INTRODUCTION:To explore the correlation between the expression of Tat interacting protein-30 (TIP30) mRNA in serum of patients with hepatitis B virus (HBV) -derived decompensated liver cirrhosis and recompensation as well as short-term prognosis. METHODS:The clinical data of 109 patients with the HBV-related decompensated cirrhosis who were hospitalized in the First Affiliated Hospital of Xi'an Jiaotong University and the First People's Hospital of Xianyang City from January 2018 to December 2023 were collected and analyzed, retrospectively, including 51 patients who occured recompensation and 58 patients who occured non-recompensation. Serum TIP30 mRNA expression was detected by Real-time polymerase reaction (RT-PCR). RESULTS:An increase in TIP30 mRNA expression after treatment was observed in the recompensation group compared to non-recompensation group (P < 0.001). Our analysis showed that serum TIP30 mRNA expression in the decompensated liver cirrhosis patients was negatively correlated with Child Pugh score, portal vein diameter, spleen length, and the morbidity in ascite, hepatic encephalopathy, hepatorenal syndrome, spontaneous peritonitis, pulmonary infection, and gastrointestinal bleeding (all P < 0.05). CONCLUSION:Detecting serum expression of TIP30 mRNA can provide a basis for evaluating the recompensation and short-term prognosis of decompensated liver cirrhosis. AS shown in .

BACKGROUND: The ligation of programmed death ligand 1 (PD-L1) on cancer cells to programmed cell death-1 (PD1) expressed on T cells is a key mechanism of immune evasion. Despite the approval of anti-PD1/PD-L1 therapy for several cancers, the limited response rate and adaptive immune resistance emphasize the necessity to investigate the mechanisms regulating PD1/PD-L1 axis. Fibrinogen-like protein 2 (FGL2) advances hepatocellular carcinoma (HCC) development by triggering various immunosuppressive processes, but its role in modulating PD1/PD-L1 pathway and cancer immunotherapy is unknown. METHODS: Tumor tissue samples were utilized to explore the relationship between FGL2 expression and clinical prognosis in patients with HCC. The association between FGL2 and immune checkpoints was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA) platform. Loss- and gain-of-function experiments were employed to examine the influence of FGL2 on PD-L1 expression. The Hepa1-6 cell line was inoculated subcutaneously or orthotopically into wild-type (WT) and Fgl2 gene knockout (Fgl2-/-) mice, and combined interference with FGL2 inhibition and PD1 blockade was investigated. RESULTS: Patients with higher FGL2 expression had significantly poorer prognosis. A positive correlation was observed between FGL2 expression and immune checkpoints including PD1, PD-L1, cytotoxic T lymphocyte-associated protein 4 (CTLA4) and so on. In mouse models, knockout of FGL2 significantly suppressed tumor growth. Within the tumor microenvironment, PD-L1 expression on hepatoma cells and PD1, CTLA4 expression on T cells were significantly lower in Fgl2-/- mice than those in WT mice. Mechanistically, FGL2 regulated the phosphorylation and nuclear translocation of transcription factor (TF) EB through activating the mammalian target of rapamycin complex 1 (mTORC1) signaling, thereby inhibiting lysosome biosynthesis and PD-L1 degradation, which ultimately led to the upregulation of PD-L1 in hepatoma cells. FGL2 depletion synergized with PD1 blockade to maximize therapeutic outcomes. Histologically, the combined interference group exhibited reduced expression of PD-L1, increased cytotoxicity of CD8+ T cells, and decreased infiltration of Tregs within the tumors. CONCLUSION: In HCC, FGL2 promotes immune escape by inhibiting the lysosomal degradation of PD-L1 via mTOR-TFEB axis. Targeting FGL2 may serve as a potential therapeutic strategy to enhance the efficacy of anti-PD1 therapy.

BackgroundPrognostic assessment in acute-on-chronic liver failure (ACLF), particularly in HBV-endemic regions, remains challenging due to the limited accuracy of conventional models. We aimed to develop and validate a novel, machine learning-based model incorporating liver reserve function to improve individualized prediction of short-term outcomes in HBV-ACLF.MethodsBaseline demographics, clinical features, laboratory findings, and 90-day follow-up data were retrospectively collected from 496 patients (training/internal subgroups) and 52 patients (external validation) with HBV-ACLF. Twelve machine learning algorithms were systematically evaluated for prognostic performance. The optimal model was established using the LASSO-RF approach, with key variables identified by SHAP values. Model accuracy was assessed by ROC analysis and compared with MELD and CTP scores. An interactive web calculator (https://syx123.shinyapps.io/deploy_shiny/) was developed to facilitate clinical use.ResultsWe initially screened 23 potential clinical risk factors for predicting ACLF prognosis. Subsequently, using the LASSO-RF model, 15 key variables were selected for model construction. The final LASSO-RF model achieved an AUC of 0.99 in the training cohort and 0.98 in the validation cohort for predicting 90-day mortality, outperforming conventional scoring systems such as MELD and CTP. To facilitate clinical application, an online tool (https://syx123.shinyapps.io/deploy_shiny/) was developed to provide real-time risk scores and 90-day mortality predictions for individual patients.ConclusionsLiver reserve function indicators, particularly EHBF and ICG-R15, play a pivotal role in prognosticating HBV-ACLF outcomes. The developed model and its accompanying online tool enable accurate risk stratification and have the potential to guide timely and individualized clinical management.

