TY - JOUR

T1 - The role of death domain proteins in host response upon SARS-CoV-2 infection

T2 - modulation of programmed cell death and translational applications

AU - Ivanisenko, Nikita V.

AU - Seyrek, Kamil

AU - Kolchanov, Nikolay A.

AU - Ivanisenko, Vladimir A.

AU - Lavrik, Inna N.

N1 - © The Author(s) 2020.

PY - 2020/12/1

Y1 - 2020/12/1

N2 - The current pandemic of novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) poses a significant global public health threat. While urgent regulatory measures in control of the rapid spread of this virus are essential, scientists around the world have quickly engaged in this battle by studying the molecular mechanisms and searching for effective therapeutic strategies against this deadly disease. At present, the exact mechanisms of programmed cell death upon SARS-CoV-2 infection remain to be elucidated, though there is increasing evidence suggesting that cell death pathways play a key role in SARS-CoV-2 infection. There are several types of programmed cell death, including apoptosis, pyroptosis, and necroptosis. These distinct programs are largely controlled by the proteins of the death domain (DD) superfamily, which play an important role in viral pathogenesis and host antiviral response. Many viruses have acquired the capability to subvert the program of cell death and evade the host immune response, mainly by virally encoded gene products that control cell signaling networks. In this mini-review, we will focus on SARS-CoV-2, and discuss the implication of restraining the DD-mediated signaling network to potentially suppress viral replication and reduce tissue damage.

AB - The current pandemic of novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) poses a significant global public health threat. While urgent regulatory measures in control of the rapid spread of this virus are essential, scientists around the world have quickly engaged in this battle by studying the molecular mechanisms and searching for effective therapeutic strategies against this deadly disease. At present, the exact mechanisms of programmed cell death upon SARS-CoV-2 infection remain to be elucidated, though there is increasing evidence suggesting that cell death pathways play a key role in SARS-CoV-2 infection. There are several types of programmed cell death, including apoptosis, pyroptosis, and necroptosis. These distinct programs are largely controlled by the proteins of the death domain (DD) superfamily, which play an important role in viral pathogenesis and host antiviral response. Many viruses have acquired the capability to subvert the program of cell death and evade the host immune response, mainly by virally encoded gene products that control cell signaling networks. In this mini-review, we will focus on SARS-CoV-2, and discuss the implication of restraining the DD-mediated signaling network to potentially suppress viral replication and reduce tissue damage.

KW - CORONAVIRUS-E PROTEIN

KW - APOPTOSIS

KW - CASPASE-8

KW - COMPLEX

KW - REVEALS

KW - INFLAMMASOME

KW - FLICE

KW - NECROPTOSIS

KW - RIPOPTOSOME

KW - ACTIVATION

UR - http://www.scopus.com/inward/record.url?scp=85092420538&partnerID=8YFLogxK

U2 - 10.1038/s41420-020-00331-w

DO - 10.1038/s41420-020-00331-w

M3 - Review article

C2 - 33072409

AN - SCOPUS:85092420538

VL - 6

JO - Cell Death Discovery

JF - Cell Death Discovery

SN - 2058-7716

IS - 1

M1 - 101

ER -