The development of predictive tools for pre‐emptive dengue vector control: a study of Aedes aegypti abundance and meteorological variables in North Queensland,Australia

Objectives To describe the meteorological influences on adult dengue vector abundance in Australia for the development of predictive models to trigger pre‐emptive control operation. Methods Multiple linear regression analyses were performed using meteorological data and female Aedes aegypti collection data from BG‐Sentinel Mosquito traps placed at 11 monitoring sites in Cairns, north Queensland. Results Considerable regression coefficients (R² = 0.64 and 0.61) for longer‐ and shorter‐term factor models respectively were derived. Longer‐term factors significantly associated with abundance of adult vectors were mean minimum temperature (lagged 6 month) and mean daily temperature (lagged 4 month), explaining the predictable increase in abundance during the wet season. Factors explaining fluctuation in abundance in the shorter term were mean relative humidity over the previous 2 week and current daily average temperature. Rainfall variables were not found to be strong predictors of A. aegypti abundance in either longer‐ or shorter‐term models. Conclusions The implications of these findings for the development of useful predictive models for vector abundance risks are discussed. Such models can be used to guide the application of pre‐emptive dengue vector control, and thereby enhance disease management.     

A functional role for NS5ATP9 in the induction of HCV NS5A‐mediated autophagy

Autophagy has been shown to facilitate replication of hepatitis C virus (HCV); however, the mechanism by which HCV induces autophagy has not been fully established. NS5A, a nonstructural protein expressed by HCV, regulates numerous cellular pathways, including autophagy, by up‐regulating Beclin 1; however, the underlying mechanism remains unclear. To obtain new insights into HCV‐regulated autophagy, NS5ATP9 was overexpressed in HepG2 and L02 cells, resulting in up‐regulation of endogenous Beclin 1 mRNA and protein levels, respectively. The luciferase‐reporter assay results showed that both NS5A and NS5ATP9 could transactivate Beclin 1 promoter activity, but that NS5A could not transactivate the Beclin 1 promoter in NS5ATP9‐silenced HepG2 and L02 cells. Up‐regulation of Beclin 1 mRNA and protein expression by NS5A could also be attenuated by NS5ATP9 knock‐down. Furthermore, the HepG2 and L02 cells that transiently overexpressed NS5ATP9 had enhanced accumulation of vacuoles carrying the autophagy marker LC3, consistent with the conversion of endogenous LC3‐I to LC3‐II. In contrast, the conversion of endogenous LC3‐I to LC3‐II could not be enhanced by NS5A in NS5ATP9‐silenced HepG2 cells. These results highlight an important potential role for NS5ATP9 in HCV NS5A‐induced hepatocyte autophagy.