There’s a scarcity of drugs effective against nonalcoholic steatohepatitis (NASH). Exosomes from Human umbilical cord mesenchymal stem cells (huc-MSCs) show potential in managing glycolipid metabolism and the immune response. Therefore, further investigations are required to explore their application in NASH and the underlying mechanisms. C57BL/6J mice were fed with a western diet for 12 weeks to induce NASH, and huc-MSCs exosomes (MSCs-exo) were administered during the feeding period. The effect of MSCs-exo was evaluated by monitoring changes in body weight, fat distribution, blood glucose, and insulin levels, and analyzing pathological alterations in liver tissue. Mechanism investigations were carried out using flow cytometry, immunofluorescence staining, and other experimental techniques. MSCs-exo could reduce liver fat, inflammation, fibrosis, and improved metabolism to alleviate the progression of NASH. Besides, MSCs-exo could decrease macrophage accumulation in the liver, encouraging M2 over M1 macrophage polarization. Furthermore, our study found that MSCs-exo had a high expression of miR-24-3p, which may regulate macrophage polarization by targeting the interferon-stimulated genes (STING) gene in macrophages, with its overexpression amplifying MSCs-exo’s NASH benefits. These findings suggest that the therapeutic effect of MSCs-exo on NASH may be attributed to the regulation of macrophage M2 polarization through miR-24-3p targeting STING. This provides a scientific basis for future clinical application.

BackgroundThe immunosuppressive nature of the HCC tumor microenvironment limits the effectiveness of current immunotherapeutic strategies. Identifying key immune-related regulators is essential for improving patient stratification and therapeutic outcomes.MethodsTranscriptomic data from TCGA and GEO datasets were integrated to screen IRDEGs. Functional enrichment, co-expression, and PPI network analyses were performed to explore the biological context. Consensus clustering based on hub gene expression was used to define immune-related molecular subtypes. Immune infiltration characteristics, immune checkpoint expression, TIDE and IPS scores, and predicted immunotherapy responses were compared. FCGR2A expression was validated in clinical HCC tissues by immunohistochemistry and western blotting. In vitro assays evaluated the effects of FCGR2A knockdown on HCC cell proliferation, migration, and invasion.ResultsA total of 21 IRDEGs were identified, among which FCGR2A was consistently upregulated and associated with poor prognosis. Enrichment analysis indicated significant involvement in immune activation and inflammatory signaling pathways. PPI network analysis identified nine hub genes, including FCGR2A. Consensus clustering revealed two distinct immune-related molecular subtypes with marked differences in immune infiltration patterns, immune checkpoint profiles, TIDE and IPS scores. GSEA demonstrated subtype-specific activation of antigen processing, T cell signaling, and inflammatory pathways. Experimental validation confirmed elevated FCGR2A expression in HCC tissues. Functional assays showed that FCGR2A knockdown significantly inhibited HCC cell proliferation, migration, and invasion.ConclusionsFCGR2A acts as both a prognostic biomarker and an immune regulatory hub in HCC, anchoring a broader gene network that defines immune subtypes and predicts therapeutic responsiveness. Incorporating FCGR2A-based stratification may optimize immunotherapeutic strategies for HCC.

