Giuseppe
Emeritus
MicroRNA Expression and Virulence in Pandemic Influenza Virus Infected Mice. (J Virol., abstract, RA-1024, edited)
J Virol. 2010 Jan 13. [Epub ahead of print]
MicroRNA Expression and Virulence in Pandemic Influenza Virus Infected Mice.
Li Y, Chan EY, Li J, Ni C, Peng X, Rosenzweig E, Tumpey TM, Katze MG. - Department of Microbiology and Washington National Primate Research Center, University of Washington, Seattle, Washington 98195-8070; Fred Hutchinson Cancer Research Center, Seattle, Washington 98109; Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America.
The worst known H1N1 influenza pandemic in history resulted in more than 20 million deaths in 1918-1919. Although the underlying mechanism causing the extreme virulence of the 1918 influenza virus is still obscure, our previous functional genomics analyses revealed a correlation between the lethality of the reconstructed 1918 influenza virus (r1918) in mice and a unique gene expression pattern associated with severe immune responses in the lungs. Lately, microRNAs have emerged as a class of crucial regulators for gene expression. To determine whether differential expression of cellular microRNAs play a role in the host response to r1918 virus infection, we compared the lung cellular "microRNAome" of mi ce infected by r1918 virus with that of mice infected by a non-lethal seasonal influenza virus, A/Texas/36/91. We found that a group of microRNAs, including miR-200a and miR-223, were differentially expressed in response to influenza virus infection, and that r1918 and A/Texas/36/91 infection induced distinct microRNA expression profiles. Moreover, we observed significant enrichment in the number of predicted cellular target mRNAs whose expression was inversely correlated with the expression of these microRNAs. Intriguingly, gene ontology analysis revealed that many of these mRNAs play roles in immune response and cell death pathways, which are known to be associated with the extreme virulence of r1918. This is the first demonstration that cellular gene expression patterns in influenza virus-infected mice may be attributed in part to microRNA regulation, and that such regulation may be a contributing factor to the extreme virulence of the r1918 virus.
PMID: 20071585 [PubMed - as supplied by publisher]
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J Virol. 2010 Jan 13. [Epub ahead of print]
MicroRNA Expression and Virulence in Pandemic Influenza Virus Infected Mice.
Li Y, Chan EY, Li J, Ni C, Peng X, Rosenzweig E, Tumpey TM, Katze MG. - Department of Microbiology and Washington National Primate Research Center, University of Washington, Seattle, Washington 98195-8070; Fred Hutchinson Cancer Research Center, Seattle, Washington 98109; Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America.
The worst known H1N1 influenza pandemic in history resulted in more than 20 million deaths in 1918-1919. Although the underlying mechanism causing the extreme virulence of the 1918 influenza virus is still obscure, our previous functional genomics analyses revealed a correlation between the lethality of the reconstructed 1918 influenza virus (r1918) in mice and a unique gene expression pattern associated with severe immune responses in the lungs. Lately, microRNAs have emerged as a class of crucial regulators for gene expression. To determine whether differential expression of cellular microRNAs play a role in the host response to r1918 virus infection, we compared the lung cellular "microRNAome" of mi ce infected by r1918 virus with that of mice infected by a non-lethal seasonal influenza virus, A/Texas/36/91. We found that a group of microRNAs, including miR-200a and miR-223, were differentially expressed in response to influenza virus infection, and that r1918 and A/Texas/36/91 infection induced distinct microRNA expression profiles. Moreover, we observed significant enrichment in the number of predicted cellular target mRNAs whose expression was inversely correlated with the expression of these microRNAs. Intriguingly, gene ontology analysis revealed that many of these mRNAs play roles in immune response and cell death pathways, which are known to be associated with the extreme virulence of r1918. This is the first demonstration that cellular gene expression patterns in influenza virus-infected mice may be attributed in part to microRNA regulation, and that such regulation may be a contributing factor to the extreme virulence of the r1918 virus.
PMID: 20071585 [PubMed - as supplied by publisher]
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