GIVE

Dr. Chelsea Smartt

Associate Professor

Our ability to mitigate epidemics is hindered by lack of knowledge about the mosquito vectors and our inability to predict dangerous vector populations and specific periods when they may become dangerous. A large part of the research being conducted in my lab is needed to fill in the missing information that has to do with vector-virus interactions. The interaction of the mosquito and the invading virus is complex and can result in physiological and gene expression alterations in the insect. In light of the above, we investigate the association of West Nile virus (WNV) and Culex pipiens quinquefasciatus mosquitoes and Dengue (DENV) and Chikungunya (CHIKV) viruses and Aedes aegypti mosquitoes that result in measureable changes in gene expression. Measurable changes in expression can be used to elucidate those genes involved in the infection and dissemination process for development of mosquito virus-transmission blocking vaccines.

To investigate the mechanism behind vector ability for West Nile virus, we identified a number of novel antiviral genes in Cx. p. quinquefasciatus shown to coincide with reduced WNV titer in the mosquito midgut when their expression is high. These novel genes were additionally shown to be involved in the same antiviral immune response pathway. Work to further characterize their involvement in WNV infection process is ongoing. We performed full transcriptome sequencing (Illumina) of two mosquito populations with variation in their vector competence and RNAseq analysis revealed involvement of several genes in differential competence to WNV and revealed the involvement of products involved in transport and signal transduction. Work is ongoing to specifically map which transport or signal transduction pathways are involved in the differences in WNV competence between the two populations.

We are also interested in the interaction of Aedes aegypti mosquitoes and the different serotypes of DENV. Our studies on an Aedes aegypti population collected in Key West FL in 2011 showed significant differences in its competence for three serotypes of dengue virus (DENV) implicated in past dengue outbreaks in Puerto Rico. The differences may be attributable to factors involved in virus genomics, viral growth kinetics, cellular receptors and/or antiviral response. In my lab we focus our studies on the interaction of mosquito genes involved in antiviral response and expression difference between infections with the 4 serotypes of DENV.

Since the recent outbreak of Chikungunya virus in Florida in 2014, we have initiated an investigation into the sudden local transmission of CHIKV and the molecular mechanisms responsible for this invasion.

 

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