Purpose: This study assessed the performance of the ultrasound-guided attenuation parameter (UGAP) in diagnosing and grading hepatic steatosis in patients with metabolic dysfunctionassociated steatotic liver disease (MASLD). Magnetic resonance imaging proton density fat fraction (MRI-PDFF) served as the reference standard.Methods: Patients with hepatic steatosis were enrolled in this prospective study and underwent UGAP measurements. MRI-PDFF values of ≥5%, ≥15%, and ≥25% were used as references for the diagnosis of steatosis grades ≥S1, ≥S2, and S3, respectively. Spearman correlation coefficients and area under the receiver operating characteristic curves (AUCs) were calculated.Results: Between July 2023 and June 2024, the study included 88 patients (median age, 40 years; interquartile range [IQR], 36 to 46 years), of whom 54.5% (48/88) were men and 45.5% (40/88) were women. Steatosis grades exhibited the following distribution: 22.7% (20/88) had S0, 50.0% (44/88) had S1, 21.6% (19/88) had S2, and 5.7% (5/88) had S3. The success rate for UGAP measurements was 100%. The median UGAP value was 0.74 dB/cm/MHz (IQR, 0.65 to 0.82 dB/ cm/MHz), and UGAP values were positively correlated with MRI-PDFF (r=0.77, P<0.001). The AUCs of UGAP for the diagnoses of ≥S1, ≥S2, and S3 steatosis were 0.91, 0.90, and 0.88, respectively. In the subgroup analysis, 98.4% (60/61) of patients had valid controlled attenuation parameter (CAP) values. UGAP measurements were positively correlated with CAP values (r=0.65, P<0.001).Conclusion: Using MRI-PDFF as the reference standard, UGAP demonstrates good diagnostic performance in the detection and grading of hepatic steatosis in patients with MASLD.

BACKGROUND:Epithelial-mesenchymal transition (EMT) is central to HCC metastasis, in which RNA-binding proteins (RBPs) play a key role. METHODS:To explore the role of RBPs in metastasis of hepatocellular carcinoma (HCC), whole transcriptome sequencing was conducted to identify differential RBPs between HCC with metastasis and HCC without metastasis. The influence of RBPs on metastasis of HCC was verified by in vitro and in vivo experiments. The interaction of RBPs with non-coding RNAs was evaluated by RNA immunoprecipitation and pull-down assays. RNA sequencing, whole-genome sequencing, and alternative splicing analysis were further performed to clarify post-transcriptional regulation mechanisms. RESULTS:Whole transcriptome sequencing results showed that expression of thioredoxin (Trx) was significantly upregulated in HCC patients with metastasis. Trx was also found to be associated with poor prognosis in HCC patients. Overexpression of Trx could promote migration and invasion of HCC cells in vitro and increase the rate of lung metastasis of HCC cells in vivo. Moreover, binding assays showed that Trx could bind to LINC00152. As a result, LINC00152 was verified to determine the pro-metastasis function of Trx by knockdown assay. Furthermore, we revealed that Trx could regulate metastasis-associated alternative splicing program. Specifically, angiopoietin 1 (ANGPT1) was the splicing target; the splicing isoform switching of ANGPT1 could activate the PI3K-Akt pathway, upregulate EMT-associated proteins, and promote migration and invasion of HCC cells. CONCLUSIONS:We found that Trx could interact with LINC00152 and promote HCC metastasis via regulating alternative splicing, indicating that Trx may serve as a novel therapeutic target for HCC treatment.

Objective Hepatitis B virus-associated acute-on-chronic liver failure (HBV-ACLF) has a high mortality rate due to severe liver function disorder, extremely poor liver regeneration capacity, and dysregulated immune responses, thus new treatment measures are urgently needed to improve the therapeutic effect. This study aimed to evaluate the effectiveness of Granulocyte-colony stimulating factor (G-CSF) treatment in HBV-ACLF. Methods The data of patients with HBV-ACLF admitted to West China Hospital from January 2022 to October 2023 were collected retrospectively. They were divided into control group and treatment group according to whether they had received additional G-CSF treatment. The survival outcomes at 30-day and 90-day were analyzed between two groups. The change of disease severity score and alpha fetoprotein (AFP) after 14 days of hospitalization were observed between two groups. The control group received standard medical therapy, while the G-CSF group received G-CSF at a dose of 5µg/kg once daily for six days on the basis of standard medical therapy. Results In this retrospective study, a total of 136 HBV-ACLF patients were divided into two groups, with 47 in the G-CSF group and 89 in the control group. The 30-day survival rate of patients receiving G-CSF treatment was 85.1%, compared to 71.9% in the control group (P = 0.084). The 90-day survival rate for patients receiving G-CSF treatment was 76.6%, while it was 59.6% for the control group (P = 0.047). Additionally, on the 14th day of hospitalization, patients receiving G-CSF treatment showed a more reduction in Model for End-Stage Liver Disease (MELD) score (P = 0.001) and Child-Turcotte-Pugh (CTP) score (P = 0.021) compared to the control group. The decrease in serum AFP in the control group was greater than that in the G-CSF group, although there was no statistical difference (P = 0.112). Conclusion G-CSF significantly improves the survival rate of HBV-ACLF patients and further promotes the recovery of liver function during hospitalization for ACLF.

