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10.3390/v13071246 http://scihub22266oqcxt.onion/10.3390/v13071246 34206990!8310277!34206990     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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Viruses 2021 ; 13 (7): ä Nephropedia Template TP {{tp|p=34206990|t=2021. Human Defensins Inhibit SARS-CoV-2 Infection by Blocking Viral Entry |pdf=|usr=}}{{34206990}} gab.com Text Human Defensins Inhibit SARS-CoV-2 Infection by Blocking Viral Entry JO: Viruses http://www.kidney.de/pget.php?&tw=1&pmid=34206990 #FOAvip Innate immunity during acute infection plays a critical role in the disease severity of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), and is likely to contribute to COVID-19 disease outcomes. Defensins are highly abundant innate immune factors in neutrophils and epithelial cells, including intestinal Paneth cells, and exhibit antimicrobial and immune-modulatory activities. In this study, we investigated the effects of human alpha- and beta-defensins and RC101, a theta-defensin analog, on SARS-CoV-2 infection. We found that human neutrophil peptides (HNPs) 1-3, human defensin (HD) 5 and RC101 exhibited potent antiviral activity against pseudotyped viruses expressing SARS-CoV-2 spike proteins. HNP4 and HD6 had weak anti-SARS-CoV-2 activity, whereas human beta-defensins (HBD2, HBD5 and HBD6) had no effect. HNP1, HD5 and RC101 also inhibited infection by replication-competent SARS-CoV-2 viruses and SARS-CoV-2 variants. Pretreatment of cells with HNP1, HD5 or RC101 provided some protection against viral infection. These defensins did not have an effect when provided post-infection, indicating their effect was directed towards viral entry. Indeed, HNP1 inhibited viral fusion but not the binding of the spike receptor-binding domain to hACE2. The anti-SARS-CoV-2 effect of defensins was influenced by the structure of the peptides, as linear unstructured forms of HNP1 and HD5 lost their antiviral function. Pro-HD5, the precursor of HD5, did not block infection by SARS-CoV-2. High virus titers overcame the effect of low levels of HNP1, indicating that defensins act on the virion. HNP1, HD5 and RC101 also blocked viral infection of intestinal and lung epithelial cells. The protective effects of defensins reported here suggest that they may be useful additives to the antivirus arsenal and should be thoroughly studied. Twit Text FOAVip Human Defensins Inhibit SARS-CoV-2 Infection by Blocking Viral Entry ????Viruses http://www.kidney.de/pget.php?&tw=1&pmid=34206990 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34206990 #FOAvip English Wikipedia <ref>{{Cite pmid|34206990}}</ref> Human Defensins Inhibit SARS-CoV-2 Infection by Blocking Viral Entry #MMPMID34206990 Xu C; Wang A; Marin M; Honnen W; Ramasamy S; Porter E; Subbian S; Pinter A; Melikyan GB; Lu W; Chang TL Viruses 2021[Jun]; 13 (7): ä PMID34206990show ga Innate immunity during acute infection plays a critical role in the disease severity of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), and is likely to contribute to COVID-19 disease outcomes. Defensins are highly abundant innate immune factors in neutrophils and epithelial cells, including intestinal Paneth cells, and exhibit antimicrobial and immune-modulatory activities. In this study, we investigated the effects of human alpha- and beta-defensins and RC101, a theta-defensin analog, on SARS-CoV-2 infection. We found that human neutrophil peptides (HNPs) 1-3, human defensin (HD) 5 and RC101 exhibited potent antiviral activity against pseudotyped viruses expressing SARS-CoV-2 spike proteins. HNP4 and HD6 had weak anti-SARS-CoV-2 activity, whereas human beta-defensins (HBD2, HBD5 and HBD6) had no effect. HNP1, HD5 and RC101 also inhibited infection by replication-competent SARS-CoV-2 viruses and SARS-CoV-2 variants. Pretreatment of cells with HNP1, HD5 or RC101 provided some protection against viral infection. These defensins did not have an effect when provided post-infection, indicating their effect was directed towards viral entry. Indeed, HNP1 inhibited viral fusion but not the binding of the spike receptor-binding domain to hACE2. The anti-SARS-CoV-2 effect of defensins was influenced by the structure of the peptides, as linear unstructured forms of HNP1 and HD5 lost their antiviral function. Pro-HD5, the precursor of HD5, did not block infection by SARS-CoV-2. High virus titers overcame the effect of low levels of HNP1, indicating that defensins act on the virion. HNP1, HD5 and RC101 also blocked viral infection of intestinal and lung epithelial cells. The protective effects of defensins reported here suggest that they may be useful additives to the antivirus arsenal and should be thoroughly studied. |A549 Cells[MESH] |Caco-2 Cells[MESH] |Defensins/classification/*pharmacology[MESH] |Epithelial Cells/virology[MESH] |HEK293 Cells[MESH] |HeLa Cells[MESH] |Humans[MESH] |SARS-CoV-2/*drug effects/physiology[MESH]Human Defensins Inhibit SARS-CoV-2 Infection by Blocking Viral Entry (epmc).pdf DeepDyve Pubget Overpricing