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Host stress hormones affect host, but not vector, infectiousness for West Nile virus

Hormones that help hosts cope with stressors also affect how hosts regulate the processes that influence their susceptibility to parasites as well as their propensity to transmit pathogens to other hosts and vectors. In birds, corticosterone (CORT), influences timing of activity, feeding behaviors, and various immune defenses that influence the number and outcomes of host interactions with vectors and parasites. No study to our knowledge, though, has investigated whether CORT in hosts affects the extrinsic incubation period (EIP) of a vector for a virus, one of the strongest drivers of vector-borne disease cycles. Our goal here was to discern whether experimental CORT alterations in zebra finches (Taeniopygia guttata) affected EIP for West Nile virus (WNV) in the mosquito, Culex quinquefasciatus, a common vector of WNV and other infections in the southern US. We experimentally manipulated CORT in birds, infected them with WNV, and then investigated whether EIP differed between vectors fed on CORT-treated or control birds. Although CORT enhanced WNV viremia in hosts, as we have observed previously, we found no effects of CORT on vector EIP or post-feeding mortality rates, another important component of epidemiological models. These results, plus our prior observations that CORT enhances host attractiveness, indicate that some but not all stages of host-vector-virus interactions are sensitive to host stress.