Abstract

Apoptosis is a form of programmed cell death, which maintains cellular homeostasis by eliminating pathogen-infected cells. It contains three signaling pathways: death receptor pathway, mitochondria-mediated pathway, and endoplasmic reticulum pathway. Its importance in host defenses is highlighted by the observation that many viruses evade, hinder or destroy apoptosis, thereby weakening the host’s immune response. Flaviviruses such as Dengue virus, Japanese encephalitis virus, and West Nile virus utilize various strategies to activate or inhibit cell apoptosis. This article reviews the research progress of apoptosis mechanism during flaviviruses infection, including flaviviruses proteins and subgenomic flaviviral RNA to regulate apoptosis by interacting with host proteins, as well as various signaling pathways involved in flaviviruses-induced apoptosis, which provides a scientific basis for understanding the pathogenesis of flaviviruses and helps in developing an effective antiviral therapy.

Highlights

  • Reviewed by: Penghua Wang, University of Connecticut Health Center, United States Philippe Desprès, Université de la Réunion, France Mukesh Kumar, Georgia State University, United States

  • We focus on reviewing the roles played by flavivirus in the regulation of cell apoptosis, and understanding the mechanism of flavivirus regulating apoptosis will be helpful for future research

  • Zika virus (ZIKV) infection is related to pro-inflammatory cytokine expression and apoptosis in placental explants, we propose that human placental explants can be used as a model for studying ZIKV infection in vitro (Ribeiro et al, 2018)

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Summary

Introduction

Reviewed by: Penghua Wang, University of Connecticut Health Center, United States Philippe Desprès, Université de la Réunion, France Mukesh Kumar, Georgia State University, United States. Another study found that accumulation of DENV1 viral protein in the ER, rather than the release of virus, can induce ER stress and activate the apoptosis pathway.

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