ABSTRACT
Toll-like receptors (TLRs) are key sensors that recognize the pathogen-associated molecular patterns (PAMPs) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to activate innate immune response to clear the invading virus. However, dysregulated immune responses may elicit the overproduction of proinflammatory cytokines and chemokines, resulting in the enhancement of immune-mediated pathology. Therefore, a proper understanding of the interaction between SARS-CoV-2 and TLR-induced immune responses is very important for the development of effective preventive and therapeutic strategies. In this review, we discuss the recognition of SARS-CoV-2 components by TLRs and the downstream signaling pathways that are activated, as well as the dual role of TLRs in regulating antiviral effects and excessive inflammatory responses in patients with coronavirus disease 2019 (COVID-19). In addition, this article describes recent progress in the development of TLR immunomodulators including the agonists and antagonists, as vaccine adjuvants or agents used to treat hyperinflammatory responses during SARS-CoV-2 infection.
ABSTRACT
Many studies have shown that patients with Coronavirus disease 2019 (COVID-19) have different degrees of liver injury. However, the mechanisms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invasion into the liver are still not fully understood. This review mainly summarizes the recently published works on the abnormal liver biochemical indicators and the mechanism of viral invasion with liver injury in COVID-19 patients. Generally, SARS-CoV-2 infection of the liver was caused by blood circulation or retrograde infection of the digestive tract, which led to the liver injury through direct cytopathic effect induced by virus or immunopathological effect caused by excessive inflammation. Besides these, hypoxia, endothelial injury and drug-induced jury were also the main reasons of liver injury in COVID-19 patients. In the liver function indicators, elevated alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, and lactate dehydrogenase levels with reduced albumin levels were observed in COVID-19 patients.
ABSTRACT
BACKGROUND: Clinical recovery does not mean full recovery. It is necessary to explore the aftereffects of COVID-19 in patients and compare the laboratory features of COVID-19 and other viral pneumonias in the recovery stages. METHODS: Forty-seven cases of COVID-19 and 45 cases of other viral pneumonias (control) were included in this study. The laboratory parameters were compared between COVID-19 and control patients as well as severe and moderate COVID-19 patients from the clinical recovery stage to the 4 weeks postdischarge recovery stage. RESULTS: A higher RDW-CV level and neutrophil percentage and lower levels of total proteins, lymphocytes, eosinophils, and MCH were found in COVID-19 patients compared with those in controls from the clinical recovery to the postdischarge recovery stages. Further analysis showed that decreases in lymphocytes, total proteins, and SOD and elevations in neutrophils, FDP, CRP, and ESR were more common in severe than moderate cases of COVID-19 during hospitalization; however, differences in these indicators, except total proteins, were not observed in the postdischarge recovery stages. Additionally, only 76.9% of COVID-19 patients were positive for IgG antibodies against SARS-CoV-2 in the convalescence stage, and one patient that was negative for specific IgG was reinfected. CONCLUSIONS: This study demonstrated that patients recovering from COVID-19 might need better care than that patients with other viral pneumonias due to the possibility of having poor immunity and nutritional conditions. These findings provide new insights to improve the understanding of COVID-19 and improve care for patients affected by these kinds of pandemics in the future.