Journal of Viral Hepatitis最新文献

The rate of HCV infection is higher in people with psychiatric conditions than in the general population. However, access to somatic care for populations with mental or dual diagnoses remains insufficient. These circumstances could constitute a barrier to the eradication of HCV infection. A retrospective study was performed in the public mental health institution of Ville Evrard. Screening for HCV infection should be systematically proposed to patients attending the institution. On-site assessment of liver disease severity and treatment with direct-acting antivirals prescribed by physicians not specialised in hepatology allowed a better continuum of care. Patients lost to follow-up after a positive HCV serology test without viral load assessment were contacted. Patients hospitalised at least once a year were included. 8520 patients out of 18,439 (46.2%) were screened for HCV infection between 2017 and 2021. The screening rate increased from 40.0% in 2017 to 65.7% in 2021. HCV seroprevalence was 2.2%. A total of 129 HCV PCRs were performed, and 27.1% were positive. In a logistic regression model, patients older than 30 years were at greater risk of having a positive HCV serology test. These positive serologies were 1.9 times higher in men than women (p < 0.001). The assessment of fibrosis was found in 45.7% of patients with a positive HCV PCR. Patients with psychiatric conditions constitute an important HCV reservoir. A strategy of screening and management of HCV infection in this population appears to be feasible. This strategy could contribute to the eradication of chronic HCV infection.

Acute-on-chronic liver failure (ACLF) is a severe clinical condition with high short-term mortality, in part due to the dysfunctional immune response. Identifying immune mechanism under ACLF is critical to understand its pathogenesis and to develop novel targeted therapeutics. Among the immune cells, how are B cells involved in ACLF remains largely unknown. We performed scRNA-seq on peripheral blood mononuclear cells from clinical ACLF patients and healthy controls. Integrated analysis was performed to identify the role of B cells in ACLF. Subsequently, different subsets of B cells in ACLF were validated through flow cytometry based on their highlighted markers. Six B-cell subgroups, including naive B cells, naive B2 cells, nonclass-switched memory B cells, class-switched memory B cells, autoimmune-related B cells and plasma B cells were identified. The proportions of naive B cells significantly expand in ACLF, compared with healthy control. Function enrichment analysis revealed the activation of inflammatory response in naive B cells. Further flow cytometry confirmed the elevated circulating naive B cells in ACLF. Our study uncovered the altered immune landscape of circulating B cells after ACLF. The proportion dynamics and functional perturbation indicate the potential of naive B cells as intervention targets in the future ACLF therapy.

Human Bocavirus (HBoV) is an emerging pathogen linked to respiratory and gastrointestinal infections in children. While its role in respiratory diseases is established, its association with liver dysfunction remains unclear. This study presents six paediatric cases of elevated liver enzymes or acute liver failure during HBoV infection, including severe outcomes such as liver transplantation and one fatality. Frequent co-infections with other pathogens were noted, complicating the clinical course. Although direct evidence of HBoV's role in liver involvement is lacking, its potential contribution warrants further investigation to guide clinical management.

Published studies on tenofovir alafenamide (TAF) therapy for preventing vertical transmission of hepatitis B virus (HBV) have primarily enrolled mothers with viremic levels of approximately 7 log₁₀ IU/mL. This study aimed to evaluate the efficacy and safety of TAF therapy in preventing mother-to-child transmission (MTCT) in mothers with exceptionally high viral loads, defined as HBV DNA levels > 2,000,000 IU/mL. Hepatitis B e antigen (HBeAg)-positive mothers with HBV DNA levels > 2,000,000 IU/mL were prospectively enrolled from four hospitals and initiated on TAF therapy between gestational weeks 26 and 28, continuing until delivery. All infants received immunoprophylaxis and were followed up to 28 weeks postpartum. The primary endpoints were the MTCT rate and the occurrence of congenital abnormalities in infants. Secondary outcomes included maternal HBV suppression at delivery and the safety of both mothers and infants. Among 137 mothers screened, 120 were enrolled in TAF therapy, and 121 infants completed the study. At delivery, 93.3% (112/120) of mothers achieved HBV DNA levels < 200,000 IU/mL. At birth, 0.8% (1/121) of infants had a congenital malformation, and 9.9% (12/121) tested positive for HBsAg. The vertical transmission rate was 2% (2/121, intention-to-treat) at 28 weeks of age. No severe adverse effects were reported in mothers or infants. On-treatment and postpartum alanine aminotransferase (ALT) flares after TAF cessation occurred in 7.5% (9/120) and 41.1% (46/112) of mothers, respectively, alongside viral rebound after cessation. Infant physical development remained within normal ranges based on national reference standards. In summary, approximately 2% of mothers on TAF therapy during late pregnancy experienced MTCT, despite proper immunoprophylaxis for their infants. Extending the treatment duration beyond 12 weeks for mothers with extremely high viral loads is recommended to improve MTCT prevention. No safety concerns were observed for either mothers or infants.

Trial Registration: ClinicalTrials.gov identifier: NCT04237376

Alpha-fetoprotein (AFP) level and its changes in chronic hepatitis B (CHB) may influence the risk of future hepatocellular carcinoma (HCC). This study aims to evaluate the HCC risk in CHB patients with no overt HCC but with elevated AFP level and to explore the prognostic role of longitudinal changes in AFP and liver-related laboratory values. This multicentre cohort study included 10,639 CHB patients without a history of HCC from seven medical facilities in South Korea. Patients with a baseline serum AFP test and no HCC diagnosis on imaging within 3 months were included. Patients were categorised into high-AFP (≥ 10 ng/mL) and normal-AFP (< 10 ng/mL) groups. The primary outcome was the incidence of HCC within 2 years, with secondary outcomes focused on longitudinal changes in AFP and liver-related laboratory values. Propensity score matching (PSM) and Cox proportional hazard models were used to assess HCC risk. After 1:4 PSM, 1278 high-AFP and 3731 normal-AFP patients were analysed. The high-AFP group had a significantly higher 2-year incidence of HCC (HR: 4.29; 95% CI: 3.31–5.57). AFP levels increased in patients who developed HCC in both groups (p < 0.01). Among the high-AFP group, patients who did not develop HCC had elevated baseline alanine aminotransferase levels (p < 0.01), which decreased during follow-up (p < 0.01) unlike those who developed HCC. In conclusion, baseline AFP elevation in CHB patients is associated with an increased risk of developing HCC within 2 years. Longitudinal monitoring of AFP and liver-related laboratory values can help in risk stratification.

Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Hepatitis B virus (HBV) is the main pathogen for HCC development. HBV covalently closed circular DNA (cccDNA) forms extra-host chromatin-like minichromosomes in the nucleus of hepatocytes with host histones, non-histones, HBV X protein (HBx) and HBV core protein (HBc). Epigenetic alterations are dynamic and reversible, which regulate gene expression without altering the DNA sequence and play a pivotal role in the regulation of HCC onset and progression. The aim of this review is to elucidate the deregulation of epigenetic mechanisms involved in the pathogenesis of HBV-related HCC (HBV-HCC), including post-translational histone and non-histone modifications, DNA hypermethylation and hypomethylation, non-coding RNA modification on HBV cccDNA minichromosomes and host factors, effecting the replication/transcription of HBV cccDNA and transcription/translation of host genes, and thus HBV-HCC progression. It is expected that the epigenetic regulation perspective provides new ways for more in-depth development of therapeutic control of HBV-HCC.