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10.1111/cpr.12953 http://scihub22266oqcxt.onion/10.1111/cpr.12953 33211371!7744835!33211371     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Prolif 2021 ; 54 (1): e12953 Nephropedia Template TP {{tp|p=33211371|t=2021. Direct inhibitory effect on viral entry of influenza A and SARS-CoV-2 viruses by azithromycin |pdf=|usr=}}{{33211371}} gab.com Text Direct inhibitory effect on viral entry of influenza A and SARS-CoV-2 viruses by azithromycin JO: Cell Prolif http://www.kidney.de/pget.php?&tw=1&pmid=33211371 #FOAvip OBJECTIVES: Using strategy of drug repurposing, antiviral agents against influenza A virus (IAV) and newly emerging SARS-coronavirus 2 (SARS-CoV-2, also as 2019-nCoV) could be quickly screened out. MATERIALS AND METHODS: A previously reported engineered replication-competent PR8 strain carrying luciferase reporter gene (IAV-luc) and multiple pseudotyped IAV and SARS-CoV-2 virus was used. To specifically evaluate the pH change of vesicles containing IAV, we constructed an A549 cell line with endosomal and lysosomal expression of pHluorin2. RESULTS: Here, we identified azithromycin (AZ) as an effective inhibitor against multiple IAV and SARS-CoV-2 strains. We found that AZ treatment could potently inhibit IAV infection in vitro. Moreover, using pseudotyped virus model, AZ could also markedly block the entry of SARS-CoV-2 in HEK293T-ACE2 and Caco2 cells. Mechanistic studies further revealed that such effect was independent of interferon signalling. AZ treatment neither impaired the binding and internalization of IAV virions, nor the viral replication, but rather inhibited the fusion between viral and vacuolar membranes. Using a NPC1-pHluorin2 reporter cell line, we confirmed that AZ treatment could alkalize the vesicles containing IAV virions, thereby preventing pH-dependent membrane fusion. CONCLUSIONS: Overall, our findings demonstrate that AZ can exert broad-spectrum antiviral effects against IAV and SARS-CoV-2, and could be served as a potential clinical anti-SARS-CoV-2 drug in emergency as well as a promising lead compound for the development of next-generation anti-IAV drugs. Twit Text FOAVip Direct inhibitory effect on viral entry of influenza A and SARS-CoV-2 viruses by azithromycin ????Cell Prolif http://www.kidney.de/pget.php?&tw=1&pmid=33211371 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33211371 #FOAvip English Wikipedia <ref>{{Cite pmid|33211371}}</ref> Direct inhibitory effect on viral entry of influenza A and SARS-CoV-2 viruses by azithromycin #MMPMID33211371 Du X; Zuo X; Meng F; Han C; Ouyang W; Han Y; Gu Y; Zhao X; Xu F; Qin FX Cell Prolif 2021[Jan]; 54 (1): e12953 PMID33211371show ga OBJECTIVES: Using strategy of drug repurposing, antiviral agents against influenza A virus (IAV) and newly emerging SARS-coronavirus 2 (SARS-CoV-2, also as 2019-nCoV) could be quickly screened out. MATERIALS AND METHODS: A previously reported engineered replication-competent PR8 strain carrying luciferase reporter gene (IAV-luc) and multiple pseudotyped IAV and SARS-CoV-2 virus was used. To specifically evaluate the pH change of vesicles containing IAV, we constructed an A549 cell line with endosomal and lysosomal expression of pHluorin2. RESULTS: Here, we identified azithromycin (AZ) as an effective inhibitor against multiple IAV and SARS-CoV-2 strains. We found that AZ treatment could potently inhibit IAV infection in vitro. Moreover, using pseudotyped virus model, AZ could also markedly block the entry of SARS-CoV-2 in HEK293T-ACE2 and Caco2 cells. Mechanistic studies further revealed that such effect was independent of interferon signalling. AZ treatment neither impaired the binding and internalization of IAV virions, nor the viral replication, but rather inhibited the fusion between viral and vacuolar membranes. Using a NPC1-pHluorin2 reporter cell line, we confirmed that AZ treatment could alkalize the vesicles containing IAV virions, thereby preventing pH-dependent membrane fusion. CONCLUSIONS: Overall, our findings demonstrate that AZ can exert broad-spectrum antiviral effects against IAV and SARS-CoV-2, and could be served as a potential clinical anti-SARS-CoV-2 drug in emergency as well as a promising lead compound for the development of next-generation anti-IAV drugs. |A549 Cells[MESH] |Antiviral Agents/*pharmacology[MESH] |Azithromycin/*pharmacology[MESH] |COVID-19 Drug Treatment[MESH] |COVID-19/genetics/*metabolism[MESH] |Caco-2 Cells[MESH] |HEK293 Cells[MESH] |HeLa Cells[MESH] |Humans[MESH] |Influenza A virus/genetics/*metabolism[MESH] |Influenza, Human/drug therapy/genetics/*metabolism[MESH] |Interferons/genetics/metabolism[MESH] |SARS-CoV-2/genetics/*metabolism[MESH] |Signal Transduction/drug effects/genetics[MESH]Direct inhibitory effect on viral entry of influenza A and SARS-CoV-2 (epmc).pdf DeepDyve Pubget Overpricing