Lymphocyte integrins mediate entry and dysregulation of T cells by SARS-CoV-2
Mengwen Huang, Xingchao Pan, Xinling Wang, Qingfei Ren, Bei Tong, Xianchi Dong, Gaoxiang Ge, Lu Lu, Shibo Jiang, Jianfeng Chen
Abstract
T-cell infection by SARS-CoV-2 and associated immune responses are correlated with disease severity and prognosis of COVID-19. Lymphopenia is associated with increased disease severity in COVID-19. Significantly lower circulating T and B cell counts were observed in patients who died from COVID-19 compared with survivors. Moreover, SARS-CoV-2 infection causes aberrant lymphocyte activation and dysfunction. COVID-19 patients displayed hyperactivated T cells which are prone to apoptosis and dysregulated cytokine responses. 1 Some evidence suggests the infection of lymphocytes by SARS-CoV-2, including colocalization of SARS-CoV-2 spike (S) protein and lymphocytes in lung tissues of COVID-19 patients and strands of SARS-CoV-2 sub-genomes in immune cells from bronchoalveolar lavage fluid (BALF) and sputum samples of severe COVID-19 patients. 2 Angiotensin-converting enzyme 2 (ACE2) and some other reported S protein receptors are barely expressed in lymphocytes. Some recent studies suggest that integrins may act as SARS-CoV-2 receptors, shedding light on the dysregulation of lymphocyte functions by SARS-CoV-2. However, a clear-cut mechanism underlying the crosstalk between SARS-CoV-2 and lymphocyte integrins remains elusive.