Organ fibrosis is a pathological process characterized by the inability of normal tissue cells to regenerate sufficiently to meet the dynamic repair demands of chronic injury, resulting in excessive extracellular matrix deposition and ultimately leading to organ dysfunction. Despite the increasing depth of research in the field of organ fibrosis and a more comprehensive understanding of its pathogenesis, effective treatments for fibrosis-related diseases are still lacking. Melatonin, a neuroendocrine hormone synthesized by the pineal gland, plays a crucial role in regulating biological rhythms, sleep, and antioxidant defenses. Recent studies have shown that melatonin may have potential in inhibiting organ fibrosis, possibly due to its functions in anti-oxidative stress, anti-inflammation, remodeling the extracellular matrix (ECM), inhibiting epithelial-mesenchymal transition (EMT), and regulating apoptosis, thereby alleviating fibrosis. This review aims to explore the therapeutic potential of melatonin in fibrosis-related human diseases using findings from various in vivo and in vitro studies. These discoveries should provide important insights for the further development of new drugs to treat fibrosis.

CD8+ T cell exhaustion is a stable dysfunctional state driven by chronic antigen stimulation in the tumor microenvironment (TME). Differentiation of exhausted CD8+ T cells (CD8+ TEXs) is accompanied by extensive transcriptional, epigenetic and metabolic reprogramming. CD8+ TEXs are mainly characterized by impaired proliferative and cytotoxic capacity as well as the increased expression of multiple co-inhibitory receptors. Preclinical tumor studies and clinical cohorts have demonstrated that T cell exhaustion is firmly associated with poor clinical outcomes in a variety of cancers. More importantly, CD8+ TEXs are regarded as the main responder to immune checkpoint blockade (ICB). However, to date, a large number of cancer patients have failed to achieve durable responses after ICB. Therefore, improving CD8+ TEXs may be a breakthrough point to reverse the current dilemma of cancer immunotherapy and eliminate cancers. Strategies to reinvigorate CD8+ TEXs in TME mainly include ICB, transcription factor-based therapy, epigenetic therapy, metabolism-based therapy and cytokine therapy, which target on different aspects of exhaustion progression. Each of them has its advantages and application scope. In this review, we mainly focus on the major advances of current strategies to reinvigorate CD8+ TEXs in TME. We summarize their efficacy and mechanisms, identify the promising monotherapy and combined therapy and propose suggestions to enhance the treatment efficacy to significantly boost anti-tumor immunity and achieve better clinical outcomes.

The coronavirus disease 2019 (COVID-19) is a highly transmissible disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that poses a major threat to global public health. Although COVID-19 primarily affects the respiratory system, causing severe pneumonia and acute respiratory distress syndrome in severe cases, it can also result in multiple extrapulmonary complications. The pathogenesis of extrapulmonary damage in patients with COVID-19 is probably multifactorial, involving both the direct effects of SARS-CoV-2 and the indirect mechanisms associated with the host inflammatory response. Recognition of features and pathogenesis of extrapulmonary complications has clinical implications for identifying disease progression and designing therapeutic strategies. This review provides an overview of the extrapulmonary complications of COVID-19 from immunological and pathophysiologic perspectives and focuses on the pathogenesis and potential therapeutic targets for the management of COVID-19.

Abstract Objectives One of the major challenges in treating patients with coronavirus disease 2019 (COVID-19) is predicting the severity of disease. We aimed to develop a new score for predicting progression from mild/moderate to severe COVID-19. Methods A total of 239 hospitalized patients with COVID-19 from two medical centers in China between February 6 and April 6, 2020 were retrospectively included. The prognostic abilities of variables, including clinical data and laboratory findings from the electronic medical records of each hospital, were analysed using the Cox proportional hazards model and Kaplan–Meier methods. A prognostic score was developed to predict progression from mild/moderate to severe COVID-19. Results Among the 239 patients, 216 (90.38%) patients had mild/moderate disease, and 23 (9.62%) progressed to severe disease. After adjusting for multiple confounding factors, pulmonary disease, age > 75, IgM, CD16+/CD56+ NK cells and aspartate aminotransferase were independent predictors of progression to severe COVID-19. Based on these five factors, a new predictive score (the ‘PAINT score’) was established and showed a high predictive value (C-index = 0.91, 0.902 ± 0.021, p < 0.001). The PAINT score was validated using a nomogram, bootstrap analysis, calibration curves, decision curves and clinical impact curves, all of which confirmed its high predictive value. Conclusions The PAINT score for progression from mild/moderate to severe COVID-19 may be helpful in identifying patients at high risk of progression.

