RESUMO
Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently the most significant public health threats in worldwide. Patients with severe COVID-19 usually have pneumonia concomitant with local inflammation and sometimes a cytokine storm. Specific components of the SARS-CoV-2 virus trigger lung inflammation, and recruitment of immune cells to the lungs exacerbates this process, although much remains unknown about the pathogenesis of COVID-19. Our study of lung type II pneumocyte cells (A549) demonstrated that ORF7, an open reading frame (ORF) in the genome of SARS-CoV-2, induced the production of CCL2, a chemokine that promotes the chemotaxis of monocytes, and decreased the expression of IL-8, a chemokine that recruits neutrophils. A549 cells also had an increased level of IL-6. The results of our chemotaxis transwell assay suggested that ORF7 augmented monocyte infiltration and reduced the number of neutrophils. We conclude that the ORF7 of SARS-CoV-2 may have specific effects on the immunological changes in tissues after infection. These results suggest that the functions of other ORFs of SARS-CoV-2 should also be comprehensively examined.
RESUMO
Acute-on-chronic liver failure (ACLF) is a clinical syndrome characterized by chronic liver disease, multiple organ failure and high mortality. ACLF patients have a high incidence of concurrent infection due to immune dysfunction. Early diagnosis of concurrent infection can initiate early anti-infection treatment and improve patient prognosis. However, ACLF complicated with infection is easy to be misdiagnosed, so searching for new diagnostic methods and biomarkers of infection can improve the reliability and accuracy of diagnosis. This article reviews the progress on epidemiology and immune-related characteristics, and their effect on diagnosis of concurrent infection in patients with ACLF.
