title: 2009 pandemic H1N1 influenza virus causes disease and upregulation of genes related to inflammatory and immune responses, cell death, and lipid metabolism in pigs.
abstract: There exists limited information about whether adaptation is needed for cross-species transmission of the 2009 pandemic H1N1 influenza virus (pH1N1). Here, we compare the pathogenesis of two pH1N1 viruses, one derived from a human patient (A/CA/04/09 [CA09]) and the other from swine (A/swine/Alberta/25/2009 [Alb09]), with that of the 1918-like classical swine influenza virus (A/swine/Iowa/1930 [IA30]) in the pig model. Both pH1N1 isolates induced clinical symptoms such as coughing, sneezing, decreased activity, fever, and labored breathing in challenged pigs, but IA30 virus did not cause any clinical symptoms except fever. Although both the pH1N1 viruses and the IA30 virus caused lung lesions, the pH1N1 viruses were shed from the nasal cavities of challenged pigs whereas the IA30 virus was not. Global gene expression analysis indicated that transcriptional responses of the viruses were distinct. pH1N1-infected pigs had an upregulation of genes related to inflammatory and immune responses at day 3 postinfection that was not seen in the IA30 infection, and expression levels of genes related to cell death and lipid metabolism at day 5 postinfection were markedly different from those of IA30 infection. These results indicate that both pH1N1 isolates are more virulent due in part to differences in the host transcriptional response during acute infection. Our study also indicates that pH1N1 does not need prior adaptation to infect pigs, has a high potential to be maintained in naïve swine populations, and might reassort with currently circulating swine influenza viruses.
authors: Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, KS 66506, USA.
authors: Wenjun
authors: W
authors: Ma
authors: Sarah E
authors: SE
authors: Belisle
authors: Derek
authors: D
authors: Mosier
authors: Xi
authors: X
authors: Li
authors: Evelyn
authors: E
authors: Stigger-Rosser
authors: Qinfang
authors: Q
authors: Liu
authors: Chuanling
authors: C
authors: Qiao
authors: Jake
authors: J
authors: Elder
authors: Richard
authors: R
authors: Webby
authors: Michael G
authors: MG
authors: Katze
authors: Juergen A
authors: JA
authors: Richt
mesh_terms: D000818:Animals; D016923:Cell Death; D004195:Disease Models, Animal; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000473:pathology* / Q000821:virology; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology* / Q000472:pathogenicity*; D050356:Lipid Metabolism; D008168:Lung / Q000473:pathology / Q000821:virology; D053858:Metabolic Networks and Pathways / Q000235:genetics*; D008969:Molecular Sequence Data; D009297:Nasal Mucosa / Q000821:virology; D009976:Orthomyxoviridae Infections / Q000276:immunology / Q000473:pathology / Q000821:virology; D017422:Sequence Analysis, DNA; D013552:Swine; D013553:Swine Diseases / Q000276:immunology / Q000473:pathology / Q000821:virology; D017201:Virus Shedding