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Structured populations of Sulfolobus acidocaldarius with susceptibility to mobile genetic elements

The impact of a structured environment on genome evolution can be determined through comparative population genomics of species that live in the same habitat. Recent work comparing three genome sequences of Sulfolobus acidocaldarius suggested that highly structured, extreme, hot spring environments do not limit dispersal of this thermoacidophile, in contrast to other co-occurring Sulfolobus species. Instead, a high level of conservation among these three S. acidocaldarius genomes was hypothesized to result from rapid, global-scale dispersal promoted by low susceptibility to viruses that sets S. acidocaldarius apart from its sister Sulfolobus species. To test this hypothesis, we conducted a comparative analysis of 47 genomes of S. acidocaldarius from spatial and temporal sampling of two hot springs in Yellowstone National Park. While we confirm the low diversity in the core genome, we observe differentiation among S. acidocaldarius populations, likely resulting from low migration among hot spring “islands” in Yellowstone National Park. Patterns of genomic variation indicate that differing geological contexts result in the elimination or preservation of diversity among differentiated populations. We observe multiple deletions associated with a large genomic island rich in glycosyltransferases, differential integrations of the Sulfolobus turreted icosahedral virus, as well as two different plasmid elements. These data demonstrate that neither rapid dispersal nor lack of mobile genetic elements result in low diversity in the S. acidocaldarius genomes. We suggest instead that significant differences in the recent evolutionary history, or the intrinsic evolutionary rates, of sister Sulfolobus species result in the relatively low diversity of the S. acidocaldarius genome.

Genome Biology and Evolution

Avian influenza virus ecology in Iceland shorebirds: intercontinental reassortment and movement

Shorebirds are a primary reservoir of avian influenza viruses (AIV). We conducted surveillance studies in Iceland shorebird populations for 3 years, documenting high serological evidence of AIV exposure in shorebirds, primarily in Ruddy Turnstones ( Arenaria interpres ; seroprevalence = 75%). However, little evidence of virus infection was found in these shorebird populations and only two turnstone AIVs (H2N7; H5N1) were able to be phylogenetically examined. These analyses showed that viruses from Iceland shorebirds were primarily derived from Eurasian lineage viruses, yet the H2 hemagglutinin gene segment was from a North American lineage previously detected in a gull from Iceland the previous year. The H5N1 virus was determined to be low pathogenic, however the PB2 gene was closely related to the PB2 from highly pathogenic H5N1 isolates from China. Multiple lines of evidence suggest that the turnstones were infected with at least one of these AIV while in Iceland and confirm Iceland as an important location where AIV from different continents interact and reassort, creating new virus genomes. Mounting data warrant continued surveillance for AIV in wild birds in the North Atlantic, including Canada, Greenland, and the northeast USA to determine the risks of new AI viruses and their intercontinental movement in this region.

Infection, Genetics and Evolution

Disease outbreaks select for mate choice and coat color in wolves

We know much about pathogen evolution and the emergence of new disease strains, but less about host resistance and how it is signaled to other individuals and subsequently maintained. The cline in frequency of black-coated wolves ( Canis lupus ) across North America is hypothesized to result from a relationship with canine distemper virus (CDV) outbreaks. We tested this hypothesis using cross-sectional data from wolf populations across North America that vary in the prevalence of CDV and the allele that makes coats black, longitudinal data from Yellowstone National Park, and modeling. We found that the frequency of CDV outbreaks generates fluctuating selection that results in heterozygote advantage that in turn affects the frequency of the black allele, optimal mating behavior, and black wolf cline across the continent.

Science

Alphacoronaviruses in new World bats: Prevalence, persistence, phylogeny, and potential for interaction with humans

Bats are reservoirs for many different coronaviruses (CoVs) as well as many other important zoonotic viruses. We sampled feces and/or anal swabs of 1,044 insectivorous bats of 2 families and 17 species from 21 different locations within Colorado from 2007 to 2009. We detected alphacoronavirus RNA in bats of 4 species: big brown bats (Eptesicus fuscus), 10% prevalence; long-legged bats (Myotis volans), 8% prevalence; little brown bats (Myotis lucifugus), 3% prevalence; and western long-eared bats (Myotis evotis), 2% prevalence. Overall, juvenile bats were twice as likely to be positive for CoV RNA as adult bats. At two of the rural sampling sites, CoV RNAs were detected in big brown and long-legged bats during the three sequential summers of this study. CoV RNA was detected in big brown bats in all five of the urban maternity roosts sampled throughout each of the periods tested. Individually tagged big brown bats that were positive for CoV RNA and later sampled again all became CoV RNA negative. Nucleotide sequences in the RdRp gene fell into 3 main clusters, all distinct from those of Old World bats. Similar nucleotide sequences were found in amplicons from gene 1b and the spike gene in both a big-brown and a long-legged bat, indicating that a CoV may be capable of infecting bats of different genera. These data suggest that ongoing evolution of CoVs in bats creates the possibility of a continued threat for emergence into hosts of other species. Alphacoronavirus RNA was detected at a high prevalence in big brown bats in roosts in close proximity to human habitations (10%) and known to have direct contact with people (19%), suggesting that significant potential opportunities exist for cross-species transmission of these viruses. Further CoV surveillance studies in bats throughout the Americas are warranted.

