Venezuelan equine encephalitis virus in the mosquito vector Aedes taeniorhynchus : Infection initiated by a small number of susceptible epithelial cells and a population bottleneck

• Published in: Virology (New York, N.Y.) N.Y.), 2008-03, Vol.372 (1), p.176-186
• Main Authors: Smith, Darci R, Adams, A. Paige, Kenney, Joan L, Wang, Eryu, Weaver, Scott C
• Format: Article
• Language: English
• Subjects: Aedes; Aedes - ultrastructure; Aedes - virology; Aedes taeniorhynchus; Alphavirus; Animals; Cell Line; Cricetinae; Digestive System - cytology; Digestive System - ultrastructure; Digestive System - virology; Encephalitis Virus, Venezuelan Equine - genetics; Encephalitis Virus, Venezuelan Equine - growth & development; Encephalitis Virus, Venezuelan Equine - pathogenicity; Encephalomyelitis, Venezuelan Equine - transmission; Encephalomyelitis, Venezuelan Equine - virology; epithelial cells; Epithelial Cells - ultrastructure; Epithelial Cells - virology; Evolution; Genetics; Green Fluorescent Proteins - genetics; Green Fluorescent Proteins - metabolism; horse diseases; Humans; Infectious Disease; insect vectors; Insect Vectors - ultrastructure; Insect Vectors - virology; Microscopy, Confocal; midgut; Mosquito; Pathogenesis; Prunus; Replicon; Venezuelan equine encephalitis virus; viral encephalitis; virus replication
• ISSN: 0042-6822; 1096-0341
• DOI: 10.1016/j.virol.2007.10.011

Abstract We evaluated infection of Aedes taeniorhynchus mosquitoes, vectors of Venezuelan equine encephalitis virus (VEEV), using radiolabeled virus and replicon particles expressing green (GFP) or cherry fluorescent protein (CFP). More epidemic VEEV bound to and infected mosquito midguts compared to an enzootic strain, and a small number of midgut cells was preferentially infected. Chimeric replicons infected midgut cells at rates comparable to those of the structural gene donor. The numbers of midgut cells infected averaged 28, and many infections were initiated in only 1–5 cells. Infection by a mixture of GFP- and CFP-expressing replicons indicated that only about 100 midgut cells were susceptible. Intrathoracic injections yielded similar patterns of replication with both VEEV strains, suggesting that midgut infection is the primary limitation to transmission. These results indicate that the structural proteins determine initial infection of a small number of midgut cells, and that VEEV undergoes population bottlenecks during vector infection.