IL-10 signaling blockade controls murine West Nile virus infection

Fengwei Bai*, Terrence Town, Feng Qian, Penghua Wang, Masahito Kamanaka, Tarah M. Connolly, David Gate, Ruth R. Montgomery, Richard A. Flavell, Erol Fikrig

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

76 Scopus citations


West Nile virus (WNV), a mosquito-borne single-stranded RNA flavivirus, can cause significant human morbidity and mortality. Our data show that interleukin-10 (IL-10) is dramatically elevated both in vitro and in vivo following WNV infection. Consistent with an etiologic role of IL-10 in WNV pathogenesis, we find that WNV infection is markedly diminished in IL-10 deficient (IL-10-/-) mice, and pharmacologic blockade of IL-10 signaling by IL-10 neutralizing antibody increases survival of WNV-infected mice. Increased production of antiviral cytokines in IL-10-/- mice is associated with more efficient control of WNV infection. Moreover, CD4 + T cells produce copious amounts of IL-10, andmay be an important cellular source of IL-10 duringWNV infection in vivo. In conclusion, IL-10 signaling plays a negative role in immunity against WNV infection, and blockade of IL-10 signaling by genetic or pharmacologic means helps to control viral infection, suggesting a novel anti-WNV therapeutic strategy.

Original languageEnglish (US)
Article numbere1000610
JournalPLoS pathogens
Issue number10
StatePublished - Oct 2009
Externally publishedYes

ASJC Scopus subject areas

  • Genetics
  • Molecular Biology
  • Virology
  • Parasitology
  • Microbiology
  • Immunology


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