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Please cite this paper as: Bateman et al. (2012) Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding. Influenza and Other Respiratory Viruses 6(6), 424-433. Background In the late 1990s, triple reassortant H3N2 influenza A viruses emerged and spread widely in the US swine population. We have shown previously that an isolate representative of this virus-lineage, A/Swine/Minnesota/593/99 (Sw/MN), exhibits phenotypic differences compared to a wholly human-lineage H3N2 virus isolated during the same time period, A/Swine/Ontario/00130/97 (Sw/ONT). Specifically, Sw/MN was more infectious for pigs and infected a significantly higher proportion of cultured primary swine respiratory epithelial cells (SRECs). In addition, reverse genetics-generated Sw/MN × Sw/ONT reassortant and point mutant viruses demonstrated that the infectivity phenotypes in SRECs were strongly dependent on three amino acids within the hemagglutinin (HA) gene. Objectives To determine the mechanism by which Sw/MN attains higher infectivity than Sw/ONT in SRECs. Methods A/Swine/Minnesota/593/99, Sw/ONT, and mutant (reverse genetics-generated HA reassortant and point mutant) viruses were compared at various HA-mediated stages of infection: initial sialic acid binding, virus entry, and the pH of virus-endosome fusion. Results/Conclusions Sialic acid binding was the sole stage where virus differences directly paralleled infectivity phenotypes in SRECs, indicating that binding is the primary mechanism responsible for differences in the infectivity levels of Sw/MN and Sw/ONT. [ABSTRACT FROM AUTHOR]

In 2004, 803 rural Iowans from the Agricultural Health Study were enrolled in a 2-year prospective study of zoonotic influenza transmission. Demographic and occupational exposure data from enrollment, 12-month, and 24-month follow-up encounters were examined for association with evidence of previous and incident influenza virus infections. When proportional odds modeling with multivariable adjustment was used, upon enrollment, swine-exposed participants (odds ratio [OR] 54.9, 95% confidence interval [CI] 13.0-232.6) and their nonswine-exposed spouses (OR 28.2, 95% CI 6.1-130.1) were found to have an increased odds of elevated antibody level to swine influenza (H1N1) virus compared with 79 nonexposed University of Iowa personnel. Further evidence of occupational swine influenza virus infections was observed through self-reported influenza-like illness data, comparisons of enrollment and follow-up serum samples, and the isolation of a reassortant swine influenza (H1N1) virus from an ill swine farmer. Study data suggest that swine workers and their nonswine-exposed spouses are at increased risk of zoonotic influenza virus infections. [ABSTRACT FROM AUTHOR]

In 1997–1998, H3N2 influenza viruses of different genotypes emerged among North American pigs. Triple reassortant H3N2 viruses containing human, classical swine and avian virus genes spread widely within the swine population and gave rise subsequently to reassortant H1N2 and H1N1 viruses. Together with wholly avian viruses recovered from North American pigs since 1999, these viruses emphasize that influenza virus interspecies transmission and reassortment in pigs can occur throughout world. They provide important research tools with which the genetic factors that control interspecies transmission can be investigated. [Copyright &y& Elsevier]

An H1N2 influenza virus (A/Duck/North Carolina/91347/01) (Dk/NC) was isolated from a wild duck in the United States in 2001. Genetic analyses showed that this duck virus has the same human/classical swine/avian reassortant genotype as the H1N2 viruses that have been isolated from pigs and turkeys in the US since 1999. Phylogenetic analyses of each gene segment further confirmed that the Dk/NC virus is closely related to the domestic animal H1N2 isolates. In particular, Dk/NC is most closely related to a swine H1N2 virus also isolated in North Carolina. These two viruses and a phylogenetically-defined subset of additional swine H1N2 viruses share a common mutation in the Sb antigenic site on the hemagglutinin protein. The recovery of Dk/NC from a wild bird raises concerns for further widespread distribution of these H1N2 viruses via waterfowl migration. [Copyright &y& Elsevier]

