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The putative mechanism of lymphopenia in COVID-19 patients
Xinling Wang1 , Zezhong Liu1 , Lu Lu1 , Shibo Jiang1,2,*
1Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Institute of Infectious Disease and Biosecurity, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China
2Department of Infectious Diseases and Shenzhen Key Lab of Endogenous Infection, Shenzhen Nanshan People’s Hospital and the Sixth Affiliated Hospital of Guangdong Medical University, Shenzhen 518052, China
*Correspondence to:Shibo Jiang , Email:shibojiang@fudan.edu.cn
J Mol Cell Biol, Volume 14, Issue 5, May 2022, mjac034,  https://doi.org/10.1093/jmcb/mjac034

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its variants have caused >500 million confirmed cases and >6 million deaths. Apart from the common clinical manifestations, 63% of admitted coronavirus disease 2019 (COVID-19) patients had lymphopenia, increasing to 85% in patients with severe disease (Huang et al., 2020). It has been reported that several genes representing the p53-mediated apoptosis signaling pathway are upregulated in peripheral blood mononuclear cells (PBMCs) of COVID-19 patients (Xiong et al., 2020). Moreover, SARS-CoV-2 RNA is detected in most immune cells, including T and B lymphocytes and NK cells (Ren et al., 2021). Therefore, unraveling the mechanism of lymphopenia in COVID-19 patients depends on whether SARS-CoV-2 directly infects immune cells to induce cell death.


Volume 14, Issue 5
May 2022