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Global host immune response: pathogenesis and transcriptional profiling of type A influenza viruses expressing the hemagglutinin and neuraminidase genes from the 1918 pandemic virus.
J Virol. 2004 Sep; 78(17):9499-511.JV

Abstract

To understand more fully the molecular events associated with highly virulent or attenuated influenza virus infections, we have studied the effects of expression of the 1918 hemagglutinin (HA) and neuraminidase (NA) genes during viral infection in mice under biosafety level 3 (agricultural) conditions. Using histopathology and cDNA microarrays, we examined the consequences of expression of the HA and NA genes of the 1918 pandemic virus in a recombinant influenza A/WSN/33 virus compared to parental A/WSN/33 virus and to an attenuated virus expressing the HA and NA genes from A/New Caledonia/20/99. The 1918 HA/NA:WSN and WSN recombinant viruses were highly lethal for mice and displayed severe lung pathology in comparison to the nonlethal New Caledonia HA/NA:WSN recombinant virus. Expression microarray analysis performed on lung tissues isolated from the infected animals showed activation of many genes involved in the inflammatory response, including cytokine, apoptosis, and lymphocyte genes that were common to all three infection groups. However, consistent with the histopathology studies, the WSN and 1918 HA/NA:WSN recombinant viruses showed increased up-regulation of genes associated with activated T cells and macrophages, as well as genes involved in apoptosis, tissue injury, and oxidative damage that were not observed in the New Caledonia HA/NA:WSN recombinant virus-infected mice. These studies document clear differences in gene expression profiles that were correlated with pulmonary disease pathology induced by virulent and attenuated influenza virus infections.

Authors+Show Affiliations

Department of Microbiology, School of Medicine, University of Washington, Seattle, Washington 98195-8070, USA. jkash@u.washington.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15308742

Citation

Kash, John C., et al. "Global Host Immune Response: Pathogenesis and Transcriptional Profiling of Type a Influenza Viruses Expressing the Hemagglutinin and Neuraminidase Genes From the 1918 Pandemic Virus." Journal of Virology, vol. 78, no. 17, 2004, pp. 9499-511.
Kash JC, Basler CF, García-Sastre A, et al. Global host immune response: pathogenesis and transcriptional profiling of type A influenza viruses expressing the hemagglutinin and neuraminidase genes from the 1918 pandemic virus. J Virol. 2004;78(17):9499-511.
Kash, J. C., Basler, C. F., García-Sastre, A., Carter, V., Billharz, R., Swayne, D. E., Przygodzki, R. M., Taubenberger, J. K., Katze, M. G., & Tumpey, T. M. (2004). Global host immune response: pathogenesis and transcriptional profiling of type A influenza viruses expressing the hemagglutinin and neuraminidase genes from the 1918 pandemic virus. Journal of Virology, 78(17), 9499-511.
Kash JC, et al. Global Host Immune Response: Pathogenesis and Transcriptional Profiling of Type a Influenza Viruses Expressing the Hemagglutinin and Neuraminidase Genes From the 1918 Pandemic Virus. J Virol. 2004;78(17):9499-511. PubMed PMID: 15308742.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Global host immune response: pathogenesis and transcriptional profiling of type A influenza viruses expressing the hemagglutinin and neuraminidase genes from the 1918 pandemic virus. AU - Kash,John C, AU - Basler,Christopher F, AU - García-Sastre,Adolfo, AU - Carter,Victoria, AU - Billharz,Rosalind, AU - Swayne,David E, AU - Przygodzki,Ronald M, AU - Taubenberger,Jeffery K, AU - Katze,Michael G, AU - Tumpey,Terrence M, PY - 2004/8/17/pubmed PY - 2004/9/17/medline PY - 2004/8/17/entrez SP - 9499 EP - 511 JF - Journal of virology JO - J. Virol. VL - 78 IS - 17 N2 - To understand more fully the molecular events associated with highly virulent or attenuated influenza virus infections, we have studied the effects of expression of the 1918 hemagglutinin (HA) and neuraminidase (NA) genes during viral infection in mice under biosafety level 3 (agricultural) conditions. Using histopathology and cDNA microarrays, we examined the consequences of expression of the HA and NA genes of the 1918 pandemic virus in a recombinant influenza A/WSN/33 virus compared to parental A/WSN/33 virus and to an attenuated virus expressing the HA and NA genes from A/New Caledonia/20/99. The 1918 HA/NA:WSN and WSN recombinant viruses were highly lethal for mice and displayed severe lung pathology in comparison to the nonlethal New Caledonia HA/NA:WSN recombinant virus. Expression microarray analysis performed on lung tissues isolated from the infected animals showed activation of many genes involved in the inflammatory response, including cytokine, apoptosis, and lymphocyte genes that were common to all three infection groups. However, consistent with the histopathology studies, the WSN and 1918 HA/NA:WSN recombinant viruses showed increased up-regulation of genes associated with activated T cells and macrophages, as well as genes involved in apoptosis, tissue injury, and oxidative damage that were not observed in the New Caledonia HA/NA:WSN recombinant virus-infected mice. These studies document clear differences in gene expression profiles that were correlated with pulmonary disease pathology induced by virulent and attenuated influenza virus infections. SN - 0022-538X UR - https://www.unboundmedicine.com/medline/citation/15308742/Global_host_immune_response:_pathogenesis_and_transcriptional_profiling_of_type_A_influenza_viruses_expressing_the_hemagglutinin_and_neuraminidase_genes_from_the_1918_pandemic_virus_ L2 - http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=15308742 DB - PRIME DP - Unbound Medicine ER -