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At least 109 records · Page 6Linked to original sources

Heightened exposure to parasites favors the evolution of immunity in brood parasitic cowbirds

Immunologists and evolutionary biologists are interested in how the immune system evolves to fit an ecological niche. We studied the relationship between exposure to parasites and strength of immunity by investigating the response of two species of New World cowbirds (genus Molothrus , Icteridae), obligate brood parasites with contrasting life history strategies, to experimental arboviral infection. The South American shiny cowbird ( M. bonariensis ) is an extreme host - generalist that lays its eggs in the nests of >225 different avian species. The Central American bronzed cowbird ( M. aeneus ) is a relative host - specialist that lays its eggs preferentially in the nests of approximately 12 orioles in a single sister genus. West Nile virus provided a strong challenge and delineated immune differences between these species. The extreme host-generalist shiny cowbird, like the North American host-generalist, the brown-headed cowbird, showed significantly lower viremia to three arboviruses than related icterid species that were not brood parasites. The bronzed cowbird showed intermediate viremia. These findings support the interpretation that repeated exposure to a high diversity of parasites favors the evolution of enhanced immunity in brood parasitic cowbirds and makes them useful models for future studies of innate immunity.

Evolutionary Biology

Heightened immune system function in polar bears using terrestrial habitats

Climate change is altering the distribution of some wildlife species while warming temperatures are facilitating the northward expansion of pathogens, potentially increasing disease risk. Melting of Arctic sea ice is causing polar bears ( Ursus maritimus ) of the Southern Beaufort Sea (SBS) to increasingly spend summer on land, where they may encounter novel pathogens. Here, we tested whether SBS polar bears on shore during summer exhibited greater immune system activity than bears remaining on the sea ice. In addition, we tested whether the type of immune response correlated with body condition, because adaptive responses (slowly-developing defenses against specific pathogens) often require less energy than innate responses (rapid defenses not based on pathogen identity). After accounting for body condition, we found that polar bears on shore exhibited higher total white blood cell counts, neutrophils, and monocytes than bears on the ice, suggesting greater infections. Lymphocytes, eosinophils, basophils and globulins did not differ. C-reactive protein, an indicator of inflammation, also did not differ between habitats. Body condition was associated with variables indicative of both innate and adaptive immunity, suggesting that neither response was uniquely limited by energy resources. Our data indicate that as more polar bears spend longer periods of time on shore, they may experience more infections. We encourage continued health monitoring of this species and studies of the long-term fitness consequences from disease.

Physiological and Biochemical Zoology

Enhanced innate immune responses in a brood parasitic cowbird species: degranulation and oxidative burst

We examined the relative effectiveness of two innate immune responses in two species of New World blackbirds (Passeriformes, Icteridae) that differ in resistance to West Nile virus (WNV). We measured degranulation and oxidative burst, two fundamental components of phagocytosis, and we predicted that the functional effectiveness of these innate immune responses would correspond to the species' relative resistance to WNV. The brown-headed cowbird (Molothrus ater), an obligate brood parasite, had previously shown greater resistance to infection with WNV, lower viremia and faster recovery when infected, and lower subsequent antibody titers than the red-winged blackbird (Agelaius phoeniceus), a close relative that is not a brood parasite. We found that cowbird leukocytes were significantly more functionally efficient than those of the blackbird leukocytes and 50% more effective at killing the challenge bacteria. These results suggest that further examination of innate immunity in the cowbird may provide insight into adaptations that underlie its greater resistance to WNV. These results support an eco-immunological interpretation that species like the cowbird, which inhabit ecological niches with heightened exposure to parasites, experience evolutionary selection for more effective immune responses.

