Programmed cell death: the battlefield between the host and alpha-herpesviruses and a potential avenue for cancer treatment
Metrics: PDF 1474 views | HTML 2102 views | ?
Chuankuo Zhao1,2,3,*, Mingshu Wang1,2,3,*, Anchun Cheng1,2,3, Qiao Yang1,2,3, Ying Wu1,2,3, Dekang Zhu2,3, Shun Chen1,2,3, Mafeng Liu1,2,3, XinXin Zhao1,2,3, Renyong Jia1,2,3, Kunfeng Sun1,2,3 and Xiaoyue Chen2,3
1Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu City 611130, Sichuan, P.R. China
2Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Wenjiang, Chengdu City 611130, Sichuan, P.R. China
3Avian Disease Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu City 611130, Sichuan, P.R. China
*These authors have contributed equally to this study and should be listed as first authors
Anchun Cheng, email: email@example.com
Mingshu Wang, email: firstname.lastname@example.org
Keywords: alpha-herpesviruses; apoptosis; autophagy; necroptosis; cancer treatment
Received: November 06, 2017 Accepted: May 24, 2018 Published: July 17, 2018
Programed cell death is an antiviral mechanism by which the host limits viral replication and protects uninfected cells. Many viruses encode proteins resistant to programed cell death to escape the host immune defenses, which indicates that programed cell death is more favorable for the host immune defense. Alpha-herpesviruses are pathogens that widely affect the health of humans and animals in different communities worldwide. Alpha-herpesviruses can induce apoptosis, autophagy and necroptosis through different molecular mechanisms. This review concisely illustrates the different pathways of apoptosis, autophagy, and necroptosis induced by alpha-herpesviruses. These pathways influence viral infection and replication and are a potential avenue for cancer treatment. This review will increase our understanding of the role of programed cell death in the host immune defense and provides new possibilities for cancer treatment.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.