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Mitochondrial protein, TBRG4, modulates KSHV and EBV reactivation from latency

Zhang, Huirong ; Wong, Jason P ; Ni, Guoxin ; Cano, Patricio ; Dittmer, Dirk P ; Damania, Blossom Zhu, Fanxiu

PLoS pathogens, 2022-11, Vol.18 (11), p.e1010990-e1010990 [Periódico revisado por pares]

United States: Public Library of Science

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Título:
Mitochondrial protein, TBRG4, modulates KSHV and EBV reactivation from latency
Autor: Zhang, Huirong ; Wong, Jason P ; Ni, Guoxin ; Cano, Patricio ; Dittmer, Dirk P ; Damania, Blossom
Zhu, Fanxiu
Assuntos: Biology and Life Sciences ; Epstein-Barr virus ; Gene expression ; Genetic aspects ; Herpesvirus 4, Human - physiology ; Herpesvirus 8, Human - physiology ; Human herpesvirus 8 ; Humans ; Medicine and Health Sciences ; Mitochondria ; Mitochondrial Proteins - metabolism ; Physiological aspects ; Reactive Oxygen Species - metabolism ; Research and Analysis Methods ; RNA-Binding Proteins - metabolism ; Viral proteins ; Virus activation ; Virus Latency ; Virus research
É parte de: PLoS pathogens, 2022-11, Vol.18 (11), p.e1010990-e1010990
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SourceType-Scholarly Journals-1
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The authors have declared that no competing interests exist.
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Descrição: Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr (EBV) are gammaherpesviruses associated with multiple human malignancies. KSHV is the etiological agent of Kaposi's Sarcoma, primary effusion lymphoma (PEL) and multicentric Castleman's disease (MCD). EBV is associated with Burkitt's lymphoma (BL), Hodgkin's lymphoma (HL), nasopharyngeal carcinoma (NPC) and gastric carcinoma (GC). KSHV and EBV establish life-long latency in the human host with intermittent periods of lytic reactivation. Here, we identified a cellular factor named transforming growth factor-beta regulator 4 (TBRG4) that plays a role in the gammaherpesvirus lifecycle. We find that TBRG4, a protein that is localized to the mitochondria, can regulate lytic reactivation from latency of both KSHV and EBV. Knockdown of TBRG4 in cells latently infected with KSHV or EBV induced viral lytic gene transcription and replication. TBRG4 deficiency causes mitochondrial stress and increases reactive oxygen species (ROS) production. Treatment with a ROS scavenger decreased viral reactivation from latency in TBRG4-depleted cells. These data suggest that TBRG4 serves as a cellular repressor of KSHV and EBV reactivation through the regulation of ROS production.
Editor: United States: Public Library of Science
Idioma: Inglês

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Mitochondrial protein, TBRG4, modulates KSHV and EBV reactivation from latency

Zhang, Huirong ; Wong, Jason P ; Ni, Guoxin ; Cano, Patricio ; Dittmer, Dirk P ; Damania, Blossom Zhu, Fanxiu

United States: Public Library of Science

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