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10.1093/infdis/jis455 http://scihub22266oqcxt.onion/10.1093/infdis/jis455 22829640!7107318!22829640     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Infect+Dis 2012 ; 206 (11): 1685-94 Nephropedia Template TP {{tp|p=22829640|t=2012. Influenza A viruses target type II pneumocytes in the human lung |pdf=|usr=}}{{22829640}} gab.com Text Influenza A viruses target type II pneumocytes in the human lung JO: J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=22829640 #FOAvip BACKGROUND: Highly pathogenic avian H5N1 influenza viruses preferentially infect alveolar type II pneumocytes in human lung. However, it is unknown whether this cellular tropism contributes to high viral virulence because the primary target cells of other influenza viruses have not been systematically studied. METHODS: We provide the first comparison of the replication, tropism, and cytokine induction of human, highly pathogenic avian influenza A virus subtype H5N1 and other animal influenza A viruses in primary human lung organ cultures. RESULTS: Subytpe H5N1 and human-adapted subtype H1N1 and H3N2 viruses replicated efficiently in the lung tissue, whereas classic swine and low-pathogenicity avian viruses propagated only poorly. Nevertheless, all viruses examined were detected almost exclusively in type II pneumocytes, with a minor involvement of alveolar macrophages. Infection with avian viruses that have a low and high pathogenicity provoked a pronounced induction of cytokines and chemokines, while human and pandemic H1N1-2009 viruses triggered only weak responses. CONCLUSIONS: These findings show that differences in the pathogenic potential of influenza A viruses in the human lung cannot be attributed to a distinct cellular tropism. Rather, high or low viral pathogenicity is associated with a strain-specific capacity to productively replicate in type II pneumocytes and to cope with the induced cytokine response. Twit Text FOAVip Influenza A viruses target type II pneumocytes in the human lung ????J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=22829640 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22829640 #FOAvip English Wikipedia <ref>{{Cite pmid|22829640}}</ref> Influenza A viruses target type II pneumocytes in the human lung #MMPMID22829640 Weinheimer VK; Becher A; Tonnies M; Holland G; Knepper J; Bauer TT; Schneider P; Neudecker J; Ruckert JC; Szymanski K; Temmesfeld-Wollbrueck B; Gruber AD; Bannert N; Suttorp N; Hippenstiel S; Wolff T; Hocke AC J Infect Dis 2012[Dec]; 206 (11): 1685-94 PMID22829640show ga BACKGROUND: Highly pathogenic avian H5N1 influenza viruses preferentially infect alveolar type II pneumocytes in human lung. However, it is unknown whether this cellular tropism contributes to high viral virulence because the primary target cells of other influenza viruses have not been systematically studied. METHODS: We provide the first comparison of the replication, tropism, and cytokine induction of human, highly pathogenic avian influenza A virus subtype H5N1 and other animal influenza A viruses in primary human lung organ cultures. RESULTS: Subytpe H5N1 and human-adapted subtype H1N1 and H3N2 viruses replicated efficiently in the lung tissue, whereas classic swine and low-pathogenicity avian viruses propagated only poorly. Nevertheless, all viruses examined were detected almost exclusively in type II pneumocytes, with a minor involvement of alveolar macrophages. Infection with avian viruses that have a low and high pathogenicity provoked a pronounced induction of cytokines and chemokines, while human and pandemic H1N1-2009 viruses triggered only weak responses. CONCLUSIONS: These findings show that differences in the pathogenic potential of influenza A viruses in the human lung cannot be attributed to a distinct cellular tropism. Rather, high or low viral pathogenicity is associated with a strain-specific capacity to productively replicate in type II pneumocytes and to cope with the induced cytokine response. |Alveolar Epithelial Cells/*classification/*virology[MESH] |Cytokines/genetics/metabolism[MESH] |Gene Expression Regulation/physiology[MESH] |Humans[MESH] |Influenza A virus/classification/pathogenicity/*physiology[MESH] |Influenza, Human/virology[MESH] |Lung/cytology[MESH] |Macrophages, Alveolar/virology[MESH] |Tissue Culture Techniques[MESH] |Viral Tropism/*physiology[MESH] |Virulence[MESH]Influenza A viruses target type II pneumocytes in the human lung (epmc).pdf DeepDyve Pubget Overpricing