Please cite this paper as: Terebuh et al. (2010) Transmission of influenza A viruses between pigs and people, Iowa, 2002-2004. Influenza and Other Respiratory Viruses 4(6), 387-396. Triple-reassortant (tr) viruses of human, avian, and swine origin, including H1N1, H1N2, and H3N2 subtypes, emerged in North American swine herds in 1998 and have become predominant. While sporadic human infections with classical influenza A (H1N1) and with tr-swine influenza viruses have been reported, relatively few have been documented in occupationally exposed swine workers (SW). We conducted a 2-year (2002-2004) prospective cohort study of transmission of influenza viruses between pigs and SW from a single pork production company in Iowa. Respiratory samples were collected and tested for influenza viruses from SW and from pigs under their care through surveillance for influenza-like illnesses (ILI). Serial blood samples from study participants were tested by hemagglutination inhibition (HI) for antibody seroconversion against human and swine influenza viruses (SIV), and antibody seroprevalence was compared to age-matched urban Iowa blood donors. During the first year, 15 of 88 SW had ILI and were sampled; all were culture-negative for influenza. During the second year, 11 of 76 SW had ILI and were sampled; one was culture-positive for a human seasonal H3N2 virus. Among 20 swine herd ILI outbreaks sampled, influenza A virus was detected by rRT-PCR from 17 with 11 trH1N1 and five trH3N2 virus isolates cultured. During both years, HI geometric mean titers were significantly higher among SW compared to blood donor controls for three SIV: classical swine Sw/WI/238/97 (H1N1), tr Sw/IN/9K035/99 (H1N2), and trSw/IA/H02NJ56371/02 (H1N1)] ( P < 0·0001). SW had serologic evidence for infection with both swine and human influenza viruses and were exposed to diverse influenza virus strains circulating in pigs. Influenza virus surveillance among pigs and SW should be encouraged to better understand cross-species transmission and diversity of influenza viruses at the human-swine interface. [ABSTRACT FROM AUTHOR]

Background: Maternal infection with influenza and other pathogens during pregnancy has been associated with increased risk for schizophrenia and neurodevelopmental disorders. In rodent studies, maternal inflammatory responses to influenza affect fetal brain development. However, to verify the relevance of these findings to humans, research is needed in a primate species with more advanced prenatal corticogenesis. Methods: Twelve pregnant rhesus monkeys were infected with influenza, A/Sydney/5/97 (H3N2), 1 month before term (early third trimester) and compared with 7 control pregnancies. Nasal swabs and blood samples confirmed viral shedding and immune activation. Structural magnetic resonance imaging was conducted at 1 year; behavioral development and cortisol reactivity were also assessed. Results: Maternal infections were mild and self-limiting. At birth, maternally derived influenza-specific immunoglobulin G was present in the neonate, but there was no evidence of direct viral exposure. Birth weight and gestation length were not affected, nor were infant neuromotor, behavioral, and endocrine responses. However, magnetic resonance imaging analyses revealed significant reductions in cortical gray matter in flu-exposed animals. Regional analyses indicated the largest gray matter reductions occurred bilaterally in cingulate and parietal areas; white matter was also reduced significantly in the parietal lobe. Conclusions: Influenza infection during pregnancy affects neural development in the monkey, reducing gray matter throughout most of the cortex and decreasing white matter in parietal cortex. These brain alterations are likely to be permanent, given that they were still present at the monkey-equivalent of older childhood and thus might increase the likelihood of later behavioral pathology. [Copyright &y& Elsevier]

Abstract: To study the receptor specificities of H1 and H3 influenza viruses isolated recently from pigs, we employed the analogues of natural receptors, namely sialyloligosaccharides conjugated with polyacrylamide in biotinylated and label free forms. All Madin-Darby canine kidney (MDCK) cell-propagated viruses with human H3 or classical swine H1 hemagglutinins bound only to Neu5Acα2–6Galβ1-bearing polymers, and not to Neu5Acα2–3Galβ1-bearing polymers. This receptor-binding pattern is typical for human influenza viruses and it differs from the previously described receptor-binding specificity of egg-adapted swine influenza viruses. Swine virus isolates with avian-like H1 and H3 hemagglutinins displayed distinct receptor specificity by binding to both Neu5Acα2–6Gal- and Neu5Acα2–3Gal-containing receptors. These viruses, as well as egg-adapted swine and turkey viruses with a classical swine HA, differed from the related duck viruses by increased affinity to sulfated sialyloligosaccaride, Su-SiaLex. Except for avian-like H3 viruses, none of the studied swine viruses bound to Neu5Gc-containing sialoglycopolymers, suggesting that binding to these sialic acid species abundantly expressed in pigs may not be essential for virus replication in this host. [Copyright &y& Elsevier]