Transcriptome Analysis of Peripheral Blood Mononuclear Cells Reveals Distinct Immune Response in Asymptomatic and Re-Detectable Positive COVID-19 Patients.

The existence of asymptomatic and re-detectable positive coronavirus disease 2019 (COVID-19) patients presents the disease control challenges of COVID-19. Most studies on immune responses in COVID-19 have focused on moderately or severely symptomatic patients; however, little is known about the immune response in asymptomatic and re-detectable positive (RP) patients. Here we performed a comprehensive analysis of the transcriptomic profiles of peripheral blood mononuclear cells (PBMCs) from 48 COVID-19 patients which included 8 asymptomatic, 13 symptomatic, 15 recovered and 12 RP patients. The weighted gene co-expression network analysis (WGCNA) identified six co-expression modules, of which the turquoise module was positively correlated with the asymptomatic, symptomatic, and recovered COVID-19 patients. The red module positively correlated with symptomatic patients only and the blue and brown modules positively correlated with the RP patients. The analysis by single sample gene set enrichment analysis (ssGSEA) revealed a lower level of IFN response and complement activation in the asymptomatic patients compared with the symptomatic, indicating a weaker immune response of the PBMCs in the asymptomatic patients. In addition, gene set enrichment analysis (GSEA) analysis showed the enrichment of TNFα/NF-κB and influenza infection in the RP patients compared with the recovered patients, indicating a hyper-inflammatory immune response in the PBMC of RP patients. Thus our findings could extend our understanding of host immune response during the progression of COVID-19 disease and assist clinical management and the immunotherapy development for COVID-19.

COVID-19-associated liver injury: from bedside to bench.

The outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been a global challenge since December 2019. Although most patients with COVID-19 exhibit mild clinical manifestations, in approximately 5% of these patients, the disease eventually progresses to severe lung injury or even multiorgan dysfunction. This situation represents various challenges to hepatology. In the context of liver injury in patients with COVID-19, several key problems need to be solved. For instance, it is important to determine whether SARS-CoV-2 can directly invade liver, especially when ACE2 appears to be negligibly expressed on hepatocytes. In addition, the mechanisms underlying liver dysfunction in COVID-19 patients are not fully understood, which are likely multifactorial and related to hyperinflammation, dysregulated immune responses, abnormal coagulation and drugs. Here, we systematically describe the potential pathogenesis of COVID-19-associated liver injury and propose several hypotheses about its etiopathogenesis.