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10.1073/pnas.2018030117 http://scihub22266oqcxt.onion/10.1073/pnas.2018030117 33082228!7668053!33082228     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33082228&cmd=llinks): Failed to open stream: HTTP request failed! 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Transcriptional and proteomic insights into the host response in fatal COVID-19 cases |pdf=|usr=}}{{33082228}} gab.com Text Transcriptional and proteomic insights into the host response in fatal COVID-19 cases JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=33082228 #FOAvip Coronavirus disease 2019 (COVID-19), the global pandemic caused by SARS-CoV-2, has resulted thus far in greater than 933,000 deaths worldwide; yet disease pathogenesis remains unclear. Clinical and immunological features of patients with COVID-19 have highlighted a potential role for changes in immune activity in regulating disease severity. However, little is known about the responses in human lung tissue, the primary site of infection. Here we show that pathways related to neutrophil activation and pulmonary fibrosis are among the major up-regulated transcriptional signatures in lung tissue obtained from patients who died of COVID-19 in Wuhan, China. Strikingly, the viral burden was low in all samples, which suggests that the patient deaths may be related to the host response rather than an active fulminant infection. Examination of the colonic transcriptome of these patients suggested that SARS-CoV-2 impacted host responses even at a site with no obvious pathogenesis. Further proteomics analysis validated our transcriptome findings and identified several key proteins, such as the SARS-CoV-2 entry-associated protease cathepsins B and L and the inflammatory response modulator S100A8/A9, that are highly expressed in fatal cases, revealing potential drug targets for COVID-19. Twit Text FOAVip Transcriptional and proteomic insights into the host response in fatal COVID-19 cases ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=33082228 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33082228 #FOAvip English Wikipedia <ref>{{Cite pmid|33082228}}</ref> Transcriptional and proteomic insights into the host response in fatal COVID-19 cases #MMPMID33082228 Wu M; Chen Y; Xia H; Wang C; Tan CY; Cai X; Liu Y; Ji F; Xiong P; Liu R; Guan Y; Duan Y; Kuang D; Xu S; Cai H; Xia Q; Yang D; Wang MW; Chiu IM; Cheng C; Ahern PP; Liu L; Wang G; Surana NK; Xia T; Kasper DL Proc Natl Acad Sci U S A 2020[Nov]; 117 (45): 28336-28343 PMID33082228show ga Coronavirus disease 2019 (COVID-19), the global pandemic caused by SARS-CoV-2, has resulted thus far in greater than 933,000 deaths worldwide; yet disease pathogenesis remains unclear. Clinical and immunological features of patients with COVID-19 have highlighted a potential role for changes in immune activity in regulating disease severity. However, little is known about the responses in human lung tissue, the primary site of infection. Here we show that pathways related to neutrophil activation and pulmonary fibrosis are among the major up-regulated transcriptional signatures in lung tissue obtained from patients who died of COVID-19 in Wuhan, China. Strikingly, the viral burden was low in all samples, which suggests that the patient deaths may be related to the host response rather than an active fulminant infection. Examination of the colonic transcriptome of these patients suggested that SARS-CoV-2 impacted host responses even at a site with no obvious pathogenesis. Further proteomics analysis validated our transcriptome findings and identified several key proteins, such as the SARS-CoV-2 entry-associated protease cathepsins B and L and the inflammatory response modulator S100A8/A9, that are highly expressed in fatal cases, revealing potential drug targets for COVID-19. |*Transcriptome[MESH] |Aged[MESH] |Aged, 80 and over[MESH] |COVID-19/genetics/immunology/*metabolism/pathology[MESH] |Colon/metabolism[MESH] |Fatal Outcome[MESH] |Female[MESH] |Humans[MESH] |Lung/metabolism/pathology/virology[MESH] |Male[MESH] |Middle Aged[MESH] |Neutrophil Activation[MESH] |Proteome/genetics/*metabolism[MESH] |SARS-CoV-2/pathogenicity[MESH]Transcriptional and proteomic insights into the host response in fatal(epmc).pdf DeepDyve Pubget Overpricing