Avian Diseases

Perfluorooctane sulfonamide induced autotoxic effects on the zebrafish immune system

Perfluorooctane sulfonamide (PFOSA) is an immediate perfluorooctanesulfonate (PFOS) precursor (PreFOS). Previous studies have shown PFOSA to induce stronger toxic responses compared to other perfluorinated compounds (PFCs). However, the specific nature of PFOSA-induced toxicity, whether autonomous or mediated by its metabolite PFOS, has not been fully elucidated. This study systematically investigates the immunomodulatory effects of PFOSA and PFOS in zebrafish ( Danio rerio ). Exposure to PFOSA compromised the zebrafish’s ability to defend against pathogenic infections, as evidenced by increased bacterial adhesion to their skin and reduced levels of the biocidal protein lysozyme (LYSO). Moreover, PFOSA exposure was associated with disruptions in inflammatory markers and immune indicators, along with a decrease in immune cell counts. The findings from this study suggest that the immunotoxicity effects of PFOSA are primarily due to its own toxicity rather than its metabolite PFOS. This conclusion was supported by dose-dependent responses, the severity of observed effects, and multivariate analysis. In addition, our experiments using NF-κB-morpholino knock-down techniques further confirmed the role of the Nuclear factor-κappa B pathway in mediating PFOSA-induced immunotoxicity. In conclusion, this study reveals that PFOSA impairs the immune system in zebrafish through an autotoxic mechanism, providing valuable insights for assessing the ecological risks of PFOSA.

Environmental Science and Technology

Do contrasting patterns of migration movements and disease outbreaks between congeneric waterfowl species reflect differing immunity?

Long-distance migrations influence the dynamics of hostpathogen interactions and understanding the role of migratory waterfowl in the spread of the highly pathogenic avian influenza viruses (HPAIV) is important. While wild geese have been associated with outbreak events, disease ecology of closely related species has not been studied to the same extent. The swan goose ( Anser cygnoides ) and the bar-headed goose ( Anser indicus ) are congeneric species with distinctly different HPAIV infection records; the former with few and the latter with numerous records. We compared movements of these species, as well as the more distantly related whooper swan ( Cygnus cygnus ) through their annual migratory cycle to better understand exposure to HPAIV events and how this compares within and between congeneric and noncongeneric species. In spite of their record of fewer infections, swan geese were more likely to come in contact with disease outbreaks than bar-headed geese. We propose two possible explanations: i) frequent prolonged contact with domestic ducks increases innate immunity in swan geese, and/or ii) the stress of high-elevation migration reduces immunity of bar-headed geese. Continued efforts to improve our understanding of species-level pathogen response is critical to assessing disease transmission risk.

Geospatial Health

Synergistic interventions to control COVID-19: Mass testing and isolation mitigates reliance on distancing

Stay-at-home orders and shutdowns of non-essential businesses are powerful, but socially costly, tools to control the pandemic spread of SARS-CoV-2. Mass testing strategies, which rely on widely administered frequent and rapid diagnostics to identify and isolate infected individuals, could be a potentially less disruptive management strategy, particularly where vaccine access is limited. In this paper, we assess the extent to which mass testing and isolation strategies can reduce reliance on socially costly non-pharmaceutical interventions, such as distancing and shutdowns. We develop a multi-compartmental model of SARS-CoV-2 transmission incorporating both preventative non-pharmaceutical interventions (NPIs) and testing and isolation to evaluate their combined effect on public health outcomes. Our model is designed to be a policy-guiding tool that captures important realities of the testing system, including constraints on test administration and non-random testing allocation. We show how strategic changes in the characteristics of the testing system, including test administration, test delays, and test sensitivity, can reduce reliance on preventative NPIs without compromising public health outcomes in the future. The lowest NPI levels are possible only when many tests are administered and test delays are short, given limited immunity in the population. Reducing reliance on NPIs is highly dependent on the ability of a testing program to identify and isolate unreported, asymptomatic infections. Changes in NPIs, including the intensity of lockdowns and stay at home orders, should be coordinated with increases in testing to ensure epidemic control; otherwise small additional lifting of these NPIs can lead to dramatic increases in infections, hospitalizations and deaths. Importantly, our results can be used to guide ramp-up of testing capacity in outbreak settings, allow for the flexible design of combined interventions based on social context, and inform future cost-benefit analyses to identify efficient pandemic management strategies.

