Human Coronavirus: Host-Pathogen Interaction.

Abstract	Human coronavirus (HCoV) infection causes respiratory diseases with mild to severe outcomes. In the last 15 years, we have witnessed the emergence of two zoonotic, highly pathogenic HCoVs: severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). Replication of HCoV is regulated by a diversity of host factors and induces drastic alterations in cellular structure and physiology. Activation of critical signaling pathways during HCoV infection modulates the induction of antiviral immune response and contributes to the pathogenesis of HCoV. Recent studies have begun to reveal some fundamental aspects of the intricate HCoV-host interaction in mechanistic detail. In this review, we summarize the current knowledge of host factors co-opted and signaling pathways activated during HCoV infection, with an emphasis on HCoV-infection-induced stress response, autophagy, apoptosis, and innate immunity. The cross talk among these pathways, as well as the modulatory strategies utilized by HCoV, is also discussed.
Authors	To Sing Fung, Ding Xiang Liu
Journal	Annual review of microbiology (Annu Rev Microbiol) Vol. 73 Pg. 529-557 (09 08 2019) ISSN: 1545-3251 [Electronic] United States
PMID	31226023 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References	Membrane Proteins Viral Proteins Glutamyl Aminopeptidase Dipeptidyl Peptidase 4 Peptidyl-Dipeptidase A
Topics	Animals Apoptosis Autophagy Chiroptera (virology) Coronavirus (genetics, growth & development, immunology, metabolism) Coronavirus Infections (immunology, pathology) Dipeptidyl Peptidase 4 (genetics, metabolism) Endoplasmic Reticulum Stress Genome, Viral Glutamyl Aminopeptidase (genetics, metabolism) Host-Pathogen Interactions (immunology) Humans Immunity, Innate Membrane Proteins (genetics, metabolism) Middle East Respiratory Syndrome Coronavirus (genetics, growth & development, immunology, metabolism) Peptidyl-Dipeptidase A (genetics, metabolism) Severe acute respiratory syndrome-related coronavirus (genetics, growth & development, immunology, metabolism) Signal Transduction Viral Proteins (genetics, metabolism) Virus Internalization Virus Replication Zoonoses

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