Limited potexvirus diversity in eastern Gulf of Mexico seagrass meadows.

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 affects host-virus interactions.

Light pollution affects West Nile virus exposure risk across Florida.

Emerging infectious diseases (EIDs) present global health threats, and their emergences are often linked to anthropogenic change. Artificial light at night (ALAN) is one form of anthropogenic change that spans beyond urban boundaries and may be relevant to EIDs through its influence on the behaviour and physiology of hosts and/or vectors. Although West Nile virus (WNV) emergence has been described as peri-urban, we hypothesized that exposure risk could also be influenced by ALAN in particular, which is testable by comparing the effects of ALAN on prevalence while controlling for other aspects of urbanization. By modelling WNV exposure among sentinel chickens in Florida, we found strong support for a nonlinear relationship between ALAN and WNV exposure risk in chickens with peak WNV risk occurring at low ALAN levels. Although our goal was not to discern how ALAN affected WNV relative to other factors, effects of ALAN on WNV exposure were stronger than other known drivers of risk (i.e. impervious surface, human population density). Ambient temperature in the month prior to sampling, but no other considered variables, strongly influenced WNV risk. These results indicate that ALAN may contribute to spatio-temporal changes in WNV risk, justifying future investigations of ALAN on other vector-borne parasites.

Light pollution increases West Nile virus competence of a ubiquitous passerine reservoir species.

Among the many anthropogenic changes that impact humans and wildlife, one of the most pervasive but least understood is light pollution. Although detrimental physiological and behavioural effects resulting from exposure to light at night are widely appreciated, the impacts of light pollution on infectious disease risk have not been studied. Here, we demonstrate that artificial light at night (ALAN) extends the infectious-to-vector period of the house sparrow (Passer domesticus), an urban-dwelling avian reservoir host of West Nile virus (WNV). Sparrows exposed to ALAN maintained transmissible viral titres for 2 days longer than controls but did not experience greater WNV-induced mortality during this window. Transcriptionally, ALAN altered the expression of gene regulatory networks including key hubs (OASL, PLBD1 and TRAP1) and effector genes known to affect WNV dissemination (SOCS). Despite mounting anti-viral immune responses earlier, transcriptomic signatures indicated that ALAN-exposed individuals probably experienced pathogen-induced damage and immunopathology, potentially due to evasion of immune effectors. A simple mathematical modelling exercise indicated that ALAN-induced increases of host infectious-to-vector period could increase WNV outbreak potential by approximately 41%. ALAN probably affects other host and vector traits relevant to transmission, and additional research is needed to advise the management of zoonotic diseases in light-polluted areas.

An experimental test of the physiological consequences of avian malaria infection.

Chronic, low-intensity parasite infections can reduce host fitness through negative impacts on reproduction and survival, even if they produce few overt symptoms. As a result, these parasites can influence the evolution of host morphology, behaviour and physiology. The physiological consequences of chronic infection can provide insight into the processes underlying parasite-driven natural selection. Here, we evaluate the physiological consequences of natural, low-intensity infection in an avian host-parasite system: adult male red-winged blackbirds (Agelaius phoeniceus) infected with haemosporidian parasites. Chronic haemosporidian infection has previously been shown to reduce both reproductive success and survival in several avian species. We used antimalarial medications to experimentally reduce haemosporidian parasitaemia (the proportion of blood cells infected with haemosporidian parasites) and measured the effect of treatment on body condition, haematology, immune function, physiological stress and oxidative state. Treatment with an antimalarial medication reduced parasitaemia for the most prevalent haemosporidian parasites from the genus Plasmodium. Treatment also increased haemoglobin and haematocrit, and decreased red blood cell production rates. We detected no effect of treatment on body condition, immune metrics, plasma corticosterone concentrations, total antioxidant capacity or reactive oxygen metabolites. Our results suggest that the damage and replacement of red blood cells during infection could be important costs of chronic haemosporidian infection. Strong links between parasitaemia and the physiological consequences of infection indicate that even for relatively low-intensity infections, measuring parasitaemia rather than only presence/absence could be important when evaluating the role of infection in influencing hosts' behaviour, physiology or fitness.

House Sparrows Vary Seasonally in Their Ability to Transmit West Nile Virus.

