,Changes in influenza viruses that infect pigs have been observed for over two decades. The evolution of these viruses has led to several new strains. For instance, one such strain known as H1N2 emerged to infect pigs in the United States in 2015. This virus recently gained prevalence after acquiring a new N1 gene. Our study aimed to determine if the new N1 gene was responsible for increased transmission of the virus among pigs. To investigate this hypothesis, we analyzed four different strains of H1N1 or H1N2 influenza A virus. Each strain had different combinations of N1 and N2 genes. We infected pigs with these viruses and observed their clinical signs as well as transmission to other pigs. Regardless of the viral genes present, all variants of the virus were transmitted from one infected pig to another at the same levels. Therefore, the new N1 gene did not seem to have direct importance in increasing the transmission of the virus. These results suggest that the increase in detection may be associated with less protection from previous vaccines or infections due to the change in N1 or N2, or changes related to pig management or movement. Understanding how influenza A viruses spread provides important insights for the swine industry for disease prevention and vaccine developers for vaccine strain selection.,

,Influenza A virus in swine hemagglutinin (HA) gene sequence data for 9 virus strains.,,

,An investigation of antigenic relationships between North American swine H3N2 influenza A viruses (IAV) and human seasonal vaccine strains was conducted to assess the zoonotic risk to humans. Human seasonal H3N2 vaccine strains isolated from 1973 to 2014 (n=20) were obtained from the World Health Organization Global Influenza Surveillance and Response Network through St. Jude Children’s Research Hospital to use for serological assays, such as hemagglutination inhibition (HI) assays. Human seasonal vaccine strains were cultured on MDCK cells or eggs and the HA gene was verified by sequencing on a Sanger method at National Animal Disease Center (NADC). A consensus HA sequence was generated using Geneious Software.,

,Data are the individual group values for oral and cloacal virus shedding and antibody titers for reach treatment group from: Mo et al., The pathogenicity and transmission of live bird market H2N2 avian influenza viruses in chickens, Pekin ducks, and guinea fowl. Vet Mic 260:109180, 2021. https://doi.org/10.1016/j.vetmic.2021.109180,Methods: Six H2N2 low pathogenic avian influenza viruses from US LBMs were selected based on recency and to represent the different genotypes present in the live birds markets during the time period (i.e., the presence or absence of a NA stalk deletion): A/duck/PA/14-030488-5/2014 (Dk/PA/14), A/chicken/NY/16-032621-2/2016 (Ck/NY/16), A/chicken/CT/17-008911-4/2017 (Ck/CT/17), A/chicken/NY/18-002471-4/2018 (CK/NY/02471/18), A/chicken/NY/18-042097-3/2018 (Ck/NY/042097/18) and A/chicken/NY/19-012787-1/2019 (Ck/NY/19). Isolates were evaluated in White Leghorn chickens (Gallus gallus), guinea fowl (Numida meleagris) and Pekin ducks (Anas platyrhynchos). Chickens and guinea fowl were challenged at 4 weeks of age and Pekin ducks were challenged at 2 weeks of age with 6log10 of virus by the intra-choanal route. “Contact” birds, which were hatch-mates of the inoculated birds, were co-housed with the inoculated birds 24hrs post inoculation to evaluate transmission. Viral loads in OP and CL swabs collected at 2, 4, 7, 10, and 14 days post inoculation were determined by quantitative real-time reverse-transcriptase polymerase chain reaction (qRT-PCR). RNA was extracted from swabs using the MagMAX96 Viral RNA Isolation Kit (Thermo Fisher Scientific, Waltham, MA) and the KingFisher Flex Magnetic Particle Processing System (Thermo Fisher Scientific), with an additional wash step to remove inhibitors (Das et al., 2009). The qRT‐PCR for AIV detection was conducted based on the standard USDA M gene AIV qRT‐PCR procedure (Spackman et al., 2002) using an Applied Biosystems® 7500 Fast Real‐Time PCR system (Thermo Fisher Scientific). Cycle threshold (Ct) values were determined by the 7500 Fast Software v2.3. For relative quantification, Ct values were converted to titer equivalents based on the standard curve method (Larionov et al., 2005). Values were established from ten-fold dilutions of the same titrated stock of the virus used to challenge the birds. The limit of detection was determined to be 0.8Log10 per reaction. Serological testing for antibodies to the virus utilized the hemagglutination inhibition (HI) assays using homologous antigens were performed to quantify antibody responses with serum collected from chickens, guinea fowl and Pekin ducks at 14 dpi based on the standard protocol (OIE, 2019). HI titers were reported as reciprocal log2 titers, and titers greater than 3 log2 (1:8) were considered positive.,,