PLOS Computational Biology

Temporal variation in viral hemorrhagic septicemia virus antibodies in freshwater drum ( Aplodinotus grunniens ) indicates cyclic transmission in Lake Winnebago, Wisconsin

Viral hemorrhagic septicemia virus (VHSV) is an emerging pathogen that causes mass mortality in multiple fish species. In 2007, the Great Lakes freshwater strain, type IVb, caused a large die-off of freshwater drum ( Aplodinotus grunniens ) in Lake Winnebago, Wisconsin, USA. To evaluate the persistence and transmission of VHSV, freshwater drum from Lake Winnebago were tested for antibodies to the virus using recently developed virus neutralization (VN) and enzyme-linked immunosorbent (ELISA) assays. Samples were also tested by real-time reverse transcription-PCR (rRT-PCR) to detect viral RNA. Of 548 serum samples tested, 44 (8.03%) were positive by VN (titers ranging from 1:16 to 1:1,024) and 45 (8.21%) were positive by ELISA, including 7 fish positive by both assays. Antibody prevalence increased with age and was higher in one northwestern area of Lake Winnebago than in other areas. Of 3,864 tissues sampled from 551 fish, 1 spleen and 1 kidney sample from a single adult female fish collected in the spring of 2012 tested positive for VHSV by rRT-PCR, and serum from the same fish tested positive by VN and ELISA. These results suggest that VHSV persists and viral transmission may be active in Lake Winnebago even in years following outbreaks and that wild fish may survive VHSV infection and maintain detectable antibody titers while harboring viral RNA. Influxes of immunologically naive juvenile fish through recruitment may reduce herd immunity, allow VHSV to persist, and drive superannual cycles of transmission that may sporadically manifest as fish kills.

Wisconsin

Developing transmissible vaccines for animal infections

Many emerging and reemerging pathogens originate from wildlife, but nearly all wild species are unreachable using conventional vaccination, which requires capture of and vaccine administration to individual animals. By enabling immunization at scales sufficient to interrupt pathogen transmission, transmissible vaccines (TVs) that spread themselves through wildlife populations by infectious processes could potentially transform the management of otherwise intractable challenges to public health, wildlife conservation, and animal welfare. However, generating TVs likely requires modifying viruses that would be intended to spread in nature, which raises concerns ranging from technical feasibility, to safety and security risks, to regulatory uncertainties ( 1 , 2 ). We propose a series of commitments and strategies for vaccine development—beginning with a priori decisions on vaccine design and continuing through to stakeholder codevelopment [see supplementary materials (SM)]—that we believe increase the likelihood that the potential risks of vaccine transmission are outweighed by benefits to conservation, animal welfare, and zoonosis prevention.

