Journal
VIROLOGY
Volume 412, Issue 1, Pages 101-109Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2011.01.003
Keywords
Flavivirus; Complement; Pathogenesis; Lectin pathway; Immunity
Categories
Funding
- NIH (the Midwest Regional Center of Excellence for Biodefense and Emerging Infectious Diseases Research) [U54 AI057160]
- MRC [G0501425, G0700859, G0801952, G1000191] Funding Source: UKRI
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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(-/-) x 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. (c) 2011 Elsevier Inc. All rights reserved.
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