,The global outbreak of clade 2.3.4.4b H5N1 highly pathogenic avian influenza (HPAI) virus has caused tremendous losses in poultry. Although turkeys are a smaller sector in poultry production compared to chickens, they tend to be affected more severely by HPAI virus because they can usually be infected with a lower dose of influenza A virus than chickens (i.e., they are more susceptible). Exposure to non-replicating proteins may help control HPAI, however data with turkeys are somewhat limited regarding how well they work and approaches to modifying surveillance have not been developed. Here, an H5N9 non-replicating protein comprised of a clade 2.3.4.4b H5 hemagglutinin from A/turkey/Indiana/22-003707-003/2022 (TK/IN/22) and a North American wild bird lineage N9 was evaluated in commercial broad breasted white turkeys by challenge to live virus. Turkeys were divided into three groups, where each group was exposed to the non-replicating protein once at 3 (3wk), 7 (7wk), or 9 (9wk) weeks of age. All birds were challenged at 10 weeks of age with TK/IN/22 HPAIV. There was 100% survival in all groups except the sham exposure group which had 100% mortality. A significant decrease in viral shedding was observed in all exposed groups compared to the shams, although the 9wk group shed significantly higher quantities by the cloacal route at seven days post challenge (DPC) compared to the 3wk group. The neuraminidase inhibition-enzyme linked lectin assay (NI-ELLA) was used as a serological test that was able to detect antibody in birds that had been infected after exposure and challenge based on antibodies to the NA protein of the challenge virus (N1 NA) in serum collected 7, 10 and 14DPC. Between 50 and 90% of turkeys, depending on age at exposure, were positive by NI-ELLA at 7DPC and 100% were positive at 14DPC regardless of age at exposure.,

This data set describes genomic sequence information from 2022 used to infer spatiotemporal trends pertaining to the introductions of highly pathogenic H5N1 avian influenza viruses into Alaska and spread among wild birds, backyard poultry, and mammals.

Data set containing avian influenza A virus (IAV) sampling information for Emperor Geese in Alaska, 2015-2017. The data are in three tables: 1) collection data and IAV screening results from fecal samples at several sites in southwestern Alaska, 2) results of blocking enzyme-linked immunosorbent assay (bELISA) tests for IAV antibodies in blood serum collected from nesting female Emperor geese near the Manokinak River on the Yukon-Kuskokwim River Delta, and 3) results of influenza virus microneutralization assays to test for the specific IAV subtypes in the Manokinak samples.

,Modern swine production facilitates indoor respiratory contact between human employees and pigs in their care, creating conditions for interspecies transmission of influenza A virus (IAV). Sow vaccination is routinely practiced in the U.S.A. to transfer maternal derived antibodies (MDA) to piglets. Weaning is a highly stressful period for piglets that requires increased human interaction. Weaned piglets potentially have mixed immunity from MDA: matched, mismatched, and naïve. Since there have been multiple introductions of human seasonal H3N2 to swine, we assessed the effect of matched and mismatched MDA acquired from vaccinated sows and the stress of weaning on the susceptibility of piglets to a human-origin H3N2 IAV. The H3N2 virus was generated by reverse genetics to mimic the 2010.1 H3N2 introduction from humans to swine. Challenged seeder piglets were divided by immune and weaning status. Two days post inoculation, naïve direct contact pigs were placed with seeders. IAV quantitative reverse transcription polymerase chain reaction (qRT-PCR) and virus titration were performed on nasal swabs and bronchoalveolar lavage fluid to evaluate shedding and transmission kinetics. Matched MDA were effective in reducing shedding in challenged pigs and minimizing transmission of the human-like H3N2 to contacts. There was an increase in shedding and transmission in weaned pigs compared to littermates that remained on the sow. These results identify critical control points in production where changing practices could mitigate human-to-swine and swine-to-swine transmission to prevent establishment of novel lineages in pig populations.,

These data describe the results of virus isolation from oropharyngeal/cloacal swabs and testing of sera by a commercial blocking enzyme-linked immunosorbent assay (bELISA) and hemagglutinin (HA) specific testing by microneutralization (MN) and hemagglutination inhibition (HI) for Lesser Scaup in both the Atlantic and Pacific Flyways and Greater Scaup in the Pacific Flyway. These data support a USGS published manuscript.