Host-pathogen interaction of human coronaviruses - apoptosis (WP4864)
Homo sapiens
This pathway describes the induction and modulation of the apoptosis system during human coronavirus infection. The information is based on the review of Fung and Liu [10.1146/annurev-micro-020518-115759]. Apoptosis is a highly controlled form of cell death that can be initiated by several internal (DNA damage) and external factors (T-cell death signal). There are some indications that induction of apoptosis in immune cells contribute to the suppression of the host immune system in some human coronavirus infections [10.1128/JVI.00269-12]. SARS-CoV induces caspase-dependent apoptosis by interfering with prosurvival BCL proteins (BCL2, BCL2L1, MCL1) and AKT1 and uses the apoptosis induced cell deconstruction it for replication, although it seems not to be depending on this mechanism for replication [10.1016/j.virusres.2014.09.016].
Authors
Friederike Ehrhart , Alex Pico , Egon Willighagen , Nhung Pham , and Eric WeitzActivity
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Organisms
Homo sapiensCommunities
COVID-19Annotations
Pathway Ontology
disease pathway apoptotic cell death pathwayDisease Ontology
severe acute respiratory syndrome viral infectious diseaseReferences
- Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Li H, Zhu H, Xu CJ, Yuan J. Cell. 1998 Aug 21;94(4):491–501. PubMed Europe PMC Scholia
- Human Coronavirus: Host-Pathogen Interaction. Fung TS, Liu DX. Annu Rev Microbiol. 2019 Sep 8;73:529–57. PubMed Europe PMC Scholia