s regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among