<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Santos Bravo M</submitter><funding>CIBER Enfermedades Infecciosas</funding><funding>Gilead Sciences</funding><pagination>e0244822</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9769853</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(6)</volume><pubmed_abstract>Remdesivir (RDV) was the first antiviral drug approved by the FDA to treat severe coronavirus disease-2019 (COVID-19) patients. RDV inhibits SARS-CoV-2 replication by stalling the non structural protein 12 (nsp12) subunit of the RNA-dependent RNA polymerase (RdRp). No evidence of global widespread RDV-resistance mutations has been reported, however, defining genetic pathways to RDV resistance and determining emergent mutations prior and subsequent antiviral therapy in clinical settings is necessary. This study identified 57/149 (38.3%) patients who did not respond to one course (5-days) (&lt;i>n&lt;/i> = 36/111, 32.4%) or prolonged (5 to 20 days) (&lt;i>n&lt;/i> = 21/38, 55.3%) RDV therapy by subgenomic RNA detection. Genetic variants in the &lt;i>nsp12&lt;/i> gene were detected in 29/49 (59.2%) non respond</pubmed_abstract><journal>Microbiology spectrum</journal><pubmed_title>Genetic Study of SARS-CoV-2 Non Structural Protein 12 in COVID-19 Patients Non Responders to Remdesivir.</pubmed_title><pmcid>PMC9769853</pmcid><funding_grant_id>IN-ES-540-6089</funding_grant_id><funding_grant_id>CB21/13/00081</funding_grant_id><pubmed_authors>Sanchez Palomino S</pubmed_authors><pubmed_authors>Villanueva JL</pubmed_authors><pubmed_authors>Puerta P</pubmed_authors><pubmed_authors>Alonso R</pubmed_authors><pubmed_authors>Vergara A</pubmed_authors><pubmed_authors>Mosquera Gutierrez MDM</pubmed_authors><pubmed_authors>Rodriguez C</pubmed_authors><pubmed_authors>Vila J</pubmed_authors><pubmed_authors>Diez-Fuertes F</pubmed_authors><pubmed_authors>Castro P</pubmed_authors><pubmed_authors>Sanzo Machuca A</pubmed_authors><pubmed_authors>Simarro Redon A</pubmed_authors><pubmed_authors>Rubio E</pubmed_authors><pubmed_authors>Cuesta G</pubmed_authors><pubmed_authors>Hurtado JC</pubmed_authors><pubmed_authors>Soriano A</pubmed_authors><pubmed_authors>Marcos MA</pubmed_authors><pubmed_authors>Martinez MJ</pubmed_authors><pubmed_authors>Alcami J</pubmed_authors><pubmed_authors>Soria D</pubmed_authors><pubmed_authors>Tuset M</pubmed_authors><pubmed_authors>Fernandez Aviles F</pubmed_authors><pubmed_authors>Bodro M</pubmed_authors><pubmed_authors>Garcia C</pubmed_authors><pubmed_authors>Santos Bravo M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic Study of SARS-CoV-2 Non Structural Protein 12 in COVID-19 Patients Non Responders to Remdesivir.</name><description>Remdesivir (RDV) was the first antiviral drug approved by the FDA to treat severe coronavirus disease-2019 (COVID-19) patients. RDV inhibits SARS-CoV-2 replication by stalling the non structural protein 12 (nsp12) subunit of the RNA-dependent RNA polymerase (RdRp). No evidence of global widespread RDV-resistance mutations has been reported, however, defining genetic pathways to RDV resistance and determining emergent mutations prior and subsequent antiviral therapy in clinical settings is necessary. This study identified 57/149 (38.3%) patients who did not respond to one course (5-days) (&lt;i>n&lt;/i> = 36/111, 32.4%) or prolonged (5 to 20 days) (&lt;i>n&lt;/i> = 21/38, 55.3%) RDV therapy by subgenomic RNA detection. Genetic variants in the &lt;i>nsp12&lt;/i> gene were detected in 29/49 (59.2%) non respond</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2026-05-28T21:31:04.738Z</modification><creation>2024-12-04T05:13:01.667Z</creation></dates><accession>S-EPMC9769853</accession><cross_references><pubmed>36354320</pubmed><doi>10.1128/spectrum.02448-22</doi></cross_references></HashMap>