Journal ArticleDOI
Brugia malayi microfilariae (Nematoda: Filaridae) enhance the infectivity of Venezuelan equine encephalitis virus to Aedes mosquitoes (Diptera: Culicidae).
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TLDR
The contrasting effects of microfilarial enhancement of viral infectivity and MF-induced mortality in mosquitoes differed among mosquito species and were determined by the nature and consequences of MF penetration through the mosquito midgut, but not to differences in mosquito susceptibilities to parenterally introduced virus.Abstract:
We examined the potentially conflicting effects that microfilarial ( MF) enhancement of viral infectivity and MF-induced mortality in mosquitoes have on the vectorial capacity of Aedes aegypti (L.), Aedes triseriatus (Say), and Aedes taeniorhynchus (Wiedemann) for Venezuelan equine encephalitis virus (VEE) when mosquitoes feed on gerbils co-infected with Brugia malayi (Buckley). Groups of mosquitoes were fed on gerbils that were either dually infected (VEE plus B. malayi MF) or singly infected (VEE only). Mosquito mortality was recorded daily, and 5-8 d later, surviving mosquitoes were assayed for disseminated viral infection. The contrasting effects of MF enhancement and MF-induced mortality differed among mosquito species and were determined by the nature and consequences of MF penetration through the mosquito midgut, but not to differences in mosquito susceptibilities to parenterally introduced virus. In Ae. aegypti, MF-induced mortality was high and tended to eliminate any significant effect of MF enhancement. In Ae. triseriatus, MF-induced mortality was low, and feeding on dually infected hosts resulted in 9 times as many mosquitoes with disseminated viral infections as did feeding on singly-infected hosts. In Ae. taeniorhynchus, MF-induced mortality was extremely high, yet under our experimental conditions, feeding on a dually infected hosts resulted in nearly 30 times as many disseminated infections as did feeding on singly infected hosts. The final outcome on vectorial capacity depended on the specific combination of MF, virus, and mosquito species involved. Therefore, future efforts toward understanding MF enhancement should be directed toward mosquito-virus-parasite species combinations that occur together in nature.read more
Citations
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Journal ArticleDOI
Immune interactions between mosquitoes and their hosts
TL;DR: The understanding of the interplay between mosquitoes and the immune system of their hosts is still in its infancy, but it is clear that there is great potential for exploiting this interplay in the control of mosquito‐borne diseases.
Journal ArticleDOI
Infection patterns of o'nyong nyong virus in the malaria-transmitting mosquito, Anopheles gambiae.
Aaron C. Brault,Brian D. Foy,Kevin M. Myles,Cindy L. H. Kelly,Stephen Higgs,Scott C. Weaver,Ken E. Olson,Barry R. Miller,Ann M. Powers,Ann M. Powers +9 more
TL;DR: A series of recombinant alphaviruses, based upon the genome of ONNV, designed for the expression of heterologous genes, that will be a valuable asset in parasite–mosquito interaction and interference research and to serve as tools for antimalaria studies.
Journal ArticleDOI
Mosquito appetite for blood is stimulated by Plasmodium chabaudi infections in themselves and their vertebrate hosts.
TL;DR: The alterations in mosquito feeding propensity reported here would occur if parasites have been selected to make infected vertebrate hosts more attractive to mosquitoes, and infected mosquitoes are more likely to seek out new blood meals.
Journal ArticleDOI
Potential for Mosquitoes (Diptera: Culicidae) From Florida to Transmit Rift Valley Fever Virus
Michael J. Turell,Seth C. Britch,Robert L. Aldridge,Daniel L. Kline,Carl Boohene,Kenneth J. Linthicum +5 more
TL;DR: Eleven species were evaluated from Florida to determine which of these species should be targeted for control should Rift Valley fever virus (RVFV) be detected in North America and how environmental factors affect transmission.
Book ChapterDOI
Pathogenesis of Rift Valley fever virus in mosquitoes--tracheal conduits & the basal lamina as an extra-cellular barrier.
William S. Romoser,Michael J. Turell,Kriangkrai Lerdthusnee,Marco Neira,David J. Dohm,George V. Ludwig,Leonard P. Wasieloski +6 more
TL;DR: Evidence indicates the existence of a salivary gland infection barrier in Anopheles stephensi and the basal lamina may prevent access to mosquito cell surface virus receptors and help explain why anopheline mosquitoes are relatively incompetent arbovirus transmitters when compared to culicines.
References
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