Virus Infection and Death Receptor-Mediated Apoptosis

doi:10.3390/v9110316

Review

. 2017 Oct 27;9(11):316.

doi: 10.3390/v9110316.

Virus Infection and Death Receptor-Mediated Apoptosis

Xingchen Zhou¹, Wenbo Jiang², Zhongshun Liu³, Shuai Liu⁴, Xiaozhen Liang⁵

Affiliations

¹ Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. xczhou@ips.ac.cn.
² Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. wbjiang@ips.ac.cn.
³ Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. zsliu@ips.ac.cn.
⁴ Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. sliu@ips.ac.cn.
⁵ Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. xzliang@ips.ac.cn.

PMID: 29077026
PMCID: PMC5707523
DOI: 10.3390/v9110316

Review

Virus Infection and Death Receptor-Mediated Apoptosis

Xingchen Zhou et al. Viruses. 2017.

. 2017 Oct 27;9(11):316.

doi: 10.3390/v9110316.

Authors

Xingchen Zhou¹, Wenbo Jiang², Zhongshun Liu³, Shuai Liu⁴, Xiaozhen Liang⁵

Affiliations

¹ Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. xczhou@ips.ac.cn.
² Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. wbjiang@ips.ac.cn.
³ Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. zsliu@ips.ac.cn.
⁴ Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. sliu@ips.ac.cn.
⁵ Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. xzliang@ips.ac.cn.

PMID: 29077026
PMCID: PMC5707523
DOI: 10.3390/v9110316

Abstract

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.

Keywords: death receptor; extrinsic apoptosis; host immune response; virus infection.

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Conflict of interest statement

The authors have no conflicts of interest.

Figures

**Figure 1**
Viral modulation of death-receptor mediated apoptosis. Death receptors Fas, TRAIL-R and TNF-R form DISC upon binding to their ligands, activate caspase cascade and subsequently initiate extrinsic apoptosis. Caspase-8 activation can cleavage BID to tBID and link to mitochondria-mediated intrinsic apoptosis pathway. Virus infection regulates death receptor-mediated extrinsic apoptosis mainly through virally encoded proteins. The regulatory mechanisms involve: (1) regulating the expression and function of death receptors/ligands; (2) interfering DISC formation and function; (3) regulating caspase activities; (4) regulating the expression and function of pro-apoptotic and anti-apoptotic proteins. Black arrow represents signal induction; grey arrow represents signal induced by viruses; grey T bar represents signal inhibited by viruses.

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References

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[1] Danthi P. Viruses and the diversity of cell death. Annu. Rev. Virol. 2016;3:533–553. doi: 10.1146/annurev-virology-110615-042435. - DOI - PubMed

[2] Danthi P. Viruses and the diversity of cell death. Annu. Rev. Virol. 2016;3:533–553. doi: 10.1146/annurev-virology-110615-042435. - DOI - PubMed

[3] Teodoro J.G., Branton P.E. Regulation of apoptosis by viral gene products. J. Virol. 1997;71:1739–1746. - PMC - PubMed

[4] Teodoro J.G., Branton P.E. Regulation of apoptosis by viral gene products. J. Virol. 1997;71:1739–1746. - PMC - PubMed

[5] Galluzzi L., Brenner C., Morselli E., Touat Z., Kroemer G. Viral control of mitochondrial apoptosis. PLoS Pathog. 2008;4:e1000018. doi: 10.1371/journal.ppat.1000018. - DOI - PMC - PubMed

[6] Galluzzi L., Brenner C., Morselli E., Touat Z., Kroemer G. Viral control of mitochondrial apoptosis. PLoS Pathog. 2008;4:e1000018. doi: 10.1371/journal.ppat.1000018. - DOI - PMC - PubMed

[7] Everett H., McFadden G. Apoptosis: An innate immune response to virus infection. Trends Microbiol. 1999;7:160–165. doi: 10.1016/S0966-842X(99)01487-0. - DOI - PubMed

[8] Everett H., McFadden G. Apoptosis: An innate immune response to virus infection. Trends Microbiol. 1999;7:160–165. doi: 10.1016/S0966-842X(99)01487-0. - DOI - PubMed

[9] Shen Y., Shenk T.E. Viruses and apoptosis. Curr. Opin. Genet. Dev. 1995;5:105–111. doi: 10.1016/S0959-437X(95)90061-6. - DOI - PubMed

[10] Shen Y., Shenk T.E. Viruses and apoptosis. Curr. Opin. Genet. Dev. 1995;5:105–111. doi: 10.1016/S0959-437X(95)90061-6. - DOI - PubMed

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Virus Infection and Death Receptor-Mediated Apoptosis

Affiliations

Virus Infection and Death Receptor-Mediated Apoptosis

Authors

Affiliations

Abstract

Conflict of interest statement

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