2. Academic Validation
  3. ACE2-independent infection of T lymphocytes by SARS-CoV-2

ACE2-independent infection of T lymphocytes by SARS-CoV-2

  • Signal Transduct Target Ther. 2022 Mar 11;7(1):83. doi: 10.1038/s41392-022-00919-x.
Xu-Rui Shen  # 1 2,  Rong Geng  # 1 2,  Qian Li  # 1 2,  Ying Chen  # 1 2,  Shu-Fen Li  # 1,  Qi Wang 1 2,  Juan Min 1,  Yong Yang 1 2,  Bei Li 1,  Ren-Di Jiang 1,  Xi Wang 1 2,  Xiao-Shuang Zheng 1 2,  Yan Zhu 1,  Jing-Kun Jia 1 2,  Xing-Lou Yang 1,  Mei-Qin Liu 1 2,  Qian-Chun Gong 3 4,  Yu-Lan Zhang 1,  Zhen-Qiong Guan 1,  Hui-Ling Li 1 2,  Zhen-Hua Zheng 1,  Zheng-Li Shi 1,  Hui-Lan Zhang 5,  Ke Peng 1 2,  Peng Zhou 6 7
Affiliations

Affiliations

  • 1 CAS Key Laboratory of Special Pathogens & State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, People's Republic of China.
  • 2 University of Chinese Academy of Sciences, Beijing, People's Republic of China.
  • 3 State Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, 200438, Shanghai, China.
  • 4 Center for Organoid and Regenerative Medicine, Greater Bay Area Institute of Precision Medicine (Guangzhou), 511462, Guangzhou, China.
  • 5 Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jie Fang Road, Han Kou District, 430030, Wuhan, China. huilanz_76@163.com.
  • 6 CAS Key Laboratory of Special Pathogens & State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, People's Republic of China. peng.zhou@wh.iov.cn.
  • 7 University of Chinese Academy of Sciences, Beijing, People's Republic of China. peng.zhou@wh.iov.cn.
  • # Contributed equally.
PMID: 35277473 DOI: 10.1038/s41392-022-00919-x
Abstract

SARS-CoV-2 induced marked lymphopenia in severe patients with COVID-19. However, whether lymphocytes are targets of viral Infection is yet to be determined, although SARS-CoV-2 RNA or antigen has been identified in T cells from patients. Here, we confirmed that SARS-CoV-2 viral antigen could be detected in patient peripheral blood cells (PBCs) or postmortem lung T cells, and the infectious virus could also be detected from viral antigen-positive PBCs. We next prove that SARS-CoV-2 infects T lymphocytes, preferably activated CD4 + T cells in vitro. Upon Infection, viral RNA, subgenomic RNA, viral protein or viral particle can be detected in the T cells. Furthermore, we show that the Infection is spike-ACE2/TMPRSS2-independent through using ACE2 knockdown or receptor blocking experiments. Next, we demonstrate that viral antigen-positive T cells from patient undergone pronounced Apoptosis. In vitro Infection of T cells induced cell death that is likely in mitochondria ROS-HIF-1a-dependent pathways. Finally, we demonstrated that LFA-1, the protein exclusively expresses in multiple leukocytes, is more likely the entry molecule that mediated SARS-CoV-2 Infection in T cells, compared to a list of other known receptors. Collectively, this work confirmed a SARS-CoV-2 Infection of T cells, in a spike-ACE2-independent manner, which shed novel insights into the underlying mechanisms of SARS-CoV-2-induced lymphopenia in COVID-19 patients.

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