment of dendritic cell (DC) function and interaction with lymphocytes after MV infection.

Main Results:

  • MV infection leads to a shift from T-helper 1 to T-helper 2 CD4+ T-cell responses.
  • Suppression of lymphocyte proliferation occurs with MV infection or exposure to viral glycoproteins.
  • Infected DCs impair mixed lymphocyte reactions and induce lymphocyte unresponsiveness.

Conclusions:

  • Measles-induced immune suppression results from complex interactions involving T-cell shifts and dysfunctional DCs.
  • Viral glycoproteins expressed by infected DCs contribute to immune suppression.
  • These mechanisms explain both the temporary immune deficits and the establishment of long-term immunity post-measles.

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