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Simian virus 40 inhibits differentiation and maturation of rhesus macaque DC-SIGN(+) dendritic cells

C Changyong1, M Sun, H Li

  • 1The State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou, PR China.

European Journal of Medical Research
|October 19, 2010
PubMed

Insights

Simian virus 40 (SV40) infection suppresses immune responses by down-regulating dendritic cell (DC) maturation markers and impairing T cell activation. This suggests SV40 may cause immune suppression through altered DC function.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Dendritic cells (DCs) are crucial for initiating and modulating immune responses.
  • Pathogenic microorganisms can evade the immune system by interfering with DC function.
  • Simian virus 40 (SV40) is a DNA tumor virus that can cause latent infections in rhesus monkeys.

Purpose of the Study:

  • To investigate the interaction between SV40 and rhesus monkey dendritic cells (DCs).
  • To analyze the effect of SV40 on DC phenotype and function, specifically DC-SIGN(+) DCs.

Main Methods:

  • Rhesus monkey peripheral blood monocyte-derived DCs were induced using recombinant human Interleukin-4 (rhIL-4) and infective SV40.
  • Phenotype and function were analyzed using flow cytometry (FCM) and mixed lymphocyte reaction (MLR).

Main Results:

  • SV40 significantly down-regulated the expression of CD83 and CD86 on DCs.
  • SV40 impaired the activation of T cell proliferation induced by DCs.
  • DC-SIGN(+) DCs showed altered phenotype and function upon SV40 infection.

Conclusions:

  • SV40 infection influences the differentiation and maturation of dendritic cells.
  • SV40 may employ immune suppression as a strategy by targeting DCs.
  • These findings highlight a potential mechanism for SV40-induced immune evasion.

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