AbstractSeasonality in infectious disease prevalence is predominantly attributed to changes in exogenous risk factors. For vectored pathogens, high abundance, activity, and/or diversity of vectors can exacerbate disease risk for hosts. Conversely, many host defenses, particularly immune responses, are seasonally variable. Seasonality in host defenses has been attributed, in part, to the proximate (i.e., metabolic) and ultimate (i.e., reproductive fitness) costs of defense. In this study, our goal was to discern whether any seasonality is observable in how a common avian host, the house sparrow (Passer domesticus), copes with a common zoonotic arbovirus, the West Nile virus (WNV), when hosts are studied under controlled conditions. We hypothesized that if host biorhythms play a role in vector-borne disease seasonality, birds would be most vulnerable to WNV when breeding and/or molting (i.e., when other costly physiological activities are underway) and thus most transmissive of WNV at these times of year (unless birds died from infection). Overall, the results only partly supported our hypothesis. Birds were most transmissive of WNV in fall (after their molt is complete and when WNV is most prevalent in the environment), but WNV resistance, WNV tolerance, and WNV-dependent mortality did not vary among seasons. These results collectively imply that natural arboviral cycles could be partially underpinned by endogenous physiological changes in hosts. However, other disease systems warrant study, as this result could be specific to the nonnative and highly commensal nature of the house sparrow or a consequence of the relative recency of the arrival of WNV to the United States.

The Diversity of Photosensitivity and its Implications for Light Pollution.

Artificial light at night (ALAN) is a pervasive anthropogenic pollutant, emanating from urban and suburban developments and reaching nearly all ecosystems from dense forests to coastlines. One proposed strategy for attenuating the consequences of ALAN is to modify its spectral composition to forms that are less disruptive for photosensory systems. However, ALAN is a complicated pollutant to manage due to the extensive variation in photosensory mechanisms and the diverse ways these mechanisms manifest in biological and ecological contexts. Here, we highlight the diversity in photosensitivity across taxa and the implications of this diversity in predicting biological responses to different forms of night lighting. We curated this paper to be broadly accessible and inform current decisions about the spectrum of electric lights used outdoors. We advocate that efforts to mitigate light pollution should consider the unique ways species perceive ALAN, as well as how diverse responses to ALAN scale up to produce diverse ecological outcomes.

Introduction to the Symposium: Effects of Light Pollution Across Diverse Natural Systems.

Light pollution, or the presence of artificial light at night (ALAN), is among the fastest growing but least understood anthropogenic stressor on the planet. While historically light pollution has not received attention comparable to climate change or chemical pollution, research over the past several decades has revealed the plethora of negative effects on humans, animals, and supporting ecosystems. As light pollution continues to grow in spatial, spectral, and temporal extent, we recognize the urgent need to understand how this affects circadian physiology, organismal fitness, life history traits and tradeoffs, population trends, and community interactions. Here, we aim to highlight background and foundational evidence of the effects of light pollution to present context and the basis for early light pollution studies. Next, we touch on several understudied topics where research is underway to fill gaps in our knowledge and provide the basis for future research. Last, we focus on questions that are vital to understanding the effects of ALAN on diverse natural systems and discuss the barriers we face conducting research on light pollution.

Distinct effects of acute versus chronic corticosterone exposure on Zebra finch responses to West Nile virus.

Wild animals are exposed to both short- (acute) and long-term (chronic) stressors. The glucocorticoid hormones, such as corticosterone (CORT), facilitate coping with such stressors, but these hormones can have quite distinct effects contingent on the duration of their elevation. Previously, we found that experimental elevation of CORT for 2 days (via implantation) affected zebra finch (Taeniopygia guttata) responses to West Nile virus (WNV). CORT-elevated birds had higher viremia for at least 2 days longer than controls, and West Nile virus (WNV)-associated mortality occurred only in CORT-elevated birds. Here, we queried how acute elevations of CORT, via injection an hour prior to WNV exposure, would affect host responses, as short-term CORT elevations can be protective in other species. Although CORT injections and implantations elevated circulating CORT to a similar degree, the type of CORT exposure had quite distinct effects on WNV responses. CORT-implanted individuals reached higher viremia and suffered more mortality to WNV than control and CORT-injected individuals. However, CORT-implanted birds maintained body mass better during infection than the other two groups. Our results further support the possibility that chronic physiological stress affects aspects of host competence and potentially community-level WNV disease dynamics.

Dim light at night: physiological effects and ecological consequences for infectious disease.

Light pollution has emerged as a pervasive component of land development over the past century. Several detrimental impacts of this anthropogenic influence have been identified in night shift workers, laboratory rodents, and a plethora of wildlife species. Circadian, or daily, patterns are interrupted by the presence of light at night and have the capacity to alter rhythmic physiological or behavioral characteristics. Indeed, biorhythm disruption can lead to metabolic, reproductive, and immunological dysfunction depending on the intensity, timing, duration, and wavelength of light exposure. Light pollution, in many forms and by many pathways, is thus apt to affect the nature of host-pathogen interactions. However, no research has yet investigated this possibility. The goal of this manuscript is to outline how dim light at night, a relevant and common form of light pollution, may affect disease dynamics by interrupting circadian rhythms and regulation of immune responses as well as opportunities for host-parasite interactions and subsequent transmission risk including spillover into humans. We close by proposing some promising interventions including alternative lighting methods or vector control efforts.