PLoS ONE

Molecular systematics of sturgeon nucleocytoplasmic large DNA viruses

Namao virus (NV) is a sturgeon nucleocytoplasmic large DNA virus (sNCLDV) that can cause a lethal disease of the integumentary system in lake sturgeon Acipenser fulvescens . As a group, the sNCLDV have not been assigned to any currently recognized taxonomic family of viruses. In this study, a data set of NV DNA sequences was generated and assembled as two non-overlapping contigs of 306,448 bp and then used to conduct a comprehensive systematics analysis using Bayesian inference of phylogeny for NV, other sNCLDV and representative members of six families of the NCLDV superfamily. The phylogeny of NV was reconstructed using protein homologues encoded by nine nucleocytoplasmic virus orthologous genes (NCVOGs): NCVOG0022 – mcp, NCVOG0038 – DNA polymerase B elongation subunit, NCVOG0076 – VV A18-type helicase, NCVOG0249 – VV A32-type ATPase, NCVOG0262 – AL2 VLTF3-like transcription factor, NCVOG0271 – RNA polymerase II subunit II, NCVOG0274 – RNA polymerase II subunit I, NCVOG0276 – ribonucleotide reductase small subunit and NCVOG1117 – mRNA capping enzyme. The accuracy of our phylogenetic method was evaluated using a combination of Bayesian statistical analysis and congruence analysis. Stable tree topologies were obtained with data sets differing in target molecule(s), sequence length and taxa. Congruent topologies were obtained in phylogenies constructed using individual protein data sets. The major capsid protein phylogeny inferred that ten representative sNCLDV form a monophyletic group comprised of four lineages within a polyphyletic Mimi-Phycodnaviridae group of taxa. Overall, the analyses revealed that Namao virus is a member of the Mimiviridae family with strong and consistent support for a clade containing NV and CroV as sister taxa.

Molecular Phylogenetics and Evolution

Genetic analyses reveal unusually high diversity of infectious haematopoietic necrosis virus in rainbow trout aquaculture

Infectious haematopoietic necrosis virus (IHNV) is the most significant virus pathogen of salmon and trout in North America. Previous studies have shown relatively low genetic diversity of IHNV within large geographical regions. In this study, the genetic heterogeneity of 84 IHNV isolates sampled from rainbow trout ( Oncorhynchus mykiss ) over a 20 year period at four aquaculture facilities within a 12 mile stretch of the Snake River in Idaho, USA was investigated. The virus isolates were characterized using an RNase protection assay (RPA) and nucleotide sequence analyses. Among the 84 isolates analysed, 46 RPA haplotypes were found and analyses revealed a high level of genetic heterogeneity relative to that detected in other regions. Sequence analyses revealed up to 7·6% nucleotide divergence, which is the highest level of diversity reported for IHNV to date. Phylogenetic analyses identified four distinct monophyletic clades representing four virus lineages. These lineages were distributed across facilities, and individual facilities contained multiple lineages. These results suggest that co-circulating IHNV lineages of relatively high genetic diversity are present in the IHNV populations in this rainbow trout culture study site. Three of the four lineages exhibited temporal trends consistent with rapid evolution.

Journal of General Virology

Genetic diversity and mutation of avian paramyxovirus serotype 1 (Newcastle disease virus) in wild birds and evidence for intercontinental spread

Avian paramyxovirus serotype 1 (APMV-1), or Newcastle disease virus, is the causative agent of Newcastle disease, one of the most economically important diseases for poultry production worldwide and a cause of periodic epizootics in wild birds in North America. In this study, we examined the genetic diversity of APMV-1 isolated from migratory birds sampled in Alaska, Japan, and Russia and assessed the evidence for intercontinental virus spread using phylogenetic methods. Additionally, we predicted viral virulence using deduced amino acid residues for the fusion protein cleavage site and estimated mutation rates for the fusion gene of class I and class II migratory bird isolates. All 73 isolates sequenced as part of this study were most closely related to virus genotypes previously reported for wild birds; however, five class II genotype I isolates formed a monophyletic clade exhibiting previously unreported genetic diversity, which met criteria for the designation of a new sub-genotype. Phylogenetic analysis of wild-bird isolates provided evidence for intercontinental virus spread, specifically viral lineages of APMV-1 class II genotype I sub-genotypes Ib and Ic. This result supports migratory bird movement as a possible mechanism for the redistribution of APMV-1. None of the predicted deduced amino acid motifs for the fusion protein cleavage site of APMV-1 strains isolated from migratory birds in Alaska, Japan, and Russia were consistent with those of previously identified virulent viruses. These data therefore provide no support for these strains contributing to the emergence of avian pathogens. The estimated mutation rates for fusion genes of class I and class II wild-bird isolates were faster than those reported previously for non-virulent APMV-1 strains. Collectively, these findings provide new insight into the diversity, spread, and evolution of APMV-1 in wild birds.

