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Editor, Senior Moderator
JVI Accepts, published online ahead of print on 7 September 2011
J. Virol. doi:10.1128/JVI.05705-11
Copyright ? 2011,American Society for Micr
2009 pandemic H1N1 virus causes disease and upregulation of genes related to inflammatory and immune response, cell death and lipid metabolism in pigs
Wenjun Ma1, Sarah E. Belisle2, Derek Mosier1, Xi Li1, Evelyn Stigger-Rosser3, Qinfang Liu1, Chuanling Qiao1, Jake Elder1, Richard Webby3, Michael G. Katze2, and Juergen A. Richt1,#
1 Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS
2 Department of Microbiology, University of Washington, Seattle, Washington
3 St. Jude Children's Research Hospital, Memphis, TN
# Corresponding author: J?rgen A. Richt, DVM, PhD, Regents Distinguished Professor, Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, KS, 66506 USA, Tel.: +1-785-532-4408, Fax: +1-785-532-4039, Email: jricht@vet.k-state.edu
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ABSTRACT
There exists limited information whether adaptation is needed for cross-species transmission of the 2009 pandemic H1N1 virus (pH1N1). Here, we compare the pathogenesis of 2 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 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 pH1N1 viruses caused similar lung lesions as IA30 virus did, both pH1N1 viruses were shed from the nasal cavities of challenged pigs but IA30 was not shed. Global gene expression analysis indicated that transcriptional response between the viruses was distinct. pH1N1-infected pigs had an upregulation of genes related to inflammatory and immune response on day 3 post infection that was not seen in the IA30 infection, and markedly differed from IA30 in expression levels of genes related to cell death and lipid metabolism on day 5 post infection. These results indicate that both pH1N1 isolates are more virulent due in part to differences in 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 na?ve swine populations and might reassort with currently circulating swine influenza viruses.
http://jvi.asm.org/cgi/content/short/JVI.05705-11v1
J. Virol. doi:10.1128/JVI.05705-11
Copyright ? 2011,American Society for Micr
2009 pandemic H1N1 virus causes disease and upregulation of genes related to inflammatory and immune response, cell death and lipid metabolism in pigs
Wenjun Ma1, Sarah E. Belisle2, Derek Mosier1, Xi Li1, Evelyn Stigger-Rosser3, Qinfang Liu1, Chuanling Qiao1, Jake Elder1, Richard Webby3, Michael G. Katze2, and Juergen A. Richt1,#
1 Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS
2 Department of Microbiology, University of Washington, Seattle, Washington
3 St. Jude Children's Research Hospital, Memphis, TN
# Corresponding author: J?rgen A. Richt, DVM, PhD, Regents Distinguished Professor, Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, KS, 66506 USA, Tel.: +1-785-532-4408, Fax: +1-785-532-4039, Email: jricht@vet.k-state.edu
arrow
ABSTRACT
There exists limited information whether adaptation is needed for cross-species transmission of the 2009 pandemic H1N1 virus (pH1N1). Here, we compare the pathogenesis of 2 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 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 pH1N1 viruses caused similar lung lesions as IA30 virus did, both pH1N1 viruses were shed from the nasal cavities of challenged pigs but IA30 was not shed. Global gene expression analysis indicated that transcriptional response between the viruses was distinct. pH1N1-infected pigs had an upregulation of genes related to inflammatory and immune response on day 3 post infection that was not seen in the IA30 infection, and markedly differed from IA30 in expression levels of genes related to cell death and lipid metabolism on day 5 post infection. These results indicate that both pH1N1 isolates are more virulent due in part to differences in 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 na?ve swine populations and might reassort with currently circulating swine influenza viruses.
http://jvi.asm.org/cgi/content/short/JVI.05705-11v1