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Virus shedding kinetics and unconventional virulence tradeoffs

Tradeoff theory, which postulates that virulence provides both transmission costs and benefits for pathogens, has become widely adopted by the scientific community. Although theoretical literature exploring virulence-tradeoffs is vast, empirical studies validating various assumptions still remain sparse. In particular, truncation of transmission duration as a cost of virulence has been difficult to quantify with robust controlled in vivo studies. We sought to fill this knowledge gap by investigating how transmission rate and duration were associated with virulence for infectious hematopoietic necrosis virus (IHNV) in rainbow trout ( Oncorhynchus mykiss ). Using host mortality to quantify virulence and viral shedding to quantify transmission, we found that IHNV did not conform to classical tradeoff theory. More virulent genotypes of the virus were found to have longer transmission durations due to lower recovery rates of infected hosts, but the relationship was not saturating as assumed by tradeoff theory. Furthermore, the impact of host mortality on limiting transmission duration was minimal and greatly outweighed by recovery. Transmission rate differences between high and low virulence genotypes were also small and inconsistent. Ultimately, more virulent genotypes were found to have the overall fitness advantage, and there was no apparent constraint on the evolution of increased virulence for IHNV. However, using a mathematical model parameterized with experimental data, it was found that host culling resurrected the virulence tradeoff and provided low virulence genotypes with the advantage. Human-induced or natural culling, as well as host population fragmentation, may be some of the mechanisms by which virulence diversity is maintained in nature. This work highlights the importance of considering non-classical virulence tradeoffs.

PLoS Pathogens↗

Surveillance for highly pathogenic influenza A viruses in California during 2014–2015 provides insights into viral evolutionary pathways and the spatiotemporal extent of viruses in the Pacific Americas Flyway

We used surveillance data collected in California before, concurrent with, and subsequent to an outbreak of highly pathogenic (HP) clade 2.3.4.4 influenza A viruses (IAVs) in 2014–2015 to (i) evaluate IAV prevalence in waterfowl, (ii) assess the evidence for spill-over infections in marine mammals and (iii) genetically characterize low-pathogenic (LP) and HP IAVs to refine inference on the spatiotemporal extent of HP genome constellations and to evaluate possible evolutionary pathways. We screened samples from 1496 waterfowl and 1142 marine mammals collected from April 2014 to August 2015 and detected IAV RNA in 159 samples collected from birds ( n = 157) and pinnipeds ( n = 2). HP IAV RNA was identified in three samples originating from American wigeon ( Anas americana ). Genetic sequence data were generated for a clade 2.3.4.4 HP IAV-positive diagnostic sample and 57 LP IAV isolates. Phylogenetic analyses revealed that the HP IAV was a reassortant H5N8 virus with gene segments closely related to LP IAVs detected in mallards ( Anas platyrhynchos ) sampled in California and other IAVs detected in wild birds sampled within the Pacific Americas Flyway. In addition, our analysis provided support for common ancestry between LP IAVs recovered from waterfowl sampled in California and gene segments of reassortant HP H5N1 IAVs detected in British Columbia, Canada and Washington, USA. Our investigation provides evidence that waterfowl are likely to have played a role in the evolution of reassortant HP IAVs in the Pacific Americas Flyway during 2014–2015, whereas we did not find support for spill-over infections in potential pinniped hosts.

Emerging Microbes & Infections↗

Viral fitness does not correlate with three genotype displacement events involving infectious hematopoietic necrosis virus

Viral genotype displacement events are characterized by the replacement of a previously dominant virus genotype by a novel genotype of the same virus species in a given geographic region. We examine here the fitness of three pairs of infectious hematopoietic necrosis virus (IHNV) genotypes involved in three major genotype displacement events in Washington state over the last 30 years to determine whether increased virus fitness correlates with displacement. Fitness was assessed using in vivo assays to measure viral replication in single infection, simultaneous co-infection, and sequential superinfection in the natural host, steelhead trout. In addition, virion stability of each genotype was measured in freshwater and seawater environments at various temperatures. By these methods, we found no correlation between increased viral fitness and displacement in the field. These results suggest that other pressures likely exist in the field with important consequences for IHNV evolution.

