There is little data on the long-term follow-up outcomes of chronic hepatitis C patients achieving sustained virological response (SVR) after treatment with peglylated interferon-α plus ribavirin. We prospectively investigated the overall clinical, biochemical, virological and histological outcomes in a ten-year cohort study of 325 patients with chronic hepatitis C achieving SVR to pegylated interferon-α and ribavirin therapy. Patients underwent consistent clinical, biochemical and virological evaluation every six months, and patients with pretherapy Ishak fibrosis score ≥2 were invited to accept a second liver biopsy at the last follow-up. Liver biopsy specimens were evaluated using Ishak's scoring system. At the end of follow-up, five patients developed decompensated liver cirrhosis. One patient (0.3%) with pretherapy cirrhosis was diagnosed with hepatocellular carcinoma (HCC). A total of 305 patients (94%) had normal serum ALT and AST levels during the entire period of follow-up. Twenty-seven patients (8%) had conclusive evidence of virological relapse. Among the 117 patients with paired pretherapy and long-term follow-up biopsies, 96 (82%) had a decreased fibrosis score. Ninety-nine (79%) had a decrease in combined inflammation score. Thirty-seven (32%) had normal or nearly normal livers on long-term follow-up biopsy. SVR achieved with PEG-IFN-α and RBV combination therapy is durable, while late virological relapse may still occur in some patients. Clinical outcomes for patients who obtain SVR are excellent, although the patients with cirrhosis are still at a low risk of hepatocellular carcinoma.

Activation of hepatic stellate cell (HSC) is the central event in liver fibrosis. NS5ATP9 is related to many malignant tumors, but little is known about its function in HSC activation. The aim of this study is to investigate the role of NS5ATP9 in HSC activation in vitro. Genes related to liver fibrosis were detected after NS5ATP9 overexpression or silencing with or without transforming growth factor (TGF)-β1 stimulation in the human HSCs by real-time polymerase chain reaction and western blotting. Cell proliferation, migration, and apoptosis were tested, and the mechanisms underlying the effect of NS5ATP9 on HSC activation were studied. We showed that NS5ATP9 suppressed HSC activation and collagen production, with or without TGF-β1 induction. Also, NS5ATP9 inhibited cell proliferation and migration and promoted apoptosis. Furthermore, NS5ATP9 reduced basal and TGF-β1-mediated Smad3/phosphorylated-Smad3 expression. The existence of a physical complex between NS5ATP9 and Smad3 was illustrated. NS5ATP9 suppresses HSC activation, extracellular matrix production, and promotes apoptosis, in part through reducing Smad3/phosphorylated-Smad3 expression.

Hepatocellular carcinoma (HCC) is a kind of malignant tumor derived from hepatocytes and hepatobiliary cells, and its occurrence is prevalent worldwide. Although medical technology is developing rapidly, the therapeutic efficacy of HCC is still poor. Emerging evidence manifests that microRNAs (miRNAs) play a crucial role in various cancers and have been regarded as cancer suppressor gene. However, the regulatory mechanisms mediated by miR-647 involved in HCC remain unclear. Hence, to clarify the regulatory mechanisms mediated by miR-647 in HCC, we studied the independent effects of miR-647 and explored protein tyrosine phosphatase receptor type F (PTPRF) in the constructed HCC cell line (HCV-huh7.5). Thereafter, we used dual-luciferase gene reporting and Western blot to investigate the relationship between PTPRF and miR-647. Furthermore, we studied the mechanism of miR-647 on PTPRF in HCV-huh7.5. We found that miR-647 could not only promote the proliferation and invasion of HCV-huh7.5 cells but also facilitate cell migration, while PTPRF has the opposite effect. Besides, the results of cell function experiment implied that the overexpression of miR-647 or inhibition of PTPFRF remarkably influenced the Erk signaling pathway, which could regulate cell proliferation, migration, and invasion. In addition, the dual luciferase reporting identified PTPRF as a direct target of miR-647. We further demonstrated that miR-647 inhibitor or PTPRF knockdown administration boosted HCV-huh7.5 cell proliferation, migration, and invasion by targeting PTPRF. These findings provided clues for the mechanism of miR-647 in promoting the biology of HCV-huh7.5 cells by inhibiting the expression level of PTPRF.

Background This study compared clinical features of the Delta variant of coronavirus disease 2019 (COVID-19) in children and adults. Methods Clinical data included 80 children and 132 adults with the Delta variant of COVID-19, hospitalized in the Affiliated Hospital of Putian College between September and October 2021. The data was analyzed retrospectively. Results The proportion of mild patients in the children group (50%) was higher than that in the adults group (17.9%). Cough (25%, 20/80) and diarrhea (1.3%, 1/80) symptoms in children group were significantly less frequent. Compared with adults, there was no significant difference in the viral load of SARS-CoV-2 in samples collected by nasopharyngeal swabs. In children, lymphocyte count was higher [1.98 (0.25–4.25) vs 1.20 (0.29–4.27) ×109/L], whereas the interleukin-6 level was lower [5.87 (1.50–61.40) vs 15.15 (1.79–166.30) pg/mL] than that in adults group. Additionally, the incidence of liver injury in children group was lower than that in adults group. There was no significant difference in the incidence of proteinuria (22/75 vs 45/112) between the two groups, but the serum creatinine level in children was lower [42.0 (28.0–73.0) vs 57.0 (32.0–94.0) µmol/L]. Conclusion Compared with adults, children with the Delta variant of COVID-19 have differences in symptoms, clinical classification, inflammatory indices, and liver/kidney function injury. Children’s illness is relatively mild. Clinicians should pay attention to their differences and use drugs accurately.

No abstract