tetano
Editor, Senior Moderator
Signal Transduct Target Ther
. 2023 Sep 20;8(1):357.
doi: 10.1038/s41392-023-01580-8. The role of cell death in SARS-CoV-2 infection
Cui Yuan[SUP] #[/SUP][SUP] 1 [/SUP], Zhenling Ma[SUP] #[/SUP][SUP] 1 [/SUP], Jiufeng Xie[SUP] 1 [/SUP], Wenqing Li[SUP] 1 [/SUP], Lijuan Su[SUP] 1 [/SUP], Guozhi Zhang[SUP] 1 [/SUP], Jun Xu[SUP] 1 [/SUP], Yaru Wu[SUP] 1 [/SUP], Min Zhang[SUP] 2 [/SUP], Wei Liu[SUP] 3 [/SUP]
Affiliations
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), showing high infectiousness, resulted in an ongoing pandemic termed coronavirus disease 2019 (COVID-19). COVID-19 cases often experience acute respiratory distress syndrome, which has caused millions of deaths. Apart from triggering inflammatory and immune responses, many viral infections can cause programmed cell death in infected cells. Cell death mechanisms have a vital role in maintaining a suitable environment to achieve normal cell functionality. Nonetheless, these processes are dysregulated, potentially contributing to disease pathogenesis. Over the past decades, multiple cell death pathways are becoming better understood. Growing evidence suggests that the induction of cell death by the coronavirus may significantly contributes to viral infection and pathogenicity. However, the interaction of SARS-CoV-2 with cell death, together with its associated mechanisms, is yet to be elucidated. In this review, we summarize the existing evidence concerning the molecular modulation of cell death in SARS-CoV-2 infection as well as viral-host interactions, which may shed new light on antiviral therapy against SARS-CoV-2.
. 2023 Sep 20;8(1):357.
doi: 10.1038/s41392-023-01580-8. The role of cell death in SARS-CoV-2 infection
Cui Yuan[SUP] #[/SUP][SUP] 1 [/SUP], Zhenling Ma[SUP] #[/SUP][SUP] 1 [/SUP], Jiufeng Xie[SUP] 1 [/SUP], Wenqing Li[SUP] 1 [/SUP], Lijuan Su[SUP] 1 [/SUP], Guozhi Zhang[SUP] 1 [/SUP], Jun Xu[SUP] 1 [/SUP], Yaru Wu[SUP] 1 [/SUP], Min Zhang[SUP] 2 [/SUP], Wei Liu[SUP] 3 [/SUP]
Affiliations
- PMID: 37726282
- DOI: 10.1038/s41392-023-01580-8
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), showing high infectiousness, resulted in an ongoing pandemic termed coronavirus disease 2019 (COVID-19). COVID-19 cases often experience acute respiratory distress syndrome, which has caused millions of deaths. Apart from triggering inflammatory and immune responses, many viral infections can cause programmed cell death in infected cells. Cell death mechanisms have a vital role in maintaining a suitable environment to achieve normal cell functionality. Nonetheless, these processes are dysregulated, potentially contributing to disease pathogenesis. Over the past decades, multiple cell death pathways are becoming better understood. Growing evidence suggests that the induction of cell death by the coronavirus may significantly contributes to viral infection and pathogenicity. However, the interaction of SARS-CoV-2 with cell death, together with its associated mechanisms, is yet to be elucidated. In this review, we summarize the existing evidence concerning the molecular modulation of cell death in SARS-CoV-2 infection as well as viral-host interactions, which may shed new light on antiviral therapy against SARS-CoV-2.