Washington↗

Interspecies transmission and limited persistence of low pathogenic avian influenza genomes among Alaska dabbling ducks

The reassortment and geographic distribution of low pathogenic avian influenza (LPAI) virus genes are well documented, but little is known about the persistence of intact LPAI genomes among species and locations. To examine persistence of entire LPAI genome constellations in Alaska, we calculated the genetic identities among 161 full-genome LPAI viruses isolated across 4 years from five species of duck: northern pintail ( Anas acuta ), mallard ( Anas platyrhynchos ), American green-winged teal ( Anas crecca ), northern shoveler ( Anas clypeata ) and American wigeon ( Anas americana ). Based on pairwise genetic distance, highly similar LPAI genomes (>99% identity) were observed within and between species and across a range of geographic distances (up to and >1000 km), but most often between isolates collected 0–10 km apart. Highly similar viruses were detected between years, suggesting inter-annual persistence, but these were rare in our data set with the majority occurring within 0–9 days of sampling. These results identify LPAI transmission pathways in the context of species, space and time, an initial perspective into the extent of regional virus distribution and persistence, and insight into why no completely Eurasian genomes have ever been detected in Alaska. Such information will be useful in forecasting the movement of foreign-origin avian influenza strains should they be introduced to North America.

Alaska↗

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↗

Spatial and temporal heterogeneity of infectious hematopoietic necrosis virus in Pacific Northwest salmonids

The aquatic rhaboviral pathogen infectious hematopoietic necrosis virus (IHNV) causes acute disease in juvenile fish of a number of populations of Pacific salmonid species. Heavily managed in both marine and freshwater environments, these fish species are cultured during the juvenile stage in freshwater conservation hatcheries, where IHNV is one of the top three infectious diseases that cause serious morbidity and mortality. Therefore, a comprehensive study of viral genetic surveillance data representing 2590 field isolates collected between 1958 and 2014 was conducted to determine the spatial and temporal patterns of IHNV in the Pacific Northwest of the contiguous United States. Prevalence of infection varied over time, fluctuating over a rough 5–7 year cycle. The genetic analysis revealed numerous subgroups of IHNV, each of which exhibited spatial heterogeneity. Within all subgroups, dominant genetic types were apparent, though the temporal patterns of emergence of these types varied among subgroups. Finally, the affinity or fidelity of subgroups to specific host species also varied, where UC subgroup viruses exhibited a more generalist profile and all other subgroups exhibited a specialist profile. These complex patterns are likely synergistically driven by numerous ecological, pathobiological, and anthropogenic factors. Since only a few anthropogenic factors are candidates for managed intervention aimed at improving the health of threatened or endangered salmonid fish populations, determining the relative impact of these factors is a high priority for future studies.

Infection, Genetics and Evolution↗

Ecological divergence of wild birds drives avian influenza spillover and global spread

The diversity of influenza A viruses (IAV) is primarily hosted by two highly divergent avian orders: Anseriformes (ducks, swans and geese) and Charadriiformes (gulls, terns and shorebirds). Studies of IAV have historically focused on Anseriformes, specifically dabbling ducks, overlooking the diversity of hosts in nature, including gull and goose species that have successfully adapted to human habitats. This study sought to address this imbalance by characterizing spillover dynamics and global transmission patterns of IAV over 10 years at greater taxonomic resolution than previously considered. Furthermore, the circulation of viral subtypes in birds that are either host-adapted (low pathogenic H13, H16) or host-generalist (highly pathogenic avian influenza—HPAI H5) provided a unique opportunity to test and extend models of viral evolution. Using Bayesian phylodynamic modelling we uncovered a complex transmission network that relied on ecologically divergent bird hosts. The generalist subtype, HPAI H5 was driven largely by wild geese and swans that acted as a source for wild ducks, gulls, land birds, and domestic geese. Gulls were responsible for moving HPAI H5 more rapidly than any other host, a finding that may reflect their long-distance, pelagic movements and their immuno-naïve status against this subtype. Wild ducks, long viewed as primary hosts for spillover, occupied an optimal space for viral transmission, contributing to geographic expansion and rapid dispersal of HPAI H5. Evidence of inter-hemispheric dispersal via both the Pacific and Atlantic Rims was detected, supporting surveillance at high latitudes along continental margins to achieve early detection. Both neutral (geographic expansion) and non-neutral (antigenic selection) evolutionary processes were found to shape subtype evolution which manifested as unique geographic hotspots for each subtype at the global scale. This study reveals how a diversity of avian hosts contribute to viral spread and spillover with the potential to improve surveillance in an era of rapid global change.

