The master antioxidant defense is activated during EBV latent infection
IMPORTANCE: To our knowledge, this is the first report delineating the activation of the master antioxidant defense during EBV latency. We show that EBV-triggered reactive oxygen species production activates the Keap1-NRF2 pathway in EBV-transformed cells, and LMP1 plays a major role in this event, and the stress-related kinase TBK1 is required for NRF2 activation. Moreover, we show that the Keap1-NRF2 pathway is important for cell proliferation and EBV latency maintenance. Our findings disclose how EBV controls the balance between oxidative stress and antioxidant defense, which greatly improve our understanding of EBV latency and pathogenesis and may be leveraged to opportunities toward the improvement of therapeutic outcomes in EBV-associated diseases.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2023 |
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Erschienen: |
2023 |
Enthalten in: |
Zur Gesamtaufnahme - volume:97 |
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Enthalten in: |
Journal of virology - 97(2023), 11 vom: 30. Nov., Seite e0095323 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Wang, Ling [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 06.12.2023 Date Revised 06.12.2023 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1128/jvi.00953-23 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM36369949X |
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245 | 1 | 4 | |a The master antioxidant defense is activated during EBV latent infection |
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500 | |a published: Print-Electronic | ||
500 | |a Citation Status MEDLINE | ||
520 | |a IMPORTANCE: To our knowledge, this is the first report delineating the activation of the master antioxidant defense during EBV latency. We show that EBV-triggered reactive oxygen species production activates the Keap1-NRF2 pathway in EBV-transformed cells, and LMP1 plays a major role in this event, and the stress-related kinase TBK1 is required for NRF2 activation. Moreover, we show that the Keap1-NRF2 pathway is important for cell proliferation and EBV latency maintenance. Our findings disclose how EBV controls the balance between oxidative stress and antioxidant defense, which greatly improve our understanding of EBV latency and pathogenesis and may be leveraged to opportunities toward the improvement of therapeutic outcomes in EBV-associated diseases | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a EBV | |
650 | 4 | |a Keap1 | |
650 | 4 | |a NRF2 | |
650 | 4 | |a antioxidant stress | |
650 | 7 | |a Antioxidants |2 NLM | |
650 | 7 | |a Kelch-Like ECH-Associated Protein 1 |2 NLM | |
650 | 7 | |a NF-E2-Related Factor 2 |2 NLM | |
650 | 7 | |a Reactive Oxygen Species |2 NLM | |
650 | 7 | |a KEAP1 protein, human |2 NLM | |
650 | 7 | |a NFE2L2 protein, human |2 NLM | |
650 | 7 | |a TBK1 protein, human |2 NLM | |
650 | 7 | |a EC 2.7.11.1 |2 NLM | |
650 | 7 | |a EBV-associated membrane antigen, Epstein-Barr virus |2 NLM | |
700 | 1 | |a Howell, Mary E A |e verfasserin |4 aut | |
700 | 1 | |a Hensley, Culton R |e verfasserin |4 aut | |
700 | 1 | |a Ning, Katharine |e verfasserin |4 aut | |
700 | 1 | |a Moorman, Jonathan P |e verfasserin |4 aut | |
700 | 1 | |a Yao, Zhi Q |e verfasserin |4 aut | |
700 | 1 | |a Ning, Shunbin |e verfasserin |4 aut | |
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