Abstract
Rift Valley fever virus (RVFV) is a mosquito-transmitted virus with proven ability to emerge into naïve geographic areas. Limited field evidence suggests that RVFV is transmitted vertically from parent mosquito to offspring, but until now this mechanism has not been confirmed in the laboratory. Furthermore, this transmission mechanism has allowed for the prediction of RVFV epizootics based on rainfall patterns collected from satellite information. However, in spite of the relevance to the initiation of epizootic events, laboratory confirmation of vertical transmission has remained an elusive research aim for thirty-five years. Herein we present preliminary evidence of the vertical transmission of RVFV by Culex tarsalis mosquitoes after oral exposure to RVFV. Progeny from three successive gonotrophic cycles were reared to adults, with infectious RVFV confirmed in each developmental stage. Virus was detected in ovarian tissues of parental mosquitoes 7 days after imbibing an infectious bloodmeal. Infection was confirmed in progeny as early as the first gonotrophic cycle, with infection rates ranging from 2.0–10.0%. Virus titers among progeny were low, which may indicate a host mechanism suppressing replication.
Highlights
Rift Valley fever virus (RVFV) is an emerging, mosquito-transmitted virus endemic to sub-Saharan Africa [1]
Rift Valley fever virus (RVFV) represents a significant threat in terms of its ability to emerge into naïve geographic areas
We present the first laboratory evidence of vertical transmission of RVFV in the susceptible North American vector, Culex tarsalis
Summary
Rift Valley fever virus (RVFV) (order: Bunyavirales; family: Phenuiviridae; genus: Phlebovirus) is an emerging, mosquito-transmitted virus endemic to sub-Saharan Africa [1]. Outbreaks are episodic and impose a significant economic, veterinary, and public health burden. Both livestock animals and humans are susceptible to infection. RVFV mortality rates among adult ruminant livestock ranges from 10% to 20%. In 1997–1998, a large transboundary outbreak of RVFV occurred in Africa, resulting in 90,000 human infections and the loss of approximately 100,000 domestic animals [5]. Much work has been conducted demonstrating that RVFV could invade and establish itself in North America because of frequent travel from endemic areas, presence of susceptible mosquito vectors, and US agricultural practices such as intensive livestock production [10,11,12,13,14,15,16]
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