PLoS Pathogens↗

A point mutation in the polymerase protein PB2 allows a reassortant H9N2 influenza isolate of wild-bird origin to replicate in human cells.

H9N2 influenza A viruses are on the list of potentially pandemic subtypes. Therefore, it is important to understand how genomic reassortment and genetic polymorphisms affect phenotypes of H9N2 viruses circulating in the wild bird reservoir. A comparative genetic analysis of North American H9N2 isolates of wild bird origin identified a naturally occurring reassortant virus containing gene segments derived from both North American and Eurasian lineage ancestors. The PB2 segment of this virus encodes 10 amino acid changes that distinguish it from other H9 strains circulating in North America. G590S, one of the 10 amino acid substitutions observed, was present in ~ 12% of H9 viruses worldwide. This mutation combined with R591 has been reported as a marker of pathogenicity for human pandemic 2009 H1N1 viruses. Screening by polymerase reporter assay of all the natural polymorphisms at these two positions identified G590/K591 and S590/K591 as the most active, with the highest polymerase activity recorded for the SK polymorphism. Rescued viruses containing these two polymorphic combinations replicated more efficiently in MDCK cells and they were the only ones tested that were capable of establishing productive infection in NHBE cells. A global analysis of all PB2 sequences identified the K591 signature in six viral HA/NA subtypes isolated from several hosts in seven geographic locations. Interestingly, introducing the K591 mutation into the PB2 of a human-adapted H3N2 virus did not affect its polymerase activity. Our findings demonstrate that a single point mutation in the PB2 of a low pathogenic H9N2 isolate could have a significant effect on viral phenotype and increase its propensity to infect mammals. However, this effect is not universal, warranting caution in interpreting point mutations without considering protein sequence context.

Infection, Genetics and Evolution↗

Virus-like particle production in atmospheric eubacteria isolates

Culturable eubacterial isolates were collected at various altitudes in Earth’s atmosphere to include ~1.5 m above ground in Tallahassee, Florida, USA, ~10.0 m above sea level over the mid-Atlantic ridge (~15oN), ~ 20 km above ground over the continental United States, ~20 km above sea level over the Pacific Ocean near southern California and from the atmosphere of Carlsbad Cavern, Carlsbad Cavern National Park, New Mexico, USA. Isolates were screened for the presence of inducible virus-like particles (VLP) through use of mitomycin C and epifluorescent direct counts. We determined that 92.7% of the isolates carried inducible (VLP) counts in exposed versus non-exposed culture controls and that the relationship was statistically significant. Further statistical analyses revealed that the numbers of isolates that demonstrated VLP production did not vary among collection sites. These data demonstrate a high prevalence of VLP generation in isolates collected in the lower atmosphere and at extreme altitudes. Also shows that species of eubacteria that are resistant to the rigors of atmospheric transport play a significant role in long-range atmospheric inter- and intra-continental dispersion of VLP and that long-range atmospheric transport of VLP may enhance rates of evolution at the microbial scale in receiving environments.

Atmosphere↗

Tick control: Trapping, bio-control, host management and other alternative strategies

Biology of Ticks is the most comprehensive work on tick biology and tick-borne diseases. This second edition is a multi-authored work, featuring the research and analyses of renowned experts across the globe. Spanning two volumes, the book examines the systematics, biology, structure, ecological adaptations, evolution, genomics and the molecular processes that underpin the growth, development and survival of these important disease-transmitting parasites. Also discussed is the remarkable array of diseases transmitted (or caused) by ticks, as well as modern methods for their control. This book should serve as a modern reference for students, scientists, physicians, veterinarians and other specialists. Volume II includes chapters on the ecology of non-nidicolous and nidicolous ticks, genetics and genomics (including the genome of the Lyme disease vector Ixodes scapularis) and immunity, including host immune responses to tick feeding and tick-host interactions, as well as the tick's innate immune system that prevents and/or controls microbial infections. Six chapters cover in depth the many diseases caused by the major tick-borne pathogens, including tick-borne protozoa, viruses, rickettsiae of all types, other types of bacteria (e.g., the Lyme disease agent) and diseases related to tick paralytic agents and toxins. The remaining chapters are devoted to tick control using vaccines, acaricides, repellents, biocontrol, and, finally, techniques for breeding ticks in order to develop tick colonies for scientific study.

