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Virus Infection and Death Receptor-Mediated Apoptosis

Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Viruses 2017, 9(11), 316; https://doi.org/10.3390/v9110316
Received: 21 September 2017 / Revised: 23 October 2017 / Accepted: 25 October 2017 / Published: 27 October 2017
(This article belongs to the Special Issue Viral Infection and Apoptosis)
Virus infection can trigger extrinsic apoptosis. Cell-surface death receptors of the tumor necrosis factor family mediate this process. They either assist persistent viral infection or elicit the elimination of infected cells by the host. Death receptor-mediated apoptosis plays an important role in viral pathogenesis and the host antiviral response. Many viruses have acquired the capability to subvert death receptor-mediated apoptosis and evade the host immune response, mainly by virally encoded gene products that suppress death receptor-mediated apoptosis. In this review, we summarize the current information on virus infection and death receptor-mediated apoptosis, particularly focusing on the viral proteins that modulate death receptor-mediated apoptosis. View Full-Text
Keywords: virus infection; death receptor; extrinsic apoptosis; host immune response virus infection; death receptor; extrinsic apoptosis; host immune response
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MDPI and ACS Style

Zhou, X.; Jiang, W.; Liu, Z.; Liu, S.; Liang, X. Virus Infection and Death Receptor-Mediated Apoptosis. Viruses 2017, 9, 316. https://doi.org/10.3390/v9110316

AMA Style

Zhou X, Jiang W, Liu Z, Liu S, Liang X. Virus Infection and Death Receptor-Mediated Apoptosis. Viruses. 2017; 9(11):316. https://doi.org/10.3390/v9110316

Chicago/Turabian Style

Zhou, Xingchen, Wenbo Jiang, Zhongshun Liu, Shuai Liu, and Xiaozhen Liang. 2017. "Virus Infection and Death Receptor-Mediated Apoptosis" Viruses 9, no. 11: 316. https://doi.org/10.3390/v9110316

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