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Viral immune evasion is crucial to the pathogenesis of hepatitis B virus (HBV) infection. However, the role of HBV in the modulation of innate immune evasion is poorly understood. A liver‐specific histone acetyltransferase 1 (Hat1) knockout (KO) mouse model and HAT1 KO cell line were established. Immunohistochemistry staining, Western blot analysis, Southern blot analysis, Northern blot analysis, immunofluorescence assays, enzyme‐linked immunosorbent assay, reverse transcription‐quantitative polymerase chain reaction, and chromatin immunoprecipitation assays were performed in the livers of mouse models, primary human hepatocytes, HepG2‐NTCP, and Huh7 and HepG2 cell lines. HBV‐elevated HAT1 increased the expression of miR‐181a‐5p targeting cyclic GMP‐AMP synthase (cGAS) messenger RNA 3′ untranslated regions through modulating acetylation of H4K5 and H4K12 in vitro and in vivo, leading to the inability of cGAS‐stimulator of interferon genes (STING) pathway and type I interferon (IFN‐I) signaling. Additionally, HBV‐elevated HAT1 promoted the expression of KPNA2 through modulating acetylation of H4K5 and H4K12 in the system, resulting in nuclear translocation of cGAS, HBx was responsible for the events by HAT1, suggesting that HBV‐elevated HAT1 controls the cGAS‐STING pathway and IFN‐I signaling to modulate viral innate immune evasion. HBV confers innate immune evasion through triggering HAT1/acetylation of H4K5/H4K12/miR‐181a‐5p or KPNA2/cGAS‐STING/IFN‐I signaling. Our finding provides new insights into the mechanism by which HBV drives viral innate immune evasion.

Background Liver transplantation (LT), resection (LR), and ablation (LA) are three curative‐intent treatment options for patients with early hepatocellular carcinoma (HCC). We aimed to develop a prognostic calculator to compare the long‐term outcomes following each of these therapies. Methods A total of 976 patients with HCC within the Milan criteria who underwent LT, LR, and LA between 2009 and 2019 from four institutions were evaluated. Multistate competing risks prediction models for recurrence‐free survival (RFS), recurrence within the Milan criteria (RWM), and HCC‐specific survival (HSS) were derived to develop a prognostic calculator. Results During a median follow‐up of 51 months, 420 (43%) patients developed recurrence. In the multivariate analysis, larger tumor size, multinodularity, older age, male, higher alpha‐fetoprotein (AFP), higher albumin‐bilirubin (ALBI) grade, and the presence of portal hypertension were significantly associated with higher recurrence and decreased survival rates. The RFS and HSS were both significantly higher among patients treated by LT than by LR or LA and significantly higher between patients treated by LR than by LA (all p < 0.001). For multinodular HCC ≤3 cm, although LT had better RFS and HSS than LR or LA, LA was noninferior to LR. An online prognostic calculator was then developed based on the preoperative clinical factors that were independently associated with outcomes to evaluate RFS, RWM, and HSS at different time intervals for all three treatment options. Conclusions Although LT resulted in the best recurrence and survival outcomes, LR and LA also offered durable long‐term alternatives. This prognostic calculator is a useful tool for clinicians to guide an informed and personalized discussion with patients based on their tumor biology and liver function.

Background/Aims: It was suggested that serum HGF,PCIII and PLT play important roles in nonalcoholic fatty liver disease (NAFLD). Thus, we aimed to evaluate their clinical utility in the diagnosis of patients with suspected NAFLD.Methods:300 Patients with NAFLD were compared to 102 matched controls.All were subjected to history taking, anthropometric measurements, and abdominal ultrasonography, as well as laboratory assessments of liver functions, fasting lipid profile, GLU, serum PLT, HGF and PCIII.Results:The levels of HGF,PCIII and PLT were higher in NAFLD cases than controls ,and with progressive increases as the severity of fatty liver increased（P<0.05）.HGF,PCIII and PLT were correlated with various clinical parameters and severity of NAFLD（P<0.05）.The optimal cut-off values for HGF in diagnosis of mild, moderate and severe fatty liver were 14.1pg/ml(AUROC 0.753,P＝0.004), 15.4pg/ml(AUROC 0.836, P < 0.001), 17.7pg/ml(AUROC 0.903, P < 0.001). PCIII had no value in differentiate mild from moderate fatty liver ,but its ability to diagnose severe fatty liver was significant. A cut-off value for PCIII to diagnose severe fatty liver was 7.9ng/L(AUROC 0.773).The optimal cut-off values for PLT in the diagnosis of mild, moderate and severe fatty liver were 194×10^9/L(AUROC 0.732), 195×10^9/L(AUROC 0.765), 200×10^9/L(AUROC 0.925), respectively with P < 0.001. When three indicators were tested together,the AUROC(95%CI)curve for diagnose NAFLD was 0.881(sensitivity0.760,specificity 0.873)(P<0.001) .Conclusion:.Combined detection of serum HGF, PCIII and PLT may be an effective non-invasive method for diagnosing NAFLD.

The Fc fragment of IgG binding protein (FCGBP) has been confirmed to play an important role in various cancers. However, the specific role of FCGBP in hepatocellular carcinoma (HCC) remains undefined. Thus, in this study, the enrichment analyses (Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Gene Set Enrichment Analysis) of FCGBP in HCC and extensive bioinformatic analyses using data of clinicopathologic characteristics, genetic expression and alterations, and immune cell infiltration were perfomed. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to verify the expression of FCGBP in both HCC tissues and cell lines. The subsequent results confirmed thatFCGBP overexpression positively correlated with poor prognosis in patients with HCC. Additionally, FCGBP expression could effectively distinguish tumor tissues from normal tissues, which was verified by qRT-PCR. The result was further confirmed by using HCC cell lines. The time-dependent survival receiver operator characteristic curve exhibited the strong ability of FCGBP to predict survival in patients with HCC. Additionally, we revealed the strong relationship between FCGBP expression and a number of classic regulatory targets and classical oncogenic signaling pathways of tumors. Finally, FCGBP was involved in the regulation of immune infiltration in HCC. Therefore, FCGBP has potential value in the diagnosis, treatment, and prognosis of HCC and may be a potential biomarker or therapeutic target.