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10.1128/JVI.02012-06 http://scihub22266oqcxt.onion/10.1128/JVI.02012-06 17079315!1797474!17079315     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=17079315&cmd=llinks): Failed to open stream: HTTP request failed! 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Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus |pdf=|usr=}}{{17079315}} gab.com Text Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=17079315 #FOAvip The severe acute respiratory syndrome (SARS), caused by a novel coronavirus (SARS-CoV), resulted in substantial morbidity, mortality, and economic losses during the 2003 epidemic. While SARS-CoV infection has not recurred to a significant extent since 2003, it still remains a potential threat. Understanding of SARS and development of therapeutic approaches have been hampered by the absence of an animal model that mimics the human disease and is reproducible. Here we show that transgenic mice that express the SARS-CoV receptor (human angiotensin-converting enzyme 2 [hACE2]) in airway and other epithelia develop a rapidly lethal infection after intranasal inoculation with a human strain of the virus. Infection begins in airway epithelia, with subsequent alveolar involvement and extrapulmonary virus spread to the brain. Infection results in macrophage and lymphocyte infiltration in the lungs and upregulation of proinflammatory cytokines and chemokines in both the lung and the brain. This model of lethal infection with SARS-CoV should be useful for studies of pathogenesis and for the development of antiviral therapies. Twit Text FOAVip Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=17079315 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17079315 #FOAvip English Wikipedia <ref>{{Cite pmid|17079315}}</ref> Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus #MMPMID17079315 McCray PB Jr; Pewe L; Wohlford-Lenane C; Hickey M; Manzel L; Shi L; Netland J; Jia HP; Halabi C; Sigmund CD; Meyerholz DK; Kirby P; Look DC; Perlman S J Virol 2007[Jan]; 81 (2): 813-21 PMID17079315show ga The severe acute respiratory syndrome (SARS), caused by a novel coronavirus (SARS-CoV), resulted in substantial morbidity, mortality, and economic losses during the 2003 epidemic. While SARS-CoV infection has not recurred to a significant extent since 2003, it still remains a potential threat. Understanding of SARS and development of therapeutic approaches have been hampered by the absence of an animal model that mimics the human disease and is reproducible. Here we show that transgenic mice that express the SARS-CoV receptor (human angiotensin-converting enzyme 2 [hACE2]) in airway and other epithelia develop a rapidly lethal infection after intranasal inoculation with a human strain of the virus. Infection begins in airway epithelia, with subsequent alveolar involvement and extrapulmonary virus spread to the brain. Infection results in macrophage and lymphocyte infiltration in the lungs and upregulation of proinflammatory cytokines and chemokines in both the lung and the brain. This model of lethal infection with SARS-CoV should be useful for studies of pathogenesis and for the development of antiviral therapies. |*Disease Models, Animal[MESH] |Animals[MESH] |Brain/cytology/pathology/virology[MESH] |Epithelial Cells/pathology/virology[MESH] |Humans[MESH] |Keratin-18/genetics/*metabolism[MESH] |Lung/cytology/pathology/virology[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Transgenic[MESH] |Peptidyl-Dipeptidase A/genetics/*metabolism[MESH] |Severe Acute Respiratory Syndrome/mortality/pathology/virology[MESH]Lethal infection of K18-hACE2 mice infected with severe acute respirat(epmc).pdf DeepDyve Pubget Overpricing