Abstract

West Nile virus (WNV) is the most common arthropod-borne flavivirus in the United States; however, the vector ligand(s) that participate in infection are not known. We now show that an Aedes aegypti C-type lectin, mosGCTL-1, is induced by WNV, interacts with WNV in a calcium-dependent manner, and facilitates infection in vivo and in vitro. A mosquito homolog of human CD45 in A. aegypti, designated mosPTP-1, recruits mosGCTL-1 to enable viral attachment to cells and to enhance viral entry. In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes. A similar phenomenon was also observed in Culex quinquefasciatus, a natural vector of WNV, further demonstrating that these genes participate in WNV infection. During the mosquito blood-feeding process, WNV infection was blocked in vivo with mosGCTL-1 antibodies. A molecular understanding of flaviviral-arthropod interactions may lead to strategies to control viral dissemination in nature.Copyright 2010 Elsevier Inc. All rights reserved. PMID: 20797779 Funding information This work was supported by: NIAID NIH HHS, United States Grant ID: N01AI50031 NIAID NIH HHS, United States Grant ID: AI 070343 NIAID NIH HHS, United States Grant ID: U01 AI070343-03 NIAID NIH HHS, United States Grant ID: N01 AI500031 Howard Hughes Medical Institute, United States NIAID NIH HHS, United States Grant ID: U54 AI057158 NIAID NIH HHS, United States Grant ID: R01 AI032947 NIAID NIH HHS, United States Grant ID: R01 AI041440 NIAID NIH HHS, United States Grant ID: AI 50031 NIAID NIH HHS, United States Grant ID: U01 AI070343 NIAID NIH HHS, United States Grant ID: U54-AI057158 More Less keyboard_arrow_down

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