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10.3390/v14010132 http://scihub22266oqcxt.onion/10.3390/v14010132 35062337!8778678!35062337     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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Viruses 2022 ; 14 (1): ä Nephropedia Template TP {{tp|p=35062337|t=2022. GNS561 Exhibits Potent Antiviral Activity against SARS-CoV-2 through Autophagy Inhibition |pdf=|usr=}}{{35062337}} gab.com Text GNS561 Exhibits Potent Antiviral Activity against SARS-CoV-2 through Autophagy Inhibition JO: Viruses http://www.kidney.de/pget.php?&tw=1&pmid=35062337 #FOAvip Since December 2019, SARS-CoV-2 has spread quickly worldwide, leading to more than 280 million confirmed cases, including over 5,000,000 deaths. Interestingly, coronaviruses were found to subvert and hijack autophagic process to allow their viral replication. Autophagy-modulating compounds thus rapidly emerged as an attractive strategy to fight SARS-CoV-2 infection, including the well-known chloroquine (CQ). Here, we investigated the antiviral activity and associated mechanism of GNS561/Ezurpimtrostat, a small lysosomotropic molecule inhibitor of late-stage autophagy. Interestingly, GNS561 exhibited antiviral activity of 6-40 nM depending on the viral strain considered, currently positioning it as the most powerful molecule investigated in SARS-CoV-2 infection. We then showed that GNS561 was located in lysosome-associated-membrane-protein-2-positive (LAMP2-positive) lysosomes, together with SARS-CoV-2. Moreover, GNS561 increased LC3-II spot size and caused the accumulation of autophagic vacuoles and the presence of multilamellar bodies, suggesting that GNS561 disrupted the autophagy mechanism. To confirm our findings, we used the K18-hACE2 mouse model and highlighted that GNS561 treatment led to a decline in SARS-CoV-2 virions in the lungs associated with a disruption of the autophagy pathway. Overall, our study highlights GNS561 as a powerful drug in the treatment of SARS-CoV-2 infection and supports the hypothesis that autophagy blockers could be an alternative strategy for COVID-19. Twit Text FOAVip GNS561 Exhibits Potent Antiviral Activity against SARS-CoV-2 through Autophagy Inhibition ????Viruses http://www.kidney.de/pget.php?&tw=1&pmid=35062337 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35062337 #FOAvip English Wikipedia <ref>{{Cite pmid|35062337}}</ref> GNS561 Exhibits Potent Antiviral Activity against SARS-CoV-2 through Autophagy Inhibition #MMPMID35062337 Bestion E; Zandi K; Belouzard S; Andreani J; Lepidi H; Novello M; Rouquairol C; Baudoin JP; Rachid M; La Scola B; Mege JL; Dubuisson J; Schinazi RF; Mezouar S; Halfon P Viruses 2022[Jan]; 14 (1): ä PMID35062337show ga Since December 2019, SARS-CoV-2 has spread quickly worldwide, leading to more than 280 million confirmed cases, including over 5,000,000 deaths. Interestingly, coronaviruses were found to subvert and hijack autophagic process to allow their viral replication. Autophagy-modulating compounds thus rapidly emerged as an attractive strategy to fight SARS-CoV-2 infection, including the well-known chloroquine (CQ). Here, we investigated the antiviral activity and associated mechanism of GNS561/Ezurpimtrostat, a small lysosomotropic molecule inhibitor of late-stage autophagy. Interestingly, GNS561 exhibited antiviral activity of 6-40 nM depending on the viral strain considered, currently positioning it as the most powerful molecule investigated in SARS-CoV-2 infection. We then showed that GNS561 was located in lysosome-associated-membrane-protein-2-positive (LAMP2-positive) lysosomes, together with SARS-CoV-2. Moreover, GNS561 increased LC3-II spot size and caused the accumulation of autophagic vacuoles and the presence of multilamellar bodies, suggesting that GNS561 disrupted the autophagy mechanism. To confirm our findings, we used the K18-hACE2 mouse model and highlighted that GNS561 treatment led to a decline in SARS-CoV-2 virions in the lungs associated with a disruption of the autophagy pathway. Overall, our study highlights GNS561 as a powerful drug in the treatment of SARS-CoV-2 infection and supports the hypothesis that autophagy blockers could be an alternative strategy for COVID-19. |*COVID-19 Drug Treatment[MESH] |Animals[MESH] |Antiviral Agents/*pharmacology/therapeutic use[MESH] |Autophagosomes/metabolism[MESH] |Autophagy/*drug effects[MESH] |COVID-19/pathology/virology[MESH] |Cell Line[MESH] |Disease Models, Animal[MESH] |Humans[MESH] |Lung/drug effects/pathology/virology[MESH] |Lysosomes/metabolism[MESH] |Mice[MESH] |SARS-CoV-2/*drug effects/physiology[MESH] |Viral Load/drug effects[MESH]GNS561 Exhibits Potent Antiviral Activity against SARS-CoV-2 through A(epmc).pdf DeepDyve Pubget Overpricing