Science

Costimulatory receptors in a teleost fish: Typical CD28, elusive CTLA4

T cell activation requires both specific recognition of the peptide-MHC complex by the TCR and additional signals delivered by costimulatory receptors. We have identified rainbow trout sequences similar to CD28 (rbtCD28) and CTLA4 (rbtCTLA4). rbtCD28 and rbtCTLA4 are composed of an extracellular Ig-superfamily V domain, a transmembrane region, and a cytoplasmic tail. The presence of a conserved ligand binding site within the V domain of both molecules suggests that these receptors likely recognize the fish homologues of the B7 family. The mRNA expression pattern of rbtCD28 and rbtCTLA4 in naive trout is reminiscent to that reported in humans and mice, because rbtCTLA4 expression within trout leukocytes was quickly up-regulated following PHA stimulation and virus infection. The cytoplasmic tail of rbtCD28 possesses a typical motif that is conserved in mammalian costimulatory receptors for signaling purposes. A chimeric receptor made of the extracellular domain of human CD28 fused to the cytoplasmic tail of rbtCD28 promoted TCR-induced IL-2 production in a human T cell line, indicating that rbtCD28 is indeed a positive costimulator. The cytoplasmic tail of rbtCTLA4 lacked obvious signaling motifs and accordingly failed to signal when fused to the huCD28 extracellular domain. Interestingly, rbtCTLA4 and rbtCD28 are not positioned on the same chromosome and thus do not belong to a unique costimulatory cluster as in mammals. Finally, our results raise questions about the origin and evolution of positive and negative costimulation in vertebrate immune systems. T cell activation is initiated through complex cell-to-cell interactions. TCRs expressed on the surface of T cells first recognize antigenic peptides presented by MHC molecules on the surface of APCs. TCRs and other surface receptors and ligands stabilize the contact between T cells and APCs, which triggers signal transduction pathways resulting in T cell activation. According to the two-signal model ( 1 , 2 ), T cell activation by Ag requires both specific recognition of the peptide by the TCR (signal 1) and additional signals delivered by other costimulatory receptors (signal 2). Among the known costimulatory receptors, CD28 and CTLA4 (also known as CD152), which are expressed on T cells and bind their corresponding ligands B7-1/B7-2 (CD80/CD86) on APCs, represent a well-studied system in mammals ( 3 ). CD28 is a glycosylated homodimeric protein expressed on the surface of double-positive thymocytes, mature CD4 + T cells, CD11b − CD8 + T cells, and γδ CD3 + T cells ( 4 , 5 ). CD28 is expressed at higher levels on activated T cells than on resting cells ( 6 ). In mammals, CD28 binds to B7-1 and B7-2, which are expressed on the surface of APCs, and delivers a critical costimulatory signal to T lymphocytes. In the absence of CD28 ligation, TCR binding either induces apoptosis or anergy in T cells ( 5 ). Engagement of CD28 alone cannot activate T cells, even if synergetic effects are provided via stimulation by T cell mitogens or anti-CD3 treatment ( 7 ). A tyrosine-based motif in cytoplasmic tail of CD28 functions as a binding site for the p85 PI3K subunit when it is phosphorylated ( 8 , 9 ). Other CD28 intracytoplasmic motifs, which associates with IL-2-inducible tyrosine kinase, lymphocyte-specific tyrosine kinase, and the adaptor growth-factor receptor bound protein-2 are responsible for signal transduction ( 10 , 11 , 12 ). The binding of growth-factor receptor bound protein-2 to CD28 also activates the GTPase RAS ( 13 ). CD28 signaling is also thought to contribute to the mobilization of lipid rafts to the immunological