Book chapter↗

Sequence variation of the glycoprotein gene identifies three distinct lineages within field isolates of viral hemorrhagic septicemia virus, a fish rhabdovirus

To evaluate the genetic diversity of viral haemorrhagic septicaemia virus (VHSV), the sequence of the glycoprotein genes (G) of 11 North American and European isolates were determined. Comparison with the G protein of representative members of the family Rhabdoviridae suggested that VHSV was a different virus species from infectious haemorrhagic necrosis virus (IHNV) and Hirame rhabdovirus (HIRRV). At a higher taxonomic level, VHSV, IHNV and HIRRV formed a group which was genetically closest to the genus Lyssavirus. Compared with each other, the G genes of VHSV displayed a dissimilar overall genetic diversity which correlated with differences in geographical origin. The multiple sequence alignment of the complete G protein, showed that the divergent positions were not uniformly distributed along the sequence. A central region (amino acid position 245-300) accumulated substitutions and appeared to be highly variable. The genetic heterogeneity within a single isolate was high, with an apparent internal mutation frequency of 1.2 x 10(-3) per nucleotide site, attesting the quasispecies nature of the viral population. The phylogeny separated VHSV strains according to the major geographical area of isolation: genotype I for continental Europe, genotype II for the British Isles, and genotype III for North America. Isolates from continental Europe exhibited the highest genetic variability, with sub-groups correlated partially with the serological classification. Neither neutralizing polyclonal sera, nor monoclonal antibodies, were able to discriminate between the genotypes. The overall structure of the phylogenetic tree suggests that VHSV genetic diversity and evolution fit within the model of random change and positive selection operating on quasispecies.

Journal of General Virology↗

Limited evidence of intercontinental dispersal of avian paramyxovirus serotype 4 by migratory birds

Avian paramyxovirus serotype 4 (APMV-4) is a single stranded RNA virus that has most often been isolated from waterfowl. Limited information has been reported regarding the prevalence, pathogenicity, and genetic diversity of AMPV-4. To assess the intercontinental dispersal of this viral agent, we sequenced the fusion gene of 58 APMV-4 isolates collected in the United States, Japan and the Ukraine and compared them to all available sequences on GenBank. With only a single exception the phylogenetic clades of APMV-4 sequences were monophyletic with respect to their continents of origin (North America, Asia and Europe). Thus, we detected limited evidence for recent intercontinental dispersal of APMV-4 in this study.

Infection, Genetics and Evolution↗

Host responses and viral traits interact to shape the impacts of climate warming on highly pathogenic avian influenza in migratory waterfowl

Emerging infectious diseases pose threats to wildlife populations, as exemplified by recent outbreaks of avian influenza viruses in wild birds. Climate change can affect infection dynamics in wildlife through direct effects on pathogens (e.g., environmental decay rates) and changes to host ecology, including shifting migration patterns. Here, we adapt an existing mechanistic model that couples migration and infection to study how traits of highly pathogenic avian influenza (HPAI) viruses contribute to HPAI outcomes in migratory waterfowl, then apply this model to explore potential impacts of climate change on HPAI dynamics. We find that the simulated impacts of HPAI on the host population under baseline climate conditions varied from no impact to 100% mortality, depending on viral traits. In most cases, traits related to transmission (i.e., contact rates, shedding rates) were more important for HPAI establishment probability, infection prevalence, and mortality than were other viral traits (e.g., environmental temperature sensitivity, cross-protective immunity). We then simulated the effects of climate change (i.e., altered temperature regimes) on HPAI dynamics both via viral environmental decay and via changes in bird migration phenology. In these simulations, we found that a 9-day advancement in spring migration timing increased the duration of HPAI outbreaks by increasing time birds spent at their breeding grounds, leading to higher mortality and fewer infections. In contrast, increased viral decay in warmer years had a smaller, but opposite impact. These patterns depended on the primary transmission mode of HPAI (i.e., direct vs. environmental) and its sensitivity to environmental temperatures. Together, these results suggest that climate change is likely to increase the impacts of HPAI on waterfowl populations if HPAI relies strongly on direct transmission and birds advance their spring migration. Further integrating host-viral co-evolution and other climatic changes (e.g., salinity, humidity) could provide more precise predictions of how HPAI dynamics could change in the future.

