Coronavirus (SARS-CoV-2) Infection and Pathogenicity: The Roles of Cell Death and Autophagy

Abstract

SARS-CoV-2, also known as COVID-19 (coronavirus disease 2019), is a serious threat to public health, the global economy, and society at large. In addition to inducing immunological and inflammatory reactions, viral infections also lead to programmed cell death in infected cells, which is essential for preserving regular cell function. Several cell death pathways have been better characterized over the last few decades. It is widely accepted that both cell autophagy and death are critical for preserving host homeostasis and playing a role in the etiology of illness. Viruses may employ a range of strategies to precisely regulate cell death. There is growing evidence that suggests the nature of these mechanisms during virus infection is dualistic. On the one hand, the virus is stopped from multiplying and spreading by killing off infected cells. On the other hand, dysregulated cell death leads to abnormal immune response and unmanageable cell damage. Meanwhile, viruses can employ cell autophagy to their advantage for immune evasion, extracellular release, and replication. Although the relationship between SARS-CoV-2, cell death, and cell autophagy is not fully understood, but previous research on SARS-CoV and MERS-CoV can provide some conclusions. Proper study of pathology and underlying mechanisms is crucial for developing effective preventative and treatment plans for this dangerous illness.