tetano
Editor, Senior Moderator
Arch Virol. 2010 Apr 7. [Epub ahead of print]
Extrapulmonary tissue responses in cynomolgus macaques (Macaca fascicularis) infected with highly pathogenic avian influenza A (H5N1) virus.
Tolnay AE, Baskin CR, Tumpey TM, Sabourin PJ, Sabourin CL, Long JP, Pyles JA, Albrecht RA, Garc?a-Sastre A, Katze MG, Bielefeldt-Ohmann H.
Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO, USA.
Abstract
The mechanisms responsible for virulence of influenza viruses in humans remain poorly understood. A prevailing hypothesis is that the highly pathogenic virus isolates cause a severe cytokinemia precipitating acute respiratory distress syndrome and multiple organ dysfunction syndrome. Cynomolgus macaques (Macaca fascicularis) infected with a human highly pathogenic avian influenza (HPAI) H5N1 virus isolate (A/Vietnam/1203/2004) or reassortants of human influenza virus A/Texas/36/91 (H1N1) containing genes from the 1918 pandemic influenza A (H1N1) virus developed severe pneumonia within 24 h postinfection. However, virus spread beyond the lungs was only detected in the H5N1 group, and signs of extrapulmonary tissue reactions, including microglia activation and sustained up-regulation of inflammatory markers, most notably hypoxia inducible factor-1alpha (HIF-1alpha), were largely limited to this group. Extrapulmonary pathology may thus contribute to the morbidities induced by H5N1 viruses.
PMID: 20372944 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/20372944
Extrapulmonary tissue responses in cynomolgus macaques (Macaca fascicularis) infected with highly pathogenic avian influenza A (H5N1) virus.
Tolnay AE, Baskin CR, Tumpey TM, Sabourin PJ, Sabourin CL, Long JP, Pyles JA, Albrecht RA, Garc?a-Sastre A, Katze MG, Bielefeldt-Ohmann H.
Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO, USA.
Abstract
The mechanisms responsible for virulence of influenza viruses in humans remain poorly understood. A prevailing hypothesis is that the highly pathogenic virus isolates cause a severe cytokinemia precipitating acute respiratory distress syndrome and multiple organ dysfunction syndrome. Cynomolgus macaques (Macaca fascicularis) infected with a human highly pathogenic avian influenza (HPAI) H5N1 virus isolate (A/Vietnam/1203/2004) or reassortants of human influenza virus A/Texas/36/91 (H1N1) containing genes from the 1918 pandemic influenza A (H1N1) virus developed severe pneumonia within 24 h postinfection. However, virus spread beyond the lungs was only detected in the H5N1 group, and signs of extrapulmonary tissue reactions, including microglia activation and sustained up-regulation of inflammatory markers, most notably hypoxia inducible factor-1alpha (HIF-1alpha), were largely limited to this group. Extrapulmonary pathology may thus contribute to the morbidities induced by H5N1 viruses.
PMID: 20372944 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/20372944