Replication of Clone 13, a naturally attenuated avirulent isolate of Rift Valley fever virus, in Aedes and Culex mosquitoes.
Rift Valley fever virus continues to cause large outbreaks of acute and febrile illness among humans and domestic animals in Africa. The high pathogenicity of the virus is mainly due to the non-structural protein derived from the S segment NSs, which was shown to inhibit the type I interferon expression at the transcriptional level and to suppress host cell RNA synthesis. Clone 13, a naturally attenuated clone containing a deletion of 70% in NSs, is a promising vaccine candidate as it has no pathogenicity for mice and is highly immunogenic leading to long-lasting immunity. If Clone 13 succeeds in inducing a transient viremia in inoculated animals, is a mosquito vector able to replicate Clone 13 and is the vector affected by viral infection? In this work, we orally infected two mosquito species, Aedes vexans and Culex pipiens quinquefasciatus, with the avirulent Clone 13. We showed that the mosquito Ae. vexans better replicated the avirulent Clone 13 than Cx. p. quinquefasciatus. Moreover, infection with Clone 13 did not cause any important changes in mosquito's life-history traits compared to noninfected females. Nevertheless, it is likely that Clone 13 would not be efficiently transmitted by mosquito vectors.
Moutailler
Sara
S
Génétique Moléculaire des Bunyavirus, Institut Pasteur, Paris, France.
Krida
Ghazi
G
Madec
Yoann
Y
Bouloy
Michèle
M
Failloux
Anna-Bella
AB
D000330:Aedes / Q000821:virology*; D000818:Animals; D003465:Culex / Q000821:virology*; D005260:Female; D008018:Life Cycle Stages; D051379:Mice; D010058:Oviposition; D012296:Rift Valley fever virus / Q000472:pathogenicity / Q000502:physiology*; D014766:Viremia; D014774:Virulence; D014779:Virus Replication / Q000502:physiology*