Abstract
The distribution and intensity of transmission of vector-borne pathogens can be strongly influenced by the competence of vectors. Vector competence, in turn, can be influenced by temperature and viral genetics. West Nile virus (WNV) was introduced into the United States of America in 1999 and subsequently spread throughout much of the Americas. Previously, we have shown that a novel genotype of WNV, WN02, first detected in 2001, spread across the US and was more efficient than the introduced genotype, NY99, at infecting, disseminating, and being transmitted by Culex mosquitoes. In the current study, we determined the relationship between temperature and time since feeding on the probability of transmitting each genotype of WNV. We found that the advantage of the WN02 genotype increases with the product of time and temperature. Thus, warmer temperatures would have facilitated the invasion of the WN02 genotype. In addition, we found that transmission of WNV accelerated sharply with increasing temperature, T, (best fit by a function of T4) showing that traditional degree-day models underestimate the impact of temperature on WNV transmission. This laboratory study suggests that both viral evolution and temperature help shape the distribution and intensity of transmission of WNV, and provides a model for predicting the impact of temperature and global warming on WNV transmission.
Highlights
The interaction between pathogens, their vectors, and vertebrate hosts is a dynamic one, and evolution in any one of the three can significantly alter transmission dynamics
The initial regressions indicated that the fraction of mosquitoes infected and the fraction with disseminated infections increased with degree days (DD = the DD model term (tT)) since feeding (Figures 1,2; Table 1)
The coefficient of this last term indicated that the fraction of mosquitoes transmitting West Nile virus (WNV) increased faster for the WN02 genotype than the NY99 genotype
Summary
The interaction between pathogens, their vectors, and vertebrate hosts is a dynamic one, and evolution in any one of the three can significantly alter transmission dynamics. Pathogens that infect and replicate well in their vertebrate hosts and vectors may decrease the survival of both which may reduce their lifespan for transmission. The distribution and intensity of transmission of vector-borne pathogens is strongly influenced by the interaction of temperature, vectors, hosts, and pathogen genetics. Temperature can determine both the latitudinal boundary and upper elevational limit of pathogen transmission if the extrinsic incubation period (EIP) is greater than the longevity of the vector [3]. Temperature has been linked to changes in the intensity of transmission of pathogens [4,5], which may be linked to temperature-induced changes in the EIP, the longevity, and the feeding rate of vectors [6,7]
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