2020 Moon Fighting COVID-19 exhausts T cells Lymphopenia is seen in severe cases of COVID-19, but the functional state of T cells in these patients is not known. Based on the retrospective study of 522 patients with COVID-19 and 40 healthy controls from Wuhan, China, this preprint study found that the age-dependent and clinical severity-dependent reduction in T cell numbers inversely correlates with serum levels of TNF, IL-6 and IL-10. The expression of T cell exhaustion markers (PD1 and TIM3) was assessed in peripheral blood cells from 14 patients with COVID-19 and 3 controls. CD8+ T cells from patients in intensive care units (ICUs) showed increased expression of PD1 compared with patients not in ICUs and healthy controls. This suggests that as disease severity progresses in patients with COVID-19, a concomitant rise in inflammatory cytokine levels may drive the depletion and exhaustion of T cell populations. 2020 Wang SARS-CoV-2 infects T lymphocytes through its spike protein-mediated membrane fusion COVID-19, the novel coronavirus disease caused by SARS-CoV-2 and outbroken at the end of 2019 in Wuhan, China,1 becomes a worldwide pandemic. SARS-CoV-2 belongs to the betacoronavirus genus and has 79.5% identity to SARS-CoV. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) as its host entry receptor.2 The clinical manifestations of COVID-19 include pneumonia, diarrhea, dyspnea, and multiple organ failure. Interestingly, lymphocytopenia, as a diagnostic indicator, is common in COVID-19 patients. Xiong et al. found upregulation of apoptosis, autophagy, and p53 pathways in PBMC of COVID-19 patients.3 Some studies reported that lymphocytopenia might be related to mortality, especially in patients with low levels of CD3+, CD4+, and CD8+ T lymphocytes.4,5 Lymphocytopenia was also found in the Middle East respiratory syndrome (MERS) cases. MERS-CoV can directly infect human primary T lymphocytes and induce T-cell apoptosis through extrinsic and intrinsic apoptosis pathways, but it cannot replicate in T lymphocytes.6 However, it is unclear whether SARS-CoV-2 can also infect T cells, resulting in lymphocytopenia.

2020 Shi COVID-19 infection: the perspectives on immune responses More than 100 years since the outbreak of the 1918 influenza pandemic, we now seem to face another pandemic. The outbreak of the new coronavirus (SARS-CoV-2) infection is spreading to every continent, forcing us to live with this virus for perhaps a long time. Scientists and clinicians have learned much of coronavirus disease 2019, COVID-19, and its pathogenesis [1]: not all people exposed to SARS-CoV-2 are infected and not all infected patients develop severe respiratory illness. Accordingly, SARS-CoV-2 infection can be roughly divided into three stages: stage I, an asymptomatic incubation period with or without detectable virus; stage II, non-severe symptomatic period with the presence of virus; stage III, severe respiratory symptomatic stage with high viral load [2]. From the point of view of prevention, individuals at stage I, the stealth carriers, are the least manageable because, at least on some occasions, they spread the virus unknowingly: indeed, the first asymptomatic transmission has been reported in Germany [3]. The role of asymptomatic SARS-CoV-2 infected individuals in disseminating the infection remains to be defined.