Alaska, California, Oregon↗

Report on the workshop ‘Next Steps in Developing Nature Futures’

The workshop ‘New Narratives for Nature: operationalizing the IPBES Nature Futures Scenarios’ was organised by the IPBES task force on scenarios and models and hosted by the Institute for Global Environmental Strategies (IGES), with support from the research team on “Predicting and Assessing Natural Capital and Ecosystem Services through an Integrated Social-Ecological Systems Approach (PANCES)” based at the University of Tokyo, the Research Institute for Humanity and Nature (RIHN), and the United Nations University, with generous financial support from the Ministry of the Environment of Japan. Due to the COVID-19 virus outbreak, most task force members participated through virtual means, with a subset of task force members meeting in person in Japan. The aim of the workshop was to build on the Nature Futures Framework (NFF) and on the ‘nature futures’ participatory scenario-development work initiated by the IPBES expert group on scenarios and models in the first IPBES work programme. This workshop aims to further elaborate the pre-workshop scenario narratives and to enrich discussions on the NFF. The workshop also served to start working on a more detailed task force work plan. These aims were achieved through: • Task force sessions on the further formulation of the Nature Futures narratives. • Task force sessions on the cross-comparison of draft narratives and the further elaboration of the historical-present narrative. • Organisational sessions to begin the drafting of sub-deliverable-specific work plans. • In parallel to the task force workshop, collaborative sessions between the task force and Japanese researchers took place to discuss the application of the Nature Futures Framework at the national scale, using existing national level scenarios from Japan. • A public seminar, in Japan, for a wider audience introducing the scenarios and models task force’s work, the concept of the Nature Futures Framework, and fostered discussions on the concept of transformative change. Summary of outputs of the workshop in Japan • 6 NEW scenario narratives drafts – an evolution of the pre-workshop work using the narrative templates, into a more coherent set of narratives fitting their locations in the Nature Futures Framework, including some illustrative visualisations. • A cross-comparison table – to identify the core similarities and differences across the 6 new narratives (including single narrative-between-narrative comparisons). • A discussion on how to continue further development, requiring identifying pathways to complete the 6 new narratives. • 1 historical-to-present narrative draft – also an evolution of work done prior to the workshop. The task force has yet to synthesize and shorten this draft, ensuring linkages with topics detailed in the 6 new narratives into a more digestible level. • Elaboration of a follow-up plan for further development of the narratives, post-workshop, through a “buddy” system of in-depth online discussions per and between narratives. • 1 Japan case study – on fitting national level scenarios into the Nature Futures Framework. A summary will be shared by the team who worked closely on this with the PANCES partners, which we expect will give interesting insights to the cross-scale application of the Nature Futures Framework. • Detailed work plan implementation drafts (ongoing post workshop in sub-groups).

Report↗

A systematic review of avian influenza virus transmission models: Gaps and opportunities

Highly pathogenic avian influenza virus (HPAIV) increasingly threatens wild birds, poultry, non-human mammals and humans, yet gaps and opportunities in avian influenza virus (AIV) transmission modelling have not been comprehensively synthesized. We reviewed 182 articles published through 2025, categorized dimensions, including modelling approaches, data, host types, biological levels, spatial scales, temporal scales and model objectives, examined associations among these dimensions, and synthesized author-stated limitations and recommendations. Statistical and mechanistic models dominated. Model data centred on population dynamics and demography, disease surveillance, host epidemiology and competence, meteorology and land use and land cover. Most studies focused on poultry or wild birds at regional spatial scales, seasonal/annual and multi-year temporal scales, population or multi-population levels, and were retrospective. Machine learning and decision- making models were less common. Immunity, behaviour and life history, community composition, morphology, viral genetics and viral persistence received less attention. Non-human mammals, individual and community biological levels, local and broader spatial scales, daily temporal scales and prospective modelling were also less frequently modelled. The authors frequently reported limitations related to data availability, surveillance sampling and reporting bias, and model simplification, while commonly recommending improved data quality and greater model complexity and realism.

