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Senecavirus A (SVA), previously known as Seneca Valley virus, was first isolated in the United States in 2002. SVA was associated with porcine idiopathic vesicular disease in Canada and the USA in 2007 and 2012, respectively. Recent increase in SVA outbreaks resulting in neonatal mortality of piglets and/or vesicular lesions in sows in Brazil, the USA and Canada point to the necessity to study the pathogenicity and molecular epidemiology of the virus. Here, we report the analysis of the complete coding sequences of SVA from 2 clinical cases and 9 assembly yard environmental samples collected in 2015 in Canada, along with 22 previously released complete genomes in the GenBank. With this combined data set, the evolution of the SVA over a 12-month period in 2015/2016 was evaluated. These SVA isolates were characterized by a rapid accumulation of genetic variations driven mainly by a high nucleotide substitution rate and purifying selection. The SVA sequences clustered in clearly defined geographical areas with reported cases of SVA infection. No transmission links were identified between assembly yards, suggesting that point source introductions may have occurred. In addition, 25 fixed non-synonymous mutations were identified across all analyzed strains when compared to the prototype SVA strain (SVV-001). This study highlights the importance of monitoring SVA mutations for their role in increased virulence and impact on SVA diagnostics.

Wholly Eurasian highly pathogenic avian influenza H5N1 clade 2.3.4.4b virus was isolated from 2 free-ranging black bears with meningoencephalitis in Quebec, Canada. We found that isolates from both animals had the D701N mutation in the polymerase basic 2 gene, previously known to promote adaptation of H5N1 viruses to mammal hosts.

We isolated a novel reassortant influenza A(H10N7) virus from a harbor seal in British Columbia, Canada, that died from bronchointerstitial pneumonia. The virus had unique genome constellations involving lineages from North America and Eurasia and polymerase basic 2 segment D701N mutation, associated with adaptation to mammals.

The GsGd lineage (A/goose/Guangdong/1/1996) H5N1 virus was introduced to Canada in 2021/2022 through the Atlantic and East Asia-Australasia/Pacific flyways by migratory birds. This was followed by unprecedented outbreaks affecting domestic and wild birds, with spillover into other animals. Here, we report sporadic cases of H5N1 in 40 free-living mesocarnivore species such as red foxes, striped skunks, and mink in Canada. The clinical presentations of the disease in mesocarnivores were consistent with central nervous system infection. This was supported by the presence of microscopic lesions and the presence of abundant IAV antigen by immunohistochemistry. Some red foxes that survived clinical infection developed anti-H5N1 antibodies. Phylogenetically, the H5N1 viruses from the mesocarnivore species belonged to clade 2.3.4.4b and had four different genome constellation patterns. The first group of viruses had wholly Eurasian (EA) genome segments. The other three groups were reassortant viruses containing genome segments derived from both North American (NAm) and EA influenza A viruses. Almost 17 percent of the H5N1 viruses had mammalian adaptive mutations (E627 K, E627V and D701N) in the polymerase basic protein 2 (PB2) subunit of the RNA polymerase complex. Other mutations that may favour adaptation to mammalian hosts were also present in other internal gene segments. The detection of these critical mutations in a large number of mammals within short duration after virus introduction inevitably highlights the need for continually monitoring and assessing mammalian-origin H5N1 clade 2.3.4.4b viruses for adaptive mutations, which potentially can facilitate virus replication, horizontal transmission and posing pandemic risks for humans.

The first Canadian H3N2 canine influenza A outbreak involving an Asian-origin H3N2 canine influenza virus (CIV) began in southwestern Ontario, Canada, in late December 2017. More H3N2 CIV cases were identified in central and eastern Ontario between March and October 2018. Based on epidemiological investigation, 5 clusters were identified (C1, C2, C3a, C3b, and C4); however, the origin of infection has only been revealed for epidemiological cluster C1. Here, we use phylogenetic analyses to unravel the links of virus transmission between the 5 epidemiological clusters and the origin of infection for all epidemiological clusters. Our results demonstrate that the Canadian H3N2 CIV sequences were grouped into four distinct phylogenetic clusters with minimal genetic diversity between these clusters. Large scale phylogenetic analysis of H3N2 CIV from around the globe showed that the Canadian CIVs formed a distinct new clade along with CIVs that have been circulating in the USA since 2017–2018 and in China since 2017. This clade shares a common ancestor of Asian origin. This study concludes that the H3N2 CIV outbreak in Ontario was driven by multiple introductions of South Korean/Chinese-origin H3N2 CIVs over 10 months.

