SARS-CoV-2 ORF7a Mutation Found in BF.5 and BF.7 Sublineages Impacts Its Functions
A feature of the SARS-CoV-2 Omicron subvariants BF.5 and BF.7 that recently circulated mainly in China and Japan was the high prevalence of the ORF7a: H47Y mutation, in which the 47th residue of ORF7a has been mutated from a histidine (H) to a tyrosine (Y). Here, we evaluated the effect of this mutation on the three main functions ascribed to the SARS-CoV-2 ORF7a protein. Our findings show that H47Y mutation impairs the ability of SARS-CoV-2 ORF7a to antagonize the type I interferon (IFN-I) response and to downregulate major histocompatibility complex I (MHC-I) cell surface levels, but had no effect in its anti-SERINC5 function. Overall, our results suggest that the H47Y mutation of ORF7a affects important functions of this protein, resulting in changes in virus pathogenesis.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:25 |
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| Enthalten in: |
International journal of molecular sciences - 25(2024), 4 vom: 16. Feb. |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Timilsina, Uddhav [VerfasserIn] |
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| Links: |
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| Themen: |
Interferon Type I |
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| Anmerkungen: |
Date Completed 26.02.2024 Date Revised 06.04.2024 published: Electronic Citation Status MEDLINE |
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| doi: |
10.3390/ijms25042351 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM368870103 |
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| 100 | 1 | |a Timilsina, Uddhav |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a SARS-CoV-2 ORF7a Mutation Found in BF.5 and BF.7 Sublineages Impacts Its Functions |
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| 500 | |a Date Revised 06.04.2024 | ||
| 500 | |a published: Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a A feature of the SARS-CoV-2 Omicron subvariants BF.5 and BF.7 that recently circulated mainly in China and Japan was the high prevalence of the ORF7a: H47Y mutation, in which the 47th residue of ORF7a has been mutated from a histidine (H) to a tyrosine (Y). Here, we evaluated the effect of this mutation on the three main functions ascribed to the SARS-CoV-2 ORF7a protein. Our findings show that H47Y mutation impairs the ability of SARS-CoV-2 ORF7a to antagonize the type I interferon (IFN-I) response and to downregulate major histocompatibility complex I (MHC-I) cell surface levels, but had no effect in its anti-SERINC5 function. Overall, our results suggest that the H47Y mutation of ORF7a affects important functions of this protein, resulting in changes in virus pathogenesis | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a major histocompatibility complex I | |
| 650 | 4 | |a mutation | |
| 650 | 4 | |a open reading frame 7a (ORF7a) | |
| 650 | 4 | |a severe acute respiratory syndrome coronavirus 2 | |
| 650 | 4 | |a type I interferon response | |
| 650 | 7 | |a Interferon Type I |2 NLM | |
| 700 | 1 | |a Ivey, Emily B |e verfasserin |4 aut | |
| 700 | 1 | |a Duffy, Sean |e verfasserin |4 aut | |
| 700 | 1 | |a Plianchaisuk, Arnon |e verfasserin |4 aut | |
| 700 | 1 | |a The Genotype To Phenotype Japan G P-Japan Consortium |e verfasserin |4 aut | |
| 700 | 1 | |a Ito, Jumpei |e verfasserin |4 aut | |
| 700 | 1 | |a Sato, Kei |e verfasserin |4 aut | |
| 700 | 1 | |a Stavrou, Spyridon |e verfasserin |4 aut | |
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