Abstract

The interaction of the mosquito and the invading virus is complex and can result in physiological and gene expression alterations in the insect. The association of West Nile virus (WNV) and Culex pipiens quinquefasciatus mosquitoes results in measurable changes in gene expression; 22 gene products were shown previously to have altered expression. Sequence analysis of one product, CQ G1A1, revealed 100% amino acid identity to gram negative bacteria binding proteins (CPQGBP) in Cx. p. quinquefasciatus, Aedes aegypti (70%) and Anopheles gambiae (63%) that function in pathogen recognition. CQ G1A1 also was differentially expressed following WNV infection in two populations of Cx. p. quinquefasciatus colonized from Florida with known differences in vector competence for WNV and showed spatial and temporal gene expression differences in midgut, thorax, and carcass tissues. These data suggest gene expression of CQ G1A1 is influenced by WNV infection and the WNV infection-controlled expression differs between populations and tissues.

Highlights

  • West Nile virus (WNV, family Flaviviridae, genus Flavivirus) is an important threat to humans and animals as it continues to cause morbidity and mortality in the United States [1] since its introduction into New York in 1999 [2]

  • In this study we describe the characterization of one gene, CQ G1A1 that was previously shown to be up-regulated in the Cx. p. quinquefasciatus midguts after exposure to WNV

  • Infection in Cx. p. quinquefasciatus. These results indicate that mosquito CQ G1A1 is constitutively expressed and its expression, not directly linked to antiviral responses, alters after infection with WNV, and the increase in expression might be due to other factors, like presence of microbial cell wall components [35]

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Summary

Introduction

West Nile virus (WNV, family Flaviviridae, genus Flavivirus) is an important threat to humans and animals as it continues to cause morbidity and mortality in the United States [1] since its introduction into New York in 1999 [2]. The virus is maintained in an enzootic transmission cycle between birds and ornothophilic mosquitoes in the genus Culex [3]. Cx. tarsalis Coquillett, and Cx. nigripalpus Theobald are all considered important vectors of WNV in the United States [4,5,6,7,8]. Culex pipiens quinquefaciatus is a vector whose competence for WNV varies between populations of mosquitoes [9,10]. Competence of a mosquito for a virus is influenced by both internal and external factors [11]. Viruses ingested with a blood meal must first infect midgut epithelial cells in order for the biological transmission of WNV to occur, and this represents the first barrier that the virus must overcome [11,12]. Barriers to infection may be influenced by several different genes [13,14]

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