Highly pathogenic avian influenza (HPAI) H5N1 clade 2.3.4.4b viruses were first detected in St. John’s, Canada in late 2021. To investigate the patterns of avian influenza virus (AIV) infection and immune responses subsequent to the arrival of H5N1, we sampled the wild urban duck population in this area for a period of 16 months after the start of the outbreak and compared these findings to those from archived samples. Antibody seroprevalence was relatively stable before the outbreak (2011–2014) at 27.6% and 3.9% for anti-AIV (i.e., NP) and H5-specific antibodies, respectively. During the winter of 2022, AIV-NP and H5-specific antibody seroprevalence both reached 100%, signifying a population-wide infection event, which was observed again in late February 2023 following a second H5N1 incursion from Eurasia. As expected, population-level immunity waned over time, with ducks seropositive for anti-AIV-NP antibodies for approximately twice as long as for H5-specific antibodies, with the population seronegative to the latter after approximately six months. We observed a clear relationship of increasing antibody levels with decreasing viral RNA loads that allowed for interpretation of the course of infection and immune response in infected individuals and applied these findings to two cases of resampled ducks to infer infection history. Our study highlights the value of applying both AIV surveillance and seroprevalence monitoring to provide a better understanding of AIV dynamics in wild populations, which may be crucial following the global dissemination of clade 2.3.4.4b H5Nx subtypes to assess the threats they pose to both wild and domestic animals, and to humans.

The recurrent incursions of A(H5N1) clade 2.3.4.4b viruses into North America have resulted in the emergence of reassortant virus genotypes. These genotypes exhibit variations in pathogenicity and host ranges. Blue-winged teal (BWTE) are the most common dabbling ducks in North America and play a crucial role in maintaining and dispersing influenza A viruses (IAVs). In some areas, the migratory pathways of BWTE overlap with densely populated commercial poultry facilities. Despite this, the role of BWTE in the maintenance and spread of A(H5N1) is not well understood, and there is limited data on their susceptibility to A(H5N1) clade 2.3.4.4b viruses. Our study demonstrates differences in BWTE susceptibility to distinct genotypes of A(H5N1) clade 2.3.4.4b viruses. The virus transmission from infected BWTE and lethality in turkeys and chickens were also influenced by the virus genotypes. The findings suggest that BWTE could contribute to the maintenance and spread of highly pathogenic avian influenza (HPAI) viruses, and active surveillance in BWTE is essential.

The Mexican lineage H7N3 highly pathogenic avian influenza virus (HPAIV) has persisted in Mexican poultry since its first isolation in 2012. To date, the detection of this virus has gradually expanded from the initial one state to 18 states in Mexico. Despite the HPAIV H7N3 outbreak occurring yearly, the transmission pathways have never been studied, disallowing the establishment of effective control measures. We used a phylogenetic approach to unravel the transmission pathways of 2022 H7N3 HPAIVs in the new outbreak areas in Northern Mexico. We present genetic data of H7N3 viruses produced from 18 poultry farms infected in the spring of 2022. Our results indicate that the virus responsible for the current outbreak in Northern Mexico evolved from the Mexican lineage H7N3 HPAIV discovered in 2012. In the current outbreak, we identified five clusters of infection with four noticeably different genetic backgrounds. It is a cluster IV-like virus that was transmitted into one northern state causing an outbreak, then spreading to another neighboring northern state, possibly via a human-mediated mechanical transmission mechanism. The long-distance transmission event highlights the necessity for the more rigorous enforcement of biosafety measures in outbreaks. Additionally, we examined the evolutionary processes shaping the viral genetic and antigenic diversities. It is imperative to enhance active surveillance to include birds, the environment, and humans to detect HPAI in domestic poultry at an earlier point and eliminate it.

