Replication, Pathogenesis and Transmission of Pandemic (H1N1) 2009 Virus in Non-Immune Pigs

Abstract

The declaration of the human influenza A pandemic (H1N1) 2009 (H1N1/09) raised important questions, including origin and host range [1], [2]. Two of the three pandemics in the last century resulted in the spread of virus to pigs (H1N1, 1918; H3N2, 1968) with subsequent independent establishment and evolution within swine worldwide [3]. A key public and veterinary health consideration in the context of the evolving pandemic is whether the H1N1/09 virus could become established in pig populations [4]. We performed an infection and transmission study in pigs with A/California/07/09. In combination, clinical, pathological, modified influenza A matrix gene real time RT-PCR and viral genomic analyses have shown that infection results in the induction of clinical signs, viral pathogenesis restricted to the respiratory tract, infection dynamics consistent with endemic strains of influenza A in pigs, virus transmissibility between pigs and virus-host adaptation events. Our results demonstrate that extant H1N1/09 is fully capable of becoming established in global pig populations. We also show the roles of viral receptor specificity in both transmission and tissue tropism. Remarkably, following direct inoculation of pigs with virus quasispecies differing by amino acid substitutions in the haemagglutinin receptor-binding site, only virus with aspartic acid at position 225 (225D) was detected in nasal secretions of contact infected pigs. In contrast, in lower respiratory tract samples from directly inoculated pigs, with clearly demonstrable pulmonary pathology, there was apparent selection of a virus variant with glycine (225G). These findings provide potential clues to the existence and biological significance of viral receptor-binding variants with 225D and 225G during the 1918 pandemic [5].

2009 Pandemic H1N1 Influenza Virus Causes Disease and Upregulation of Genes Related to Inflammatory and Immune Responses, Cell Death, and Lipid Metabolism in Pigs

“…Our study confirms that pigs are susceptible to either the swine or human 2009 pH1N1 isolates, as reported previously (5,25,55). In addition, we found that virus replication in pH1N1-infected and classical IA30 virus-infected pigs was similar, but pH1N1 induced clear symptoms in pigs while IA30 did not.…”

Emergence of the pandemic H1N1 2009 influenza A virus in swine herds in Poland

“…In order to test the capability of the new virus to be established in swine population, an experimental infection and transmission studies were performed (3,16). The obtained results clearly demonstrated that pdm H1N1 2009 virus is entirely capable of becoming established in global pig populations.…”

Influenza A Virus Acquires Enhanced Pathogenicity and Transmissibility after Serial Passages in Swine

“…More importantly, the three viruses had enhanced contact transmissibility in both pigs and guinea pigs. Their enhanced virulence and contact transmissibility were similar to that of the H1N1/2009 virus (38)(39)(40). Since the virulence and contact transmissibility were comparable between the L2, N9, and L18 viruses, these acquired traits were determined primarily by the five consensus mutations (PB1 A469T, PA I129T, NA N329D, NS1 N205K, and NEP T48N) found in all three virus species.…”