Recent H3N2 swine influenza virus with haemagglutinin and nucleoprotein genes similar to 1975 human strains

Bikour, M. H.; Frost, Éric; Deslandes, Sylvie; Talbot, Brian G.; Weber, J; Elazhary, Youssef

doi:10.1099/0022-1317-76-3-697

Cited by 31 publications

(13 citation statements)

References 25 publications

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“…Also, human H3 viruses have established stable lineages in European swine populations after the 1968 “Hong Kong” pandemic, and are still circulating in the form of human-avian H3N2 reassortant viruses [50]. It is possible that these new swine viruses would also remain “antigenically frozen”, leading to potential human pandemic H3 and H1 viruses in the future [51],[52]. As such, surveillance and containment of swine influenza viruses is desirable for the prevention of future pandemic episodes.…”

Section: Discussionmentioning

confidence: 99%

Protection of Mice against Lethal Challenge with 2009 H1N1 Influenza A Virus by 1918-Like and Classical Swine H1N1 Based Vaccines

et al. 2010

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The recent 2009 pandemic H1N1 virus infection in humans has resulted in nearly 5,000 deaths worldwide. Early epidemiological findings indicated a low level of infection in the older population (>65 years) with the pandemic virus, and a greater susceptibility in people younger than 35 years of age, a phenomenon correlated with the presence of cross-reactive immunity in the older population. It is unclear what virus(es) might be responsible for this apparent cross-protection against the 2009 pandemic H1N1 virus. We describe a mouse lethal challenge model for the 2009 pandemic H1N1 strain, used together with a panel of inactivated H1N1 virus vaccines and hemagglutinin (HA) monoclonal antibodies to dissect the possible humoral antigenic determinants of pre-existing immunity against this virus in the human population. By hemagglutinination inhibition (HI) assays and vaccination/challenge studies, we demonstrate that the 2009 pandemic H1N1 virus is antigenically similar to human H1N1 viruses that circulated from 1918–1943 and to classical swine H1N1 viruses. Antibodies elicited against 1918-like or classical swine H1N1 vaccines completely protect C57B/6 mice from lethal challenge with the influenza A/Netherlands/602/2009 virus isolate. In contrast, contemporary H1N1 vaccines afforded only partial protection. Passive immunization with cross-reactive monoclonal antibodies (mAbs) raised against either 1918 or A/California/04/2009 HA proteins offered full protection from death. Analysis of mAb antibody escape mutants, generated by selection of 2009 H1N1 virus with these mAbs, indicate that antigenic site Sa is one of the conserved cross-protective epitopes. Our findings in mice agree with serological data showing high prevalence of 2009 H1N1 cross-reactive antibodies only in the older population, indicating that prior infection with 1918-like viruses or vaccination against the 1976 swine H1N1 virus in the USA are likely to provide protection against the 2009 pandemic H1N1 virus. This data provides a mechanistic basis for the protection seen in the older population, and emphasizes a rationale for including vaccination of the younger, naïve population. Our results also support the notion that pigs can act as an animal reservoir where influenza virus HAs become antigenically frozen for long periods of time, facilitating the generation of human pandemic viruses.

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Section: Discussionmentioning

confidence: 99%

Protection of Mice against Lethal Challenge with 2009 H1N1 Influenza A Virus by 1918-Like and Classical Swine H1N1 Based Vaccines

et al. 2010

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“…Although the HA and NA of Sw/MN are both of human influenza virus origin, previous work has shown that many of the early triple reassortant H3N2 viruses (including Sw/MN) contain 12 amino acid differences in their HA protein that are unique to the swine triple reassortant viruses and are not present in the most closely related human H3 virus HAs (including Sw/ONT) (18,43). The sites of these amino acid differences include residues previously implicated in species specificity (3,5,10), receptor binding (18,42,43), and/or glycosylation (18). Given the fact that viruses with the triple reassortant genotype have spread throughout the U.S. swine population while Sw/ONT has not, these differences are of interest as potential swine adaptation mutations.…”

Section: Resultsmentioning

confidence: 99%

Restricted Infectivity of a Human-Lineage H3N2 Influenza A Virus in Pigs Is Hemagglutinin and Neuraminidase Gene Dependent

et al. 2006

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Influenza A viruses cause pandemics at sporadic intervals. Pandemic viruses can potentially be introduced into the human population through in toto transfer of an avian influenza virus or through reassortment between avian and human strains. Pigs are believed to play a central role in the creation of pandemic viruses through reassortment because of their susceptibility to infection with both avian and human influenza viruses. However, we recently found that a human-lineage H3N2 influenza virus was highly restricted in its ability to infect pigs after intranasal inoculation. We hypothesized that this restricted infectivity phenotype was controlled by the hemagglutinin (HA) and neuraminidase (NA). To test this, we infected pigs with reverse genetics-created HA plus NA reassortant viruses. Specifically, introduction of the HA and NA genes of a contemporary H3N2 swine virus into the genetic background of the wholly human virus resulted in a significant increase in virus shedding and pathogenicity. These data indicate that the HA/NA can play important roles in controlling human influenza virus infectivity in pigs. The results further support the premise that a barrier exists to human influenza virus infection in pigs, which may limit the role of pigs in pandemic virus creation through reassortment of human and avian influenza viruses.

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“…Following the 1968 H3N2 human pandemic, there was serological evidence for infection of pigs with H3N2; however, no stable swine lineage was established at that time (reviewed in Vincent et al., 2008). In 1991, an H3N2 virus that was antigenically similar to one circulating in humans was isolated from pigs in Quebec, Canada (Bikour et al., 1995). Despite these earlier introductions, the H3N2 subtype did not become established in the North American pig population until 1998.…”

Section: Introductionmentioning

confidence: 99%

Molecular and Antigenic Characterization of Triple-Reassortant H3N2 Swine Influenza Viruses Isolated from Pigs, Turkey and Quail in Canada

Nfon¹,

Berhane²,

Zhang³

et al. 2011

Transboundary and Emerging Diseases

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In 2005, triple-reassortant H3N2 (trH3N2) influenza A viruses were isolated from swine and turkeys in Canada. Subsequently, these viruses were isolated from humans and mink in 2006 and 2007, respectively. Following full genome sequencing, H3N2 viruses isolated from turkeys (2005), quail (2008) and swine (2009) in Canada, were characterized as trH3N2. The 2005 turkey isolate was found to be almost identical to other viruses isolated in that year, with quail and pig isolates related very closely to the 2005 trH3N2. Minimal antigenic evolution of the swine isolates relative to the reference 2005 virus was observed. These results suggest the establishment of a stable lineage of trH3N2 in Canadian pigs, with evidence for interspecies transmission to turkeys and quails.

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Recent H3N2 swine influenza virus with haemagglutinin and nucleoprotein genes similar to 1975 human strains

Cited by 31 publications

References 25 publications

Protection of Mice against Lethal Challenge with 2009 H1N1 Influenza A Virus by 1918-Like and Classical Swine H1N1 Based Vaccines

Protection of Mice against Lethal Challenge with 2009 H1N1 Influenza A Virus by 1918-Like and Classical Swine H1N1 Based Vaccines

Restricted Infectivity of a Human-Lineage H3N2 Influenza A Virus in Pigs Is Hemagglutinin and Neuraminidase Gene Dependent

Molecular and Antigenic Characterization of Triple-Reassortant H3N2 Swine Influenza Viruses Isolated from Pigs, Turkey and Quail in Canada

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