KSHV Reprogramming of Host Energy Metabolism for Pathogenesis
Reprogramming of energy metabolism is a key for cancer development. Kaposi’s sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated b...
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| Published in | Frontiers in cellular and infection microbiology Vol. 11; p. 621156 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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12.05.2021
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| Abstract | Reprogramming of energy metabolism is a key for cancer development. Kaposi’s sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated by three pathways of central carbon metabolism, including aerobic glycolysis, glutaminolysis, and fatty acid synthesis. Increasing evidence has shown that KSHV infection can alter central carbon metabolic pathways to produce biomass for viral replication, as well as the survival and proliferation of infected cells. In this review, we summarize recent studies exploring how KSHV manipulates host cell metabolism to promote viral pathogenesis, which provides the potential therapeutic targets and strategies for KSHV-associated cancers. |
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| AbstractList | Reprogramming of energy metabolism is a key for cancer development. Kaposi’s sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated by three pathways of central carbon metabolism, including aerobic glycolysis, glutaminolysis, and fatty acid synthesis. Increasing evidence has shown that KSHV infection can alter central carbon metabolic pathways to produce biomass for viral replication, as well as the survival and proliferation of infected cells. In this review, we summarize recent studies exploring how KSHV manipulates host cell metabolism to promote viral pathogenesis, which provides the potential therapeutic targets and strategies for KSHV-associated cancers. Reprogramming of energy metabolism is a key for cancer development. Kaposi's sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated by three pathways of central carbon metabolism, including aerobic glycolysis, glutaminolysis, and fatty acid synthesis. Increasing evidence has shown that KSHV infection can alter central carbon metabolic pathways to produce biomass for viral replication, as well as the survival and proliferation of infected cells. In this review, we summarize recent studies exploring how KSHV manipulates host cell metabolism to promote viral pathogenesis, which provides the potential therapeutic targets and strategies for KSHV-associated cancers.Reprogramming of energy metabolism is a key for cancer development. Kaposi's sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated by three pathways of central carbon metabolism, including aerobic glycolysis, glutaminolysis, and fatty acid synthesis. Increasing evidence has shown that KSHV infection can alter central carbon metabolic pathways to produce biomass for viral replication, as well as the survival and proliferation of infected cells. In this review, we summarize recent studies exploring how KSHV manipulates host cell metabolism to promote viral pathogenesis, which provides the potential therapeutic targets and strategies for KSHV-associated cancers. |
| Author | Cai, Qiliang Wei, Fang Zhu, Caixia Wang, Yuyan Liu, Xiaoqing |
| AuthorAffiliation | 1 Ministry of Education (MOE) & National Health Committee (NHC) & Chinese Academy of Medical Science (CAMS), Key Laboratory of Medical Molecular Virology, Department of Medical Microbiology and Parasitology, School of Basic Medicine, Shanghai Medical College, Fudan University , Shanghai , China 2 Sheng Yushou Center of Cell Biology and Immunology, School of Life Science and Biotechnology, Shanghai Jiao Tong University , Shanghai , China |
| AuthorAffiliation_xml | – name: 1 Ministry of Education (MOE) & National Health Committee (NHC) & Chinese Academy of Medical Science (CAMS), Key Laboratory of Medical Molecular Virology, Department of Medical Microbiology and Parasitology, School of Basic Medicine, Shanghai Medical College, Fudan University , Shanghai , China – name: 2 Sheng Yushou Center of Cell Biology and Immunology, School of Life Science and Biotechnology, Shanghai Jiao Tong University , Shanghai , China |
| Author_xml | – sequence: 1 givenname: Xiaoqing surname: Liu fullname: Liu, Xiaoqing – sequence: 2 givenname: Caixia surname: Zhu fullname: Zhu, Caixia – sequence: 3 givenname: Yuyan surname: Wang fullname: Wang, Yuyan – sequence: 4 givenname: Fang surname: Wei fullname: Wei, Fang – sequence: 5 givenname: Qiliang surname: Cai fullname: Cai, Qiliang |
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