synapse ( 14 ), the region of contact between T cell and APC, which lowers the overall threshold of TCR engagement required for effective cytokine production and proliferation ( 15 ). In contrast, CTLA4 is a powerful negative regulator of T cell activation and was first cloned via differential screening of a cytotoxic T cell cDNA library ( 16 ). CD28 and CTLA4 belong to the same family and share high sequence similarity to each other ( 16 , 17 ). Both receptors interact with B7-1 and/or B7-2 but induce different signals: CD28 amplifies signaling triggered by the TCR-CD3 complex, whereas CTLA4 generates negative signals that inhibit T cell activation ( 18 ). CTLA4 has higher affinity for B7-1 and B7-2 compared with CD28, and its expression is also induced by TCR engagement ( 19 ). The mechanisms of CTLA4-mediated suppression likely involve both competition with CD28 for B7-1/B7-2 binding and potent inhibitory signals delivered by CTLA4 ( 20 ). The inhibitory signaling mechanisms triggered by CTLA4 are not clear. The CTLA4 cytoplasmic tail lacks typical ITIM motifs and shares with CD28 a p85 binding site ( 21 ). Thus, the extent of an immune response is likely controlled through the finely tuned expression of costimulatory receptors from the CD28/CTLA4 family on the surface of activated T cells ( 22 , 23 ). Very little is known about T cell responses and activation in bony fish. TCR-αβ cDNAs ( 24 , 25 , 26 , 27 ) and polymorphic class IA and class IIA/B MHC molecules ( 28 , 29 , 30 ) have been reported in several species, suggesting that the fish TCR recognizes antigenic peptides presented by MHC molecules similar to that of mammals. T cell-mediated responses in fish are supported by several lines of evidence. Allograft rejection provided the first experimental indications suggesting that bony fish possess a functional T cell-mediated immune response ( 31 , 32 ). In vitro assays for allospecific cytotoxicity have also been established using clonal and nonclonal catfish cell lines ( 33 , 34 ) or clonal rainbow trout ( 35 ). Autologous cell-mediated specific lysis of virus-infected syngenic target cells has also been reported in cloned goldfish ( 36 , 37 ). Finally, both public and private T cell-specific expansions have been observed in rainbow trout during secondary immune responses to viral hemorrhagic septicemia virus (VHSV), 3 a fish rhabdovirus, using TCR-β CDR3-length spectratyping ( 38 ). TCR-MHC-peptide interactions induce signaling events through CD3 in mammals and most likely in lower vertebrates because a complete set of CD3 genes, including TCR ζ, CD3 ε, and CD3 γδ, has been found in Pufferfish and Xenopus ( 39 , 40 ). CD8α has been identified in rainbow trout ( 41 ); however, the cytoplasmic tail lacks the consensus p56 lck motif, suggesting that TCR/CD3/CD8-mediated signaling events may be different in teleosts. In this study, we have identified and initially characterized two members of the CD28 family in rainbow trout, rbtCD28 and rbtCTLA4. Their sequence features and expression patterns suggest that they are the likely homologues of mammalian CD28 and CTLA4. The potential costimulatory capacities of these fish receptors were investigated using a human T cell line expressing chimeric receptors composed of the extracellular domain of human CD28 (hCD28) fused to the cytoplasmic tail of rbtCD28 or rbtCTLA4. The chimeric hCD28-rbtCD28 receptor mediated enhanced TCR-induced IL-2 production, suggesting a costimulatory function for rbtCD28. In contrast, the divergent cytoplasmic tail from rbtCTLA4 did not mediate similar signaling activities. This study therefore provides the first characterization of costimulatory receptors in lower vertebrates.

