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10.1016/j.celrep.2021.109364 http://scihub22266oqcxt.onion/10.1016/j.celrep.2021.109364 34214467!8220945!34214467     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34214467&cmd=llinks): Failed to open stream: HTTP request failed! 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Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell |pdf=|usr=}}{{34214467}} gab.com Text Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=34214467 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) variants govern transmissibility, responsiveness to vaccination, and disease severity. In a screen for new models of SARS-CoV-2 infection, we identify human H522 lung adenocarcinoma cells as naturally permissive to SARS-CoV-2 infection despite complete absence of angiotensin-converting enzyme 2 (ACE2) expression. Remarkably, H522 infection requires the E484D S variant; viruses expressing wild-type S are not infectious. Anti-S monoclonal antibodies differentially neutralize SARS-CoV-2 E484D S in H522 cells as compared to ACE2-expressing cells. Sera from vaccinated individuals block this alternative entry mechanism, whereas convalescent sera are less effective. Although the H522 receptor remains unknown, depletion of surface heparan sulfates block H522 infection. Temporally resolved transcriptomic and proteomic profiling reveal alterations in cell cycle and the antiviral host cell response, including MDA5-dependent activation of type I interferon signaling. These findings establish an alternative SARS-CoV-2 host cell receptor for the E484D SARS-CoV-2 variant, which may impact tropism of SARS-CoV-2 and consequently human disease pathogenesis. Twit Text FOAVip Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=34214467 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34214467 #FOAvip English Wikipedia <ref>{{Cite pmid|34214467}}</ref> Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell #MMPMID34214467 Puray-Chavez M; LaPak KM; Schrank TP; Elliott JL; Bhatt DP; Agajanian MJ; Jasuja R; Lawson DQ; Davis K; Rothlauf PW; Liu Z; Jo H; Lee N; Tenneti K; Eschbach JE; Shema Mugisha C; Cousins EM; Cloer EW; Vuong HR; VanBlargan LA; Bailey AL; Gilchuk P; Crowe JE Jr; Diamond MS; Hayes DN; Whelan SPJ; Horani A; Brody SL; Goldfarb D; Major MB; Kutluay SB Cell Rep 2021[Jul]; 36 (2): 109364 PMID34214467show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) variants govern transmissibility, responsiveness to vaccination, and disease severity. In a screen for new models of SARS-CoV-2 infection, we identify human H522 lung adenocarcinoma cells as naturally permissive to SARS-CoV-2 infection despite complete absence of angiotensin-converting enzyme 2 (ACE2) expression. Remarkably, H522 infection requires the E484D S variant; viruses expressing wild-type S are not infectious. Anti-S monoclonal antibodies differentially neutralize SARS-CoV-2 E484D S in H522 cells as compared to ACE2-expressing cells. Sera from vaccinated individuals block this alternative entry mechanism, whereas convalescent sera are less effective. Although the H522 receptor remains unknown, depletion of surface heparan sulfates block H522 infection. Temporally resolved transcriptomic and proteomic profiling reveal alterations in cell cycle and the antiviral host cell response, including MDA5-dependent activation of type I interferon signaling. These findings establish an alternative SARS-CoV-2 host cell receptor for the E484D SARS-CoV-2 variant, which may impact tropism of SARS-CoV-2 and consequently human disease pathogenesis. |*Receptors, Virus/metabolism[MESH] |Amino Acid Substitution[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Animals[MESH] |Antibodies, Monoclonal/immunology[MESH] |Antibodies, Viral/immunology[MESH] |COVID-19/*immunology/*metabolism[MESH] |Cell Cycle[MESH] |Cell Line, Tumor[MESH] |Chlorocebus aethiops[MESH] |Gene Expression Profiling[MESH] |Heparitin Sulfate/metabolism[MESH] |Humans[MESH] |Interferon Type I/metabolism[MESH] |Interferon-Induced Helicase, IFIH1/metabolism[MESH] |Models, Biological[MESH] |Protein Binding[MESH] |Protein Domains[MESH] |Proteomics[MESH] |SARS-CoV-2[MESH] |Serine Endopeptidases/metabolism[MESH] |Signal Transduction[MESH] |Spike Glycoprotein, Coronavirus/genetics/*metabolism[MESH] |Vero Cells[MESH] |Virus Internalization[MESH]Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human (epmc).pdf DeepDyve Pubget Overpricing