Reactome | Severe acute respiratory syndrome coronavirus type 1 (SARS-C...

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created	[InstanceEdit:9704665] Shamovsky, Veronica, 2020-10-10
dbId	9704656
displayName	Severe acute respiratory syndrome coronavirus type 1 (SARS-C...
literatureReference	[LiteratureReference:9704670] Bcl-xL inhibits T-cell apoptosis induced by expression of SARS coronavirus E protein in the absence of growth factors [LiteratureReference:9704674] Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19) [LiteratureReference:9704654] T cell responses in patients with COVID-19
modified	[InstanceEdit:9713615] Shamovsky, Veronica, 2021-01-27
schemaClass	Summation
text	Severe acute respiratory syndrome coronavirus type 1 (SARS-CoV-1) E protein induced apoptosis upon expression in the human Jurkat T-cells in the absence of growth factors (Yang Y et al. 2005). Overexpressed anti-apoptotic Bcl-2-like protein 1 (BCL2L1, also known as BCLX, Bcl-xL) inhibited T-cell apoptosis induced by SARS-CoV-1. BCL2L1 was found to interact with the viral E protein via the BH3 domain of BCL2L1 and a BH3-like domain of E protein. SARS-CoV-1 E protein is thought to induce apoptosis by sequestering anti-apoptotic BCL2L1 to membranes of the endoplasmic reticulum (ER) and Golgi, where the viral E protein is located (Yang Y et al. 2005). High levels of expression of pro?apoptotic molecules may contribute to the depletion of T lymphocytes by apoptosis, leading to the lymphopenia observed in severely affected SARS patients (Diao B et al. 2020; Chen Z & Wherry EJ 2020).

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