NO elicited normal appetitive and consummatory behaviors leading to the deposition of cordons containing egg capsules without eggs. The sites at which NO acts were investigated. The latency to egg deposition in response to a NO donor was shorter than that in

response to other stimuli, consistent with NO acting at downstream sites from those affected by the other stimuli. The NO donor does not act on neurons in GDC-0973 inhibitor the head ganglia presynaptic to the bag cells or on the bag cells. Ligating the small hermaphroditic duct connecting the gonad to the accessory genital mass blocked egg laying in response to bag cell homogenates, but not in response to exogenous NO, indicating that NO does not act on the gonad. NO is released by transport of eggs along the small hermaphroditic duct, and NO directly acts on the accessory genital mass which packages eggs. NO also acts at a second site, independent of the BAY 73-4506 effect on the accessory genital mass. A NO donor activates appetitive behaviors that normally precede egg laying even in A. californica that are unable to lay eggs.”
“Background: Rift Valley fever (RVF) is a severe mosquito-borne disease affecting humans and domestic ruminants. Mosquito saliva contains compounds that counteract the hemostatic, inflammatory, and immune responses of the host. Modulation of these defensive responses may facilitate virus

infection. Indeed, Aedes mosquito saliva played a crucial role in the vector’s capacity to effectively transfer arboviruses such as the

Cache Valley and West Nile viruses. The role of mosquito saliva in the transmission of Rift Valley fever virus (RVFV) has not been investigated.\n\nObjective: Using a murine model, we explored the potential for mosquitoes to impact the course of RVF disease by determining whether differences in pathogenesis occurred in the presence or absence of mosquito saliva and salivary gland extract.\n\nMethods: C57BL/6NRJ male mice were infected with the ZH548 strain of RVFV via intraperitoneal or intradermal route, or via bites from RVFV-exposed mosquitoes. The virus titers in mosquitoes BKM120 nmr and mouse organs were determined by plaque assays.\n\nFindings: After intraperitoneal injection, RVFV infection primarily resulted in liver damage. In contrast, RVFV infection via intradermal injection caused both liver and neurological symptoms and this route best mimicked the natural infection by mosquitoes. Co-injections of RVFV with salivary gland extract or saliva via intradermal route increased the mortality rates of mice, as well as the virus titers measured in several organs and in the blood. Furthermore, the blood cell counts of infected mice were altered compared to those of uninfected mice.\n\nInterpretation: Different routes of infection determine the pattern in which the virus spreads and the organs it targets. Aedes saliva significantly increases the pathogenicity of RVFV.