Although West Nile virus (WNV) and other arthropod-borne viruses are a major public health problem, the mechanisms of antiviral immunity in mosquitoes are poorly understood. Dicer-2, responsible for the RNAi-mediated response through the C-terminal RNase-III domain, also contains an N-terminal DExD/H-box helicase domain similar to mammalian RIG-I/MDA5 which, in Drosophila, was found to be required for activation of an antiviral gene, Vago. Here we show that the Culex orthologue of Vago (CxVago) is up-regulated in response to WNV infection in a Dicer-2-dependent manner. Further, our data show that CxVago is a secreted peptide that restricts WNV infection by activation of the Jak-STAT pathway. Thus, Vago appears to function as an IFN-like antiviral cytokine in mosquitoes.innate immunity | insect cytokine

[1] We present a coupled hydrology and entomology model for the mechanistic simulation of local-scale response of malaria transmission to hydrological and climatological determinants in semiarid, desert fringe environments. The model is applied to the Sahel village of Banizoumbou, Niger, to predict interannual variability in malaria vector mosquito populations that lead to variations in malaria transmission. Using a highresolution, small-scale distributed hydrology model that incorporates remotely sensed data for land cover and topography, we simulate the formation and persistence of the pools constituting the primary breeding habitat of Anopheles gambiae s.l. mosquitoes, the principal regional malaria vector mosquitoes. An agent-based mosquito population model is coupled to the distributed hydrology model, with aquatic-stage and adult-stage components. Through a dependence of aquatic-stage mosquito development and adult emergence on pool persistence, we model small-scale hydrology as a dominant control of mosquito abundance. For each individual adult mosquito, the model tracks attributes relevant to population dynamics and malaria transmission, which are updated as mosquitoes interact with their environment, humans, and animals.

-Re-emergence of human cases of plague after decades of silence does not necessarily mean that plague foci are re-emerging. Most often, Yersinia pestis bacteria have been maintained and circulating at low levels in the rodent populations. It seems therefore more appropriate to speak in terms of expansion or regression phases for sylvatic rodent plague foci and to reserve the term reemergence for human cases. From the analysis of well-documented human plague cases in Madagascar, we underline the causes of re-emergence that can be generalized to most world foci, and can help define environments at risk where the threat of new emergence lurks. In all recent plague outbreaks, usually more than one risk factor was at the origin of the re-emergence. The reduction or discontinuance of surveillance and control, as well as poverty and insalubrity are the main factors in the re-emergence of human cases, allowing increased contacts with infected rodents and fleas. Environment changes (i.e. climatic changes, deforestation, urbanization) induce changes in flea and rodent populations by (i) extension of rodent habitats (for example by replacing forests by steppes or farmlands); (ii) modifications in population dynamics (possible outbreaks due to an increase of available food resources); but also, (iii) emergence of new vectors, reservoirs and new Y. pestis genotypes. Numerous and spontaneous genomic rearrangements occur at high frequencies in Y. pestis, which may confer selective advantages, enhancing the ability of Y. pestis to survive, to be transmitted to new hosts, and to colonize new environments. Therefore, any environmental change should be taken as a warning signal and active surveillance programs should be initiated.