•The antigenic relationship of three anti-FMDV/A sera with field isolates was analyzed.•The IRQ/24/64, IRN/05, and ARG/01 sera showed different matches to the field isolates.•Together antigenic sites 1 and 3 contributed about 71% of the amino acid variations.•The substitutions at the antigenic sites influenced the vaccine matching results.•Genetic monitoring should include VP1, VP2, and VP3 for vaccine determination. Foot–and–mouth disease (FMD) is a severe, highly contagious viral disease that affects a wide variety of domestic and wild cloven-hoofed animals. FMD vaccines can play a vital role in disease control and are very widely used globally each year. However, due to the diversity of FMDV, the choice of FMD vaccine is still a huge challenge. In this study, 45 FMDV/A isolates were phylogenetically categorized into three topotypes: ASIA (n = 31), AFRICA (n = 10), and EURO–SA (n = 4). Three sera collected from vaccinated cattle with FMDV A22/IRQ/24/64, A/IRN/05, and A/ARG/01 were used to evaluate their antigenic relationship (r1) with the field isolates. The IRQ/24/64 serum demonstrated a 39% (17/44) match (r1 ≥ 0.3) to the field isolates, whereas IRN/05 serum and ARG/01serum showed an 18% (8/44) and a 2% (1/44) match (r1 ≥ 0.3) to the field isolates, respectively. The A22/IRQ/24/64 matched with isolates mainly from topotype ASIA, with limited cross–topotype match with isolates from topotypes AFRICA and EURO–SA. However, the A/IRN/05 did not show a cross–topotype match with topotype AFRICA isolates and A/ARG/01 failed to match any isolates from topotypes ASIA and AFRICA. After analyzing the amino acid variation of the known antigenic sites of 45 strains of FMDV/A, it was found that together antigenic sites 1 and 3 contributed about 71% of the amino acid changes to the vaccine evaluated. Based on the capsid sequences, the FMDV/A evolved unequally among topotypes. The topotypes of ASIA and AFRICA evolves faster than that of EURO–SA. The FMDV/A continues to show a high level of genetic diversity driven by a high substitution rate, purifying selection, and positive selection concentrated on antigenic sites or near antigenic sites. The current research shows the challenges of the FMDV/A vaccine selection and emphasizes the importance of continuous monitoring of antigenic evolution for the selection of effective vaccines.

We have demonstrated for the first time a comprehensive evolutionary analysis of the Mexican lineage H5N2 avian influenza virus (AIV) using complete genome sequences (n = 189), from its first isolation in 1993 until 2019. Our study showed that the Mexican lineage H5N2 AIV originated from the North American wild bird gene pool viruses around 1990 and is currently circulating in poultry populations of Mexico, the Dominican Republic, and Taiwan. Since the implementation of vaccination in 1995, the highly pathogenic AIV (HPAIV) H5N2 virus was eradicated from Mexican poultry in mid-1995. However, the low pathogenic AIV (LPAIV) H5N2 virus has continued to circulate in domestic poultry populations in Mexico, eventually evolving into five distinct clades. In the current study, we demonstrate that the evolution of Mexican lineage H5N2 AIVs involves gene reassortments and mutations gained over time. The current circulating Mexican lineage H5N2 AIVs are classified as LPAIV based on the amino acid sequences of the hemagglutinin (HA) protein cleavage site motif as well as the results of the intravenous pathogenicity index (IVPI). The immune pressure from vaccinations most likely has played a significant role in the positive selection of antigenic drift mutants within the Mexican H5N2 AIVs. Most of the identified substitutions in these viruses are located on the critical antigenic residues of the HA protein and as a result, might have contributed to vaccine failures. This study highlights and stresses the need for vaccine updates while emphasizing the importance of continued molecular monitoring of the HA protein for its antigenic changes compared to the vaccines used.