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10.1128/JVI.79.12.7819-7826.2005 http://scihub22266oqcxt.onion/10.1128/JVI.79.12.7819-7826.2005 C1143636!1143636!15919935     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=15919935&cmd=llinks): Failed to open stream: HTTP request failed! 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Cytokine Responses in Severe Acute Respiratory Syndrome Coronavirus-Infected Macrophages In Vitro: Possible Relevance to Pathogenesis |pdf=|usr=}}{{15919935}} gab.com Text Cytokine Responses in Severe Acute Respiratory Syndrome Coronavirus-Infected Macrophages In Vitro: Possible Relevance to Pathogenesis JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=15919935 #FOAvip The pathogenesis of severe acute respiratory syndrome (SARS) remains unclear. Macrophages are key sentinel cells in the respiratory system, and it is therefore relevant to compare the responses of human macrophages to infections with the SARS coronavirus (SARS-CoV) and other respiratory viruses. Primary human monocyte-derived macrophages were infected with SARS-CoV in vitro. Virus replication was monitored by measuring the levels of positive- and negative-strand RNA, by immunofluorescence detection of the SARS-CoV nucleoprotein, and by titration of the infectious virus. The gene expression profiles of macrophages infected with SARS-CoV, human coronavirus 229E, and influenza A (H1N1) virus were compared by using microarrays and real-time quantitative reverse transcriptase PCR. Secreted cytokines were measured with an enzyme-linked immunosorbent assay. SARS-CoV initiated viral gene transcription and protein synthesis in macrophages, but replication was abortive and no infectious virus was produced. In contrast to the case with human coronavirus 229E and influenza A virus, there was little or no induction of beta interferon (IFN-?) in SARS-CoV-infected macrophages. Furthermore, SARS-CoV induced the expression of chemokines such as CXCL10/IFN-?-inducible protein 10 and CCL2/monocyte chemotactic protein 1. The poor induction of IFN-?, a key component of innate immunity, and the ability of the virus to induce chemokines could explain aspects of the pathogenesis of SARS. Twit Text FOAVip Cytokine Responses in Severe Acute Respiratory Syndrome Coronavirus-Infected Macrophages In Vitro: Possible Relevance to Pathogenesis ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=15919935 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=15919935 #FOAvip English Wikipedia <ref>{{Cite pmid|15919935}}</ref> Cytokine Responses in Severe Acute Respiratory Syndrome Coronavirus-Infected Macrophages In Vitro: Possible Relevance to Pathogenesis #MMPMID15919935 Cheung CY; Poon LLM; Ng IHY; Luk W; Sia SF; Wu MHS; Chan KH; Yuen KY; Gordon S; Guan Y; Peiris JSM J Virol 2005[Jun]; 79 (12): 7819-26 PMID15919935show ga The pathogenesis of severe acute respiratory syndrome (SARS) remains unclear. Macrophages are key sentinel cells in the respiratory system, and it is therefore relevant to compare the responses of human macrophages to infections with the SARS coronavirus (SARS-CoV) and other respiratory viruses. Primary human monocyte-derived macrophages were infected with SARS-CoV in vitro. Virus replication was monitored by measuring the levels of positive- and negative-strand RNA, by immunofluorescence detection of the SARS-CoV nucleoprotein, and by titration of the infectious virus. The gene expression profiles of macrophages infected with SARS-CoV, human coronavirus 229E, and influenza A (H1N1) virus were compared by using microarrays and real-time quantitative reverse transcriptase PCR. Secreted cytokines were measured with an enzyme-linked immunosorbent assay. SARS-CoV initiated viral gene transcription and protein synthesis in macrophages, but replication was abortive and no infectious virus was produced. In contrast to the case with human coronavirus 229E and influenza A virus, there was little or no induction of beta interferon (IFN-?) in SARS-CoV-infected macrophages. Furthermore, SARS-CoV induced the expression of chemokines such as CXCL10/IFN-?-inducible protein 10 and CCL2/monocyte chemotactic protein 1. The poor induction of IFN-?, a key component of innate immunity, and the ability of the virus to induce chemokines could explain aspects of the pathogenesis of SARS. äCytokine Responses in Severe Acute Respiratory Syndrome Coronavirus-In(epmc).pdf DeepDyve Pubget Overpricing