The lectin pathway of complement activation contributes to protection from West Nile virus infection

Anja Fuchs, Amelia K. Pinto, Wilhelm J. Schwaeble, Michael S. Diamond

Research output: Contribution to journalArticle

51 Scopus citations

Abstract

The function of the lectin pathway of complement activation in vivo against West Nile virus (WNV) or many other pathogenic viruses has not been defined. Mice deficient in lectin pathway recognition molecules (mannose binding lectin-A (MBL-A) and mannose binding lectin-C (MBL-C)) or the effector enzyme mannan-binding lectin-associated serine protease-2 (MASP-2), were more vulnerable to WNV infection than wild type mice. Compared with studies of mice deficient in factors of the classical or alternative pathway, MBL-A-/- × MBL-C-/- or MASP-2-/- mice showed a less severe course of WNV infection. Indeed, a deficiency in lectin pathway activation did not significantly affect the kinetics of viral spread to the central nervous system (CNS) nor did it profoundly alter generation of adaptive B and T cell immune responses. We conclude that MBL-mediated recognition and lectin pathway activation have important yet subordinate functions in protecting against WNV infection and disease.

Original languageEnglish
Pages (from-to)101-109
Number of pages9
JournalVirology
Volume412
Issue number1
DOIs
StatePublished - Mar 30 2011

Keywords

  • Complement
  • Flavivirus
  • Immunity
  • Lectin pathway
  • Pathogenesis

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