Journal of Immunology

Prevention and control of viral diseases of salmonids

Three viral diseases of salmonids are of worldwide concern: infectious pancreatic necrosis (IPN) viral hemorrhagic septicemia (VHS), and infectious hematopoietic necrosis (IHN). Six principal approaches are being used to prevent or control these diseases: 1) preventing contact o the pathogen with the host, 2) environmental manipulation, 3) immunization, 4) chemotherapy, 5 selective breeding for disease resistance, and 6) reducing stress conditions which augment disease conditions. Preventing the introduction of a pathogen into a new stock of fish has been accomplished mainly by implementing stringent laws to prevent transport of infected fish into uninfected areas. Stocks of fish already infected are sometimes destroyed, and the hatchery is disinfected and restocked with fish free of specific pathogens. Environmental manipulation (elevated water temperature) has been successfully used to control IHN. Chemotherapeutics such as povidone-iodine for IPN and benzipyrene for IHN show promise of controlling mortalities; however, the practicality of using these drugs to eliminate the carrier fish has not been evaluated. Salmonids are capable of developing immune responses to viruses; however, development of effective vaccines, selective breeding for disease resistance, and identification of stress conditions which augment disease are still in the experimental phase.

Journal of the Fisheries Research Board of Canada

Experimental susceptibility of Wood Ducks ( Aix sponsa ) for West Nile virus

Detection of West Nile virus (WNV) has been reported in a variety of wild ducks in the US, but little is known about the pathogenesis and outcome of exposure of the disease in these species. Previous experimental studies of WNV in ducks either have challenged a small number of ducks with WNV or have tested domesticated ducks. To determine susceptibility and immune response, we challenged 7-wk-old Wood Ducks ( Aix sponsa ) with a 1999 American Crow ( Corvus brachyrhynchos ) isolate of WNV. Wood Ducks were susceptible to infection with the virus, and, although clinical signs or mortality were not observed, microscopic lesions were noted, particularly in the heart and brain. West Nile virus viremia peaked on day 2 postinfection (pi) at 10 4.54 plaque-forming units (PFU) of virus/mL serum and WNV was shed orally (between 10 2 and 10 2.9 PFU per swab) and cloacally. Specific anti-WNV antibody response was rapid, with anti-WNV IgM detected on day 3 pi followed on day 5 pi by anti-WNV IgG. Neutralizing antibodies were detected by plaque-reduction neutralization assay in one duck on day 4 pi, and in all sampled ducks on day 5. These results indicate that Wood Ducks are susceptible to WNV, but it is unlikely that significant WNV mortality events occur in Wood Ducks or that ducks play a significant role in transmission. However, WNV viremia was sufficient, in theory, to infect mosquitoes, and oral and cloacal shedding of the virus may increase the risk of infection to other waterbirds.

Journal of Wildlife Diseases

Pathophysiology of infectious hematopoietic necrosis virus disease in rainbow trout (Salmo gairdneri): early changes in blood and aspects of the immune Response after Injection of IHN Virus

Juvenile rainbow trout ( Salmo gairdneri ) were injected with infectious hematopoietic necrosis (IHN) virus and various hematological and blood chemical changes were monitored over 9 days. The packed cell volume, hemoglobin, red blood cell count, and plasma bicarbonate were significantly depressed by day 4. Plasma chloride, calcium, phosphorus, total protein, and blood cell types did not change during the 9 days. Furthermore, plasma LDH isozyme was significantly increased by the fourth day, and fish infected with infectious pancreatic necrosis virus, Vibrio anguillarum , Aeromonas salmonicida , and redmouth bacterium did not show specific LDH isozyme alterations. Acid-base alterations occurred at 10 C but not at 18 C. The acid-base imbalance and elevation of the LDH isozyme were consistently associated with the early development of the disease.The immune response after injection of IHN virus was determined and protection from disease was tested by passive immunization. Actively immunized fish developed IHN-neutralizing antibodies within 54 days after injection of virus, and the antibodies were protective when juvenile fish were passively immunized and experimentally challenged with IHN virus.

Journal of the Fisheries Research Board of Canada

Why does bee health matter? The science surrounding honey bee health concerns and what we can do about it

A colony of honey bees is an amazing organism when it is healthy; it is a superorganism in many senses of the word. As with any organism, maintaining a state of health requires cohesiveness and interplay among cells and tissues and, in the case of a honey bee colony, the bees themselves. The individual bees that make up a honey bee colony deliver to the superorganism what it needs: pollen and nectar collected from flowering plants that contain nutrients necessary for growth and survival. Honey bees with access to better and more complete nutrition exhibit improved immune system function and behavioral defenses for fighting off effects of pathogens and pesticides (Evans and Spivak 2010; Mao, Schuler, and Berenbaum 2013; Wahl and Ulm 1983). Sadly, as this story is often told in the headlines, the focus is rarely about what it means for a honey bee colony to be healthy and is instead primarily focused on colony survival rates. Bee colonies are chronically exposed to parasitic mites, viruses, diseases, miticides, pesticides, and poor nutrition, which weaken and make innate defenses insufficient at overcoming these combined stressors. Colonies that are chronically weakened can be even more susceptible to infections and levels of pesticide exposure that might otherwise be innocuous, further promoting a downward spiral of health. Sick and weakened bees diminish the colony’s resiliency, ultimately leading to a breakdown in the social structure, production, efficiency, immunity, and reproduction of the colony, and eventual or sudden colony death.