Archives of Virology

Book review: Quasispecies as a unifying concept in population dynamics

The quasispecies concept had two independent origins. One source was the theoretical ideas of Manfred Eigen and Peter Schuster in the 1970s. Studying the self-organization and evolution of primitive RNA molecules, they defined quasispecies as a distribution of mutant viral genomes generated by the mutation-selection process. In particular, the quasispecies nucleotide distribution consists of a singular fittest genotype, called the master sequence, surrounded by similar mutant spectra. The other source of the quasispecies concept can be traced to the growing empirical knowledge on RNA viruses formulated around the same time. Genomic sequencing of viral RNA indicated a variety of nucleotide sequences, or a distribution of sequences. Mutations in both Eigen’s theoretical system in the RNA viruses are not rare, as RNA is structurally less stable than RNA, but common, preventing the fittest genotype from becoming dominant. Virologists have adopted the quasispecies concept, with some papers on Covid-19 using the construct to explain that virus’s behavior.

Mathematical Biosciences

The genetic diversity and epizootiology of infectious hematopoietic necrosis virus

Infectious hematopoietic necrosis virus (IHNV) is a rhabdovirus which causes a serious disease in salmondd fish. The T1 ribonuclease fingerprinttin method was used to compare the RNA genomes of 26 isolates of IHNV recovered from sockeye salmon ( Oncorhynchus nerka ), chinook salmon ( O. tshawytscha ), and steelhead trout ( O. mykiss ) throughout the enzootic portion of western North America. Most of the isolates as a source of genetic variation. In from a single year (1987) to limit time of isolation as a source of genetic variation. In addition, isolates from different years collected at three sites were analyzed to investigate genetic drift or evolution of IHNV within specific locations. All of the isolates examined by T1 fingerprint analysis contained less than a 50% variation in spot location and were represented by a single fingerprint group. The observed variation was estimated to correspond to less than 5% variation in the nucleic acid sequence. However, sufficient variation was detected to separate the isolates into four subgroups which appeared to correlate to different geographic regions. Host species appeared not to be a significant source of variation. The evolutionary and epizootiologic significance of these findings and their relationship to other evidence of genetic variation in IHNV isolates are discussed.

Virus Research

Evidence for common ancestry among viruses isolated from wild birds in Beringia and highly pathogenic intercontinental reassortant H5N1 and H5N2 influenza A viruses

Highly pathogenic clade 2.3.4.4 H5N8, H5N2, and H5N1 influenza A viruses were first detected in wild, captive, and domestic birds in North America in November–December 2014. In this study, we used wild waterbird samples collected in Alaska prior to the initial detection of clade 2.3.4.4 H5 influenza A viruses in North America to assess the evidence for: (1) dispersal of highly pathogenic influenza A viruses from East Asia to North America by migratory birds via Alaska and (2) ancestral origins of clade 2.3.4.4 H5 reassortant viruses in Beringia. Although we did not detect highly pathogenic influenza A viruses in our sample collection from western Alaska, we did identify viruses that contained gene segments sharing recent common ancestry with intercontinental reassortant H5N2 and H5N1 viruses. Results of phylogenetic analyses and estimates for times of most recent common ancestry support migratory birds sampled in Beringia as maintaining viral diversity closely related to novel highly pathogenic influenza A virus genotypes detected in North America. Although our results do not elucidate the route by which highly pathogenic influenza A viruses were introduced into North America, genetic evidence is consistent with the hypothesized trans-Beringian route of introduction via migratory birds.

Infection, Genetics and Evolution

Temporal, geographic, and host distribution of avian paramyxovirus 1 (Newcastle disease virus)

Newcastle disease is caused by virulent forms of avian paramyxovirus of serotype 1 (APMV-1) and has global economic importance. The disease reached panzootic proportions within two decades after first being identified in 1926 in the United Kingdom and Indonesia and still remains endemic in many countries across the world. Here we review information on the host, temporal, and geographic distribution of APMV-1 genetic diversity based on the evolutionary systematics of the complete coding region of the fusion gene. Strains of APMV-1 are phylogenetically separated into two classes (class I and class II) and further classified into genotypes based on genetic differences. Class I viruses are genetically less diverse, generally present in wild waterfowl, and are of low virulence. Class II viruses are genetically and phenotypically more diverse, frequently isolated from poultry with occasional spillovers into wild birds, and exhibit a wider range of virulence. Waterfowl, cormorants, and pigeons are natural reservoirs of all APMV-1 pathotypes, except viscerotropic velogenic viruses for which natural reservoirs have not been identified. Genotypes I and II within class II include isolates of high and low virulence, the latter often being used as vaccines. Viruses of genotypes III and IX that emerged decades ago are now isolated rarely, but may be found in domestic and wild birds in China. Containing only virulent viruses and responsible for the majority of recent outbreaks in poultry and wild birds, viruses from genotypes V, VI, and VII, are highly mobile and have been isolated on different continents. Conversely, virulent viruses of genotypes XI (Madagascar), XIII (mainly Southwest Asia), XVI (North America) and XIV, XVII and XVIII (Africa) appear to have a more limited geographic distribution and have been isolated predominantly from poultry.

Infection, Genetics and Evolution

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

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