The lymphopenia as a major immunological abnormality occurs in the majority of severe COVID‐19 patients, which is strongly associated with mortality rate. A low proportion of lymphocytes may express the main receptor for SARS‐CoV‐2, called angiotensin‐converting enzyme 2 (ACE2). Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) can also use ACE2‐independent pathways to enter lymphocytes. Both SARS‐CoV‐2‐ and immune‐mediated mechanisms may contribute to the occurrence of lymphopenia through influencing the lymphocyte production, survival or tissue re‐distribution. The metabolic and biochemical changes can also affect the production and survival of lymphocytes in COVID‐19 patients. Lymphopenia can cause general immunosuppression and promote cytokine storm, both of them play an important role in the viral persistence, viral replication, multi‐organ failure and eventually death. Here, a comprehensive view concerning the possible mechanisms that may lead to the lymphocyte reduction in COVID‐19 patients is provided, while highlighting the potential intervention approaches to prevent lymphopenia.

中文翻译：

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淋巴细胞减少症是COVID-19患者重要的免疫学异常：可能的机制

淋巴细胞减少是主要的免疫学异常，在大多数重症COVID-19患者中均发生，这与死亡率密切相关。低比例的淋巴细胞可能表达SARS-CoV-2的主要受体，称为血管紧张素转换酶2（ACE2）。严重的急性呼吸系统综合症冠状病毒2（SARS-CoV-2）也可以使用ACE2独立的途径进入淋巴细胞。SARS-CoV-2和免疫介导的机制都可能通过影响淋巴细胞的产生，存活或组织的重新分布而导致淋巴细胞减少。代谢和生化变化也会影响COVID-19患者的淋巴细胞产生和存活。淋巴细胞减少症可引起全身性免疫抑制并促进细胞因子风暴，两者在病毒持久性，病毒复制，多器官衰竭，最终死亡。在此，提供了有关可能导致COVID-19患者淋巴细胞减少的可能机制的全面观点，同时强调了预防淋巴细胞减少的潜在干预方法。