Report

Functional variation at an expressed MHC class IIß locus associates with Ranavirus infection intensity in larval anuran populations

Infectious diseases are causing catastrophic losses to biodiversity globally. Iridoviruses in the genus Ranavirus are among the leading causes of amphibian disease-related mortality. Polymorphisms in major histocompatibility complex (MHC) genes are significantly associated with variation in amphibian susceptibility to pathogens. MHC genes encode diverse cell-surface molecules that can recognize and bind to a wide array of pathogen peptides, and are divided into two classes. While MHC class I genes are the classic mediators of viral acquired immunity, larval amphibians do not express them. However, MHC class II gene diversity may be an important predictor of Ranavirus susceptibility in larval amphibians, the life stage most susceptible to Ranavirus. We surveyed natural populations of larval wood frogs (Lithobates sylvaticus), which are highly susceptible to Ranavirus, across 17 ponds and two years in Maryland, USA. We sequenced the peptide-binding region of an expressed MHC class IIß locus and assessed allelic and genetic diversity. We converted alleles to functional supertypes and determined if physiochemical properties of peptide-binding regions influenced host responses to Ranavirus. Among 334 sampled individuals, 26% were infected with Ranavirus, and among infected individuals the average intensity was 7.12 x 107 virus copies. We recovered 20 unique MHC class IIß alleles that fell into two deeply diverged clades and seven functional supertypes. Variation in MHC supertypes were associated with Ranavirus infection intensity, but not prevalence. MHC supertype heterozygotes and individuals with the MHC supertype genotype ST1/ST7 had significantly lower Ranavirus infection intensity compared to homozygotes and all other genotypes. We conclude that MHC class IIß functional genetic variation is an important component of Ranavirus susceptibility. Identifying immune system gene signatures linked to variation in disease susceptibility can inform mitigation strategies for combatting global amphibian declines.

Immunogenetics

Up in arms: Immune and nervous system response to sea star wasting disease

Echinoderms, positioned taxonomically at the base of deuterostomes, provide an important system for the study of the evolution of the immune system. However, there is little known about the cellular components and genes associated with echinoderm immunity. The 2013–2014 sea star wasting disease outbreak is an emergent, rapidly spreading disease, which has led to large population declines of asteroids in the North American Pacific. While evidence suggests that the signs of this disease, twisting arms and lesions, may be attributed to a viral infection, the host response to infection is still poorly understood. In order to examine transcriptional responses of the sea star Pycnopodia helianthoides to sea star wasting disease, we injected a viral sized fraction (0.2 μm) homogenate prepared from symptomatic P. helianthoides into apparently healthy stars. Nine days following injection, when all stars were displaying signs of the disease, specimens were sacrificed and coelomocytes were extracted for RNA-seq analyses. A number of immune genes, including those involved in Toll signaling pathways, complement cascade, melanization response, and arachidonic acid metabolism, were differentially expressed. Furthermore, genes involved in nervous system processes and tissue remodeling were also differentially expressed, pointing to transcriptional changes underlying the signs of sea star wasting disease. The genomic resources presented here not only increase understanding of host response to sea star wasting disease, but also provide greater insight into the mechanisms underlying immune function in echinoderms.

PLoS ONE

Chemical and mineralogical characteristics of French green clays used for healing

