Programmed Cell Death in SARS-CoV-2 Infection: A Short Review

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the latest variant in the coronavirus family, causing COVID-19, has resulted in global pandemic since early 2020 leading to severe public health concern. So far, the pandemic has caused more than 200 million infections and 4 million deaths worldwide. Most of the studies are focused on developing prevention, intervention, and therapeutic strategies. However, underlying pathophysiology of the disease is important as well, which needs further attention. Cell death is one of the major causative mechanisms that leads to severe inflammation, and it is also an a posteriori consequence of the hyperinflammatory storm that renders poor prognosis of the disease. Substantial cell death has been reported in biopsy samples from post mortem patients. Among the distinct cell death pathways, apoptosis, the regulated programmed cell death plays an important role in the pathogenesis of the disease. Understanding the role of SARS-CoV-2 infection in apoptosis is critical to linearize the pathogenesis of the virus as well as the resultant disease, that may uncover novel therapeutic targets in treatment of COVID-19 patients. Here, we review the current progress on the underlying molecular mechanism(s) of SARS-CoV-2-induced apoptosis, not only at the level of the virus but also at its individual proteins.

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“…The primary network highlighted the fact that cell death, widely acknowledged as an essential and crucial step in disease pathogenesis (Deshpande and Zou, 2021;Li et al, 2022;Tojo, 2023;Yuan et al, 2023) was not present in any of the AOPs, hence in the network. Therefore, the KE "cell death" KE1825 present in the Wiki was added as a new node connecting "increased coronavirus production" (KE1847 from AOP430) to "increased, secretion of proinflammatory mediators (KE 1496 from AOP392).…”