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The Alphavirus genus within the Togaviridae family contains several important mosquito-borne arboviruses. Other than the antiviral activity of RNAi, relatively little is known about alphavirus interactions with insect cell defences. Here we show that Semliki Forest virus (SFV) infection of Aedes albopictus-derived U4.4 mosquito cells reduces cellular gene expression. Activation prior to SFV infection of pathways involving STAT/IMD, but not Toll signaling reduced subsequent virus gene expression and RNA levels. These pathways are therefore not only able to mediate protective responses against bacteria but also arboviruses. However, SFV infection of mosquito cells did not result in activation of any of these pathways and suppressed their subsequent activation by other stimuli.

Abstract: Mosquitoes vary in their competence or ability to transmit arthropod-borne viruses (arboviruses). Many arboviruses cause disease in humans and animals. Identifying the environmental and genetic causes of variation in mosquito competence for arboviruses is one of the great challenges in public health. Progress identifying genetic (nature) and environmental (nurture) factors influencing mosquito competence for arboviruses is reviewed. There is great complexity in the various traits that comprise mosquito competence. The complex interactions between environmental and genetic factors controlling these traits and the factors shaping variation in Nature are largely unknown. The norms of reaction of specific genes influencing competence, their distributions in natural populations and the effects of genetic polymorphism on phenotypic variation need to be determined. Mechanisms influencing competence are not likely due to natural selection because of the direct effects of the arbovirus on mosquito fitness. More likely the traits for mosquito competence for arboviruses are the effects of adaptations for other functions of these competence mechanisms. Determining these other functions is essential to understand the evolution and distributions of competence for arboviruses. This information is needed to

www.elsevier.com/locate/meegid Merging the field of epidemiology with those of evolutionary and behavioural ecology can generate considerable fundamental knowledge, as well as help to guide public health policies. An attempt is made here to integrate these disciplines by focusing on parasitic manipulation in vectorborne diseases. Parasitic manipulation is a fascinating strategy of transmission which occurs when a parasite alters phenotypic trait(s) of its hostina way that enhances its probability of transmission. Vector-borne parasites are responsible for many of the most harmful diseases affecting humans, and thus represent public health priority. It has been shown for several decades that viruses, bacteria and protozoa can alter important features of their arthropod vector and vertebrate host in a way that increases their probability of transmission. Here, we review these changes, including, the feeding behaviour, survival and immune system of the vector, as well as attraction, defensive behaviour, blood characterictics and immune system of the vertebrate host. Based on the classic measure of vector-borne disease transmission R0, additional changes, such as, vertebrate host choice by infected vectors or parasite development duration in the vector are expected. Reported or expected phenotypic changes are discussed in terms of costs and benefits to the parasite, its vector, and the vertebrate host. Introducing the parasitic manipulation concept into vector-borne diseases clearly highlights fruitful avenues not only for fundamental research, but also for developing strategies for disease control.