Methods in Ecology and Evolution↗

Transmission routes maintaining a viral pathogen of steelhead trout within a complex multi-host assemblage

This is the first comprehensive region wide, spatially explicit epidemiologic analysis of surveillance data of the aquatic viral pathogen infectious hematopoietic necrosis virus (IHNV) infecting native salmonid fish. The pathogen has been documented in the freshwater ecosystem of the Pacific Northwest of North America since the 1950s, and the current report describes the disease ecology of IHNV during 2000–2012. Prevalence of IHNV infection in monitored salmonid host cohorts ranged from 8% to 30%, with the highest levels observed in juvenile steelhead trout. The spatial distribution of all IHNV-infected cohorts was concentrated in two sub-regions of the study area, where historic burden of the viral disease has been high. During the study period, prevalence levels fluctuated with a temporal peak in 2002. Virologic and genetic surveillance data were analyzed for evidence of three separate but not mutually exclusive transmission routes hypothesized to be maintaining IHNV in the freshwater ecosystem. Transmission between year classes of juvenile fish at individual sites (route 1) was supported at varying levels of certainty in 10%–55% of candidate cases, transmission between neighboring juvenile cohorts (route 2) was supported in 31%–78% of candidate cases, and transmission from adult fish returning to the same site as an infected juvenile cohort was supported in 26%–74% of candidate cases. The results of this study indicate that multiple specific transmission routes are acting to maintain IHNV in juvenile fish, providing concrete evidence that can be used to improve resource management. Furthermore, these results demonstrate that more sophisticated analysis of available spatio-temporal and genetic data is likely to yield greater insight in future studies.

Idaho, Oregon, Washington↗

Estimating distemper virus dynamics among wolves and grizzly bears using serology and Bayesian state‐space models

Many parasites infect multiple hosts, but estimating the transmission across host species remains a key challenge in disease ecology. We investigated the within and across host species dynamics of canine distemper virus (CDV) in grizzly bears ( Ursus arctos ) and wolves ( Canis lupus ) of the Greater Yellowstone Ecosystem (GYE). We hypothesized that grizzly bears may be more likely to be exposed to CDV during outbreaks in the wolf population because grizzly bears often displace wolves while scavenging carcasses. We used serological data collected from 1984 to 2014 in conjunction with Bayesian state‐space models to infer the temporal dynamics of CDV. These models accounted for the unknown timing of pathogen exposure, and we assessed how different testing thresholds and the potential for testing errors affected our conclusions. We identified three main CDV outbreaks (1999, 2005, and 2008) in wolves, which were more obvious when we used higher diagnostic thresholds to qualify as seropositive. There was some evidence for increased exposure rates in grizzly bears in 2005, but the magnitude of the wolf effect on bear exposures was poorly estimated and depended upon our prior distributions. Grizzly bears were exposed to CDV prior to wolf reintroduction and during time periods outside of known wolf outbreaks, thus wolves are only one of several potential routes for grizzly bear exposures. Our modeling approach accounts for several of the shortcomings of serological data and is applicable to many wildlife disease systems, but is most informative when testing intervals are short. CDV circulates in a wide range of carnivore species, but it remains unclear whether the disease persists locally within the GYE carnivore community or is periodically reintroduced from distant regions with larger host populations.

Ecology and Evolution↗

Increased mortality rates caused by highly pathogenic avian influenza virus in a migratory raptor

Highly pathogenic avian influenza virus (HPAIV) has caused extensive mortalities in wild birds with a disproportionate impact on raptors since 2021. The population-level impact of HPAIV can be informed by telemetry studies that track large samples of initially healthy, wild birds. We leveraged movement data from 71 rough-legged hawks ( Buteo lagopus ) across all major North American migratory bird flyways concurrent with the 2022–2023 HPAIV outbreak and identified a total of 29 mortalities, of which 11 were confirmed, and an additional ~9 were estimated to have been caused by HPAIV. We estimated a 28% HPAIV cause-specific mortality rate among rough-legged hawks during a single year concurrent with the HPAIV outbreak in North America. Additionally, the overall mortality rate during the HPAIV outbreak (47%) was significantly higher than baseline annual mortality rates (3%–17%) suggesting that HPAIV-caused deaths were additive above baseline mortality levels. HPAIV mortalities were concentrated within the Central and Atlantic flyways during prebreeding migration and peaked in April 2022 when large-scale HPAIV mortalities were reported in other wild birds throughout North America. HPAIV exposure was most likely caused by scavenging or preying on infected waterfowl, as rough-legged hawks are known to opportunistically scavenge during the nonbreeding season. We utilized movement data to identify a continental-scale HPAIV cause-specific mortality event in rough-legged hawks that has the potential to exacerbate ongoing population declines. Our study highlights the usefulness of monitoring movement data to pinpoint sources of mortality that can help better understand the drivers of population change, even if studies are focused on other research questions.

Ecology and Evolution↗