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Kernbach, M. E.

Publications and source records attributed to Kernbach, M. E..

4 recordsLinked to original sources

Degenerate PCR primers for potexvirus detection in seagrasses

2.Turtlegrass virus X, which infects the seagrass Thalassia testudinum, is the only potexvirus known to infect marine flowering plants. We investigated potexvirus distribution in seagrasses using a degenerate reverse transcription polymerase chain reaction (RT-PCR) assay originally designed to capture potexvirus diversity in terrestrial plants. The assay, which implements Potex-5 and Potex-2RC primers, successfully amplified a 584 nt RNA-dependent RNA polymerase (RdRp) fragment from TVX-infected seagrasses. Following validation, we screened 74 opportunistically collected, apparently healthy seagrass samples for potexviruses using this RT-PCR assay. The survey examined the host species T. testudinum, Halodule wrightii, Halophila stipulacea, Syringodium filiforme, Ruppia maritima, and Zostera marina. Potexvirus PCR products were successfully generated only from T. testudinum samples and phylogenetic analysis of sequenced PCR products revealed five distinct TVX sequence variants. Although the RT-PCR assay revealed limited potexvirus diversity in seagrasses, the expanded geographic distribution of TVX shown here emphasizes the importance of future studies to investigate T. testudinum populations across its native range and understand how the observed fine-scale genetic diversity a?ects host-virus interactions. 3. Impact statementPotexviruses are widespread in terrestrial plants; however, the recent discovery of TVX in the seagrass Thalassia testudinum extends their host range to marine flowering plants. Here we use existing Potex-5 and Potex-2RC degenerate primers to explore potexvirus infections in several seagrass species. TVX sequence variants were detected in T. testudinum collected from the eastern Gulf of Mexico, uncovering previously unknown genetic diversity of this poorly understood virus. 4. Data summaryAll sequence data are available in NCBI GenBank under the accession numbers OR827692-OR827705, OR854648, OR863396, OR879052-OR879056, and PP430548-PP430571. The authors confirm all supporting data, code and protocols have been provided within the article or through supplementary data files.

microbiology↗

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.

ecology↗

Light pollution affects West Nile virus exposure risk across Florida.

Emerging infectious diseases (EIDs), including zoonotic arboviruses, present a global health threat. Multiple components of human land use change have been linked to arboviral emergence, but one pervasive factor that has received comparatively little attention is light pollution. Although often considered a component of built environments, artificial light at night (ALAN) outpaces the growth and spatial extent of urbanization, and thus affects areas where human population density and anthropogenic land changes are modest. West Nile virus (WNV) emergence has been described as peri-urban, but recent research suggests that its relative ubiquity in human-altered environments might actually be due to ALAN. Indeed, we found previously that experimental ALAN exposure enhanced avian competence to transmit WNV to mosquitoes. In the present study, we asked whether such organismal effects manifest ecologically by determining whether WNV exposure among sentinel chickens in Florida is related to local ALAN conditions. We found strong support for a nonlinear relationship between ALAN and WNV exposure in chickens with peak WNV risk occurring at low ALAN levels. Importantly, effects of ALAN on WNV exposure were stronger than other aspects of urbanization; only ambient temperature in the month prior to sampling had a comparable effect to ALAN. These results represent the first field evidence that ALAN might affect infectious disease exposure risk. We advocate for further research on how ALAN influences zoonotic risk, as well as efforts to study alternative nighttime lighting methods to reduce such risk. Significance StatementLight pollution associated with human development is a globally pervasive and rapidly expanding anthropogenic stressor; but despite documented effects on host immune functions and vector behaviors, how it affects infectious disease risk is unknown. Using data from the Florida Department of Health arbovirus surveillance program, we show that light pollution is a stronger predictor of variation in West Nile virus (WNV) exposure risk than many other previously implicated anthropogenic and natural environmental variables. Light pollution effects are nonlinear, so risk is highest in areas with dim light pollution. Our results highlight a new way that light pollution might affect human and wildlife health.

ecology↗

Light Pollution Increases West Nile Virus Competence in a Ubiquitous Passerine Reservoir Species

One sentence summaryLight pollution increases host infectiousness.\n\nAbstractLight pollution is a growing problem, but its impacts on infectious disease risk have not been considered. Previous research has revealed that dim light at night (dLAN) dysregulates various immune functions and biorhythms, which hints that dLAN could change the risk of disease epidemics. Here, we demonstrate that dLAN enhances infectiousness of the house sparrow (Passer domesticus), an urban-dwelling avian host of West Nile virus (WNV). Sparrows exposed to dLAN maintained viral titers above the transmission threshold to a biting vector (105 plaque-forming units) for two days longer than controls but did not die at higher rates. A mathematical model revealed that such effects could increase WNV outbreak potential by ~41%. dLAN likely affects other host and vector traits relevant to transmission, so additional research is needed to advise management of zoonotic diseases in light polluted areas.

pathology↗