The worldwide emergence of infectious diseases, together with the increasing incidence of antibiotic-resistant bacteria, elevate the need to properly detect, prevent, and effectively treat these infections. The overuse and misuse of common antibiotics in recent decades stimulates the need to identify new inhibitory agents. Therefore, natural products like clays, that display antibacterial properties, are of particular interest. The absorptive properties of clay minerals are well documented for healing skin and gastrointestinal ailments. However, the antibacterial properties of clays have received less scientific attention. French green clays have recently been shown to heal Buruli ulcer, a necrotic or ‘flesh-eating’ infection caused by Mycobacterium ulcerans . Assessing the antibacterial properties of these clays could provide an inexpensive treatment for Buruli ulcer and other skin infections. Antimicrobial testing of the two clays on a broad-spectrum of bacterial pathogens showed that one clay promotes bacterial growth (possibly provoking a response from the natural immune system), while another kills bacteria or significantly inhibits bacterial growth. This paper compares the mineralogy and chemical composition of the two French green clays used in the treatment of Buruli ulcer. Mineralogically, the two clays are dominated by 1 Md illite and Fe-smectite. Comparing the chemistry of the clay minerals and exchangeable ions, we conclude that the chemistry of the clay, and the surface properties that affect pH and oxidation state, control the chemistry of the water used to moisten the clay poultices and contribute the critical antibacterial agent(s) that ultimately debilitate the bacteria.

Clays and Clay Minerals

Monkeypox virus in animals: Current knowledge of viral transmission and pathogenesis in wild animal reservoirs and captive animal models

Mpox, formerly called monkeypox, is now the most serious orthopoxvirus (OPXV) infection in humans. This zoonotic disease has been gradually re-emerging in humans with an increasing frequency of cases found in endemic areas, as well as an escalating frequency and size of epidemics outside of endemic areas in Africa. Currently, the largest known mpox epidemic is spreading throughout the world, with over 85,650 cases to date, mostly in Europe and North America. These increased endemic cases and epidemics are likely driven primarily by decreasing global immunity to OPXVs, along with other possible causes. The current unprecedented global outbreak of mpox has demonstrated higher numbers of human cases and greater human-to-human transmission than previously documented, necessitating an urgent need to better understand this disease in humans and animals. Monkeypox virus (MPXV) infections in animals, both naturally occurring and experimental, have provided critical information about the routes of transmission; the viral pathogenicity factors; the methods of control, such as vaccination and antivirals; the disease ecology in reservoir host species; and the conservation impacts on wildlife species. This review briefly described the epidemiology and transmission of MPXV between animals and humans and summarizes past studies on the ecology of MPXV in wild animals and experimental studies in captive animal models, with a focus on how animal infections have informed knowledge concerning various aspects of this pathogen. Knowledge gaps were highlighted in areas where future research, both in captive and free-ranging animals, could inform efforts to understand and control this disease in both humans and animals.

Viruses

Comparison of immune responses of brown-headed cowbird and related blackbirds to West Nile and other mosquito-borne encephalitis viruses

The rapid geographic spread of West Nile virus (family Flaviviridae , genus Flavivirus , WNV) across the United States has stimulated interest in comparative host infection studies to delineate competent avian hosts critical for viral amplification. We compared the host competence of four taxonomically related blackbird species (Icteridae) after experimental infection with WNV and with two endemic, mosquito-borne encephalitis viruses, western equine encephalomyelitis virus (family Togaviridae , genus Alphavirus , WEEV), and St, Louis encephalitis virus (family Flaviviridae , genus Flavivirus , SLEV). We predicted differences in disease resistance among the blackbird species based on differences in life history, because they differ in geographic range and life history traits that include mating and breeding systems. Differences were observed among the response of these hosts to all three viruses, Red-winged Blackbirds were more susceptible to SLEV than Brewer's Blackbirds, whereas Brewer's Blackbirds were more susceptible to WEEV than Red-winged Blackbirds. In response to WNV infection, cowbirds showed the lowest mean viremias, cleared their infections faster, and showed lower antibody levels than concurrently infected species. Brown-headed Cowbirds also exhibited significantly lower viremia responses after infection with SLEV and WEEV as well as coinfection with WEEV and WNV than concurrently infected icterids. We concluded that cowbirds may be more resistant to infection to both native and introduced viruses because they experience heightened exposure to a variety of pathogens of parenting birds during the course of their parasitic life style.

Journal of Wildlife Diseases