tetano
Editor, Senior Moderator
iScience
. 2024 Mar 29;27(5):109597.
doi: 10.1016/j.isci.2024.109597. eCollection 2024 May 17. Longitudinal analysis of genomic mutations in SARS-CoV-2 isolates from persistent COVID-19 patient
Hiroki Futatsusako[SUP] 1 [/SUP], Rina Hashimoto[SUP] 1 [/SUP], Masaki Yamamoto[SUP] 2 [/SUP], Jumpei Ito[SUP] 3 4 5 [/SUP], Yasufumi Matsumura[SUP] 2 [/SUP], Hajime Yoshifuji[SUP] 6 [/SUP], Kotaro Shirakawa[SUP] 7 [/SUP], Akifumi Takaori-Kondo[SUP] 7 [/SUP]; Genotype to Phenotype Japan (G2P-Japan) Consortium; Kei Sato[SUP] 3 4 5 8 9 10 11 [/SUP], Miki Nagao[SUP] 2 [/SUP], Kazuo Takayama[SUP] 1 12 [/SUP]
Affiliations
A primary reason for the ongoing spread of coronavirus disease 2019 (COVID-19) is the continuous acquisition of mutations by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the mechanism of acquiring mutations is not fully understood. In this study, we isolated SARS-CoV-2 from an immunocompromized patient persistently infected with Omicron strain BF.5 for approximately 4 months to analyze its genome and evaluate drug resistance. Although the patient was administered the antiviral drug remdesivir (RDV), there were no acquired mutations in RDV binding site, and all isolates exhibited susceptibility to RDV. Notably, upon analyzing the S protein sequence of the day 119 isolate, we identified mutations acquired by mutant strains emerging from the BF.5 variant, suggesting that viral genome analysis in persistent COVID-19 patients may be useful in predicting viral evolution. These results suggest mutations in SARS-CoV-2 are acquired during long-term viral replication rather than in response to antiviral drugs.
Keywords: Genomics; Microbiology and Virology.
. 2024 Mar 29;27(5):109597.
doi: 10.1016/j.isci.2024.109597. eCollection 2024 May 17. Longitudinal analysis of genomic mutations in SARS-CoV-2 isolates from persistent COVID-19 patient
Hiroki Futatsusako[SUP] 1 [/SUP], Rina Hashimoto[SUP] 1 [/SUP], Masaki Yamamoto[SUP] 2 [/SUP], Jumpei Ito[SUP] 3 4 5 [/SUP], Yasufumi Matsumura[SUP] 2 [/SUP], Hajime Yoshifuji[SUP] 6 [/SUP], Kotaro Shirakawa[SUP] 7 [/SUP], Akifumi Takaori-Kondo[SUP] 7 [/SUP]; Genotype to Phenotype Japan (G2P-Japan) Consortium; Kei Sato[SUP] 3 4 5 8 9 10 11 [/SUP], Miki Nagao[SUP] 2 [/SUP], Kazuo Takayama[SUP] 1 12 [/SUP]
Affiliations
- PMID: 38638575
- PMCID: PMC11024907
- DOI: 10.1016/j.isci.2024.109597
A primary reason for the ongoing spread of coronavirus disease 2019 (COVID-19) is the continuous acquisition of mutations by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the mechanism of acquiring mutations is not fully understood. In this study, we isolated SARS-CoV-2 from an immunocompromized patient persistently infected with Omicron strain BF.5 for approximately 4 months to analyze its genome and evaluate drug resistance. Although the patient was administered the antiviral drug remdesivir (RDV), there were no acquired mutations in RDV binding site, and all isolates exhibited susceptibility to RDV. Notably, upon analyzing the S protein sequence of the day 119 isolate, we identified mutations acquired by mutant strains emerging from the BF.5 variant, suggesting that viral genome analysis in persistent COVID-19 patients may be useful in predicting viral evolution. These results suggest mutations in SARS-CoV-2 are acquired during long-term viral replication rather than in response to antiviral drugs.
Keywords: Genomics; Microbiology and Virology.