Background: Albuvirtide (ABT), a fusion inhibitor against human immunodeficiency virus ( HIV) infection, has good efficacy and tolerability for HIV treatment. However, there is a paucity of data regarding ABT-based regimen as second-line therapy. This current study evaluated the efficacy and safety of switching to ABT + ritonavir-boosted lopinavir (LPV/r) treatment in a cohort of HIV-infected individuals who failed initial treatment. Methods: This retrospective comparative cohort study included patients who failed initial treatment and switched to either ABT + LPV/r (the ABT group) or two nucleotide reverse transcriptase inhibitors (NRTIs) + LPV/r (the NRTI group) between November 2019 and December 2020 in the People's Hospital of Zhaojue County in Liangshan Yi Autonomous Prefecture, China. All individuals were followed up from baseline to 12 weeks after conversion, or until the patient developed unacceptable toxic effects or was loss of follow-up. The proportion of patients who achieved virological suppression (viral load <50 copies/mL) at week 12 was considered a primary efficacy endpoint. Safety outcomes included the incidence of adverse events and laboratory abnormalities. All participants underwent resistance testing before regimen conversion. The linear regression model was applied to evaluate the association of CD4(+) T cell count with the patient's clinical characteristics. Results: A total of 71 patients were included in this study, the two groups were comparable at baseline in terms of age, sex, CD4(+) T cell count, and viral load. The suppression of HIV-1 RNA to levels <50 copies/mL was achieved in 82.4% (28/ 31) and 29.7% (11/34) of patients in the ABT group and the NRTI group, respectively (P<0.001). Older age (P=0.016) and higher alkaline phosphatase (ALP) levels (P=0.038), but not rescue regimen, were associated with attenuated CD4(+) T cell recovery. Most adverse events mild in severity, with abdominal pain as the most reported event in two groups (26.8%, 19/71), and no severe adverse events were detected. Conclusions: Conversion to ABT + LPV/ r therapy appears to be an effective and safe strategy. This treatment regimen has great potential to be generalized in the HIV-infected population, although further testing in a larger patient population is required to verify these results.

Background Leishmaniasis is a zoonotic disease caused by Leishmania spp. and spreads through sandfly bites. Owing to the wide range of nonspecific clinical symptoms, patients with leishmaniasis are frequently misdiagnosed or underdiagnosed. Methods The study participants were 7 metagenomic next-generation sequencing (mNGS)-diagnosed patients with leishmaniasis who could not be diagnosed using conventional methods. Clinical data were retrospectively collected and analyzed. When searching PubMed for mNGS and leishmaniasis, 8 peer-reviewed case reports in English were retrieved. Results A total of 7 patients with recurrent fever, pancytopenia, and significant splenomegaly were included in this study. Only 3 individuals tested positive for rK39. Two individuals, 1 of whom was HIV-positive, had Leishmania amastigotes identified in their bone marrow. However, all patients' blood mNGS findings pointed to Leishmania infection, and they were finally diagnosed with leishmaniasis. Sodium stibogluconate therapy with a short course of amphotericin B was administered to all patients. The prognosis for the remaining patients was good, except for 1 who died of multiple organ failure. Conclusions mNGS could be used to identify leishmaniasis, particularly in patients who are difficult to diagnose using conventional approaches.

Chronic hepatitis B virus (CHB) infection is one of the primary risk factors associated with the development of hepatocellular carcinoma (HCC). Despite having been extensively studied, diagnosing early-stage HCC remains challenging, and diagnosed patients have a poor (3–5%) survival rate. Identifying new approaches to detect changes in the serum metabolic profiles of patients with CHB and liver cirrhosis (LC) may provide a valuable approach to better detect HCC at an early stage when it is still amenable to treatment, thereby improving patient prognosis and survival. In the present study, we, therefore, employed a liquid chromatography-mass spectrometry (LC-MS)-based approach to evaluate the serum metabolic profiles of 30 CHB patients, 29 LC patients, and 30 HCC patients. We then employed appropriate statistical methods to identify those metabolites that were best able to distinguish HCC cases from LC and CHB controls. A mass-based database was then used to putatively identify these metabolites. We then confirmed the identities of a subset of these metabolites through comparisons with the MS/MS fragmentation patterns and retention times of reference standards. The serum samples were then reanalyzed to quantify the levels of these selected metabolites and of other metabolites that have previously been identified as potential HCC biomarkers. Through this approach, we observed clear differences in the metabolite profiles of the CHB, LC, and HCC patient groups in both positive- and negative-ion modes. We found that the levels of taurodeoxy cholic acid (TCA) and 1,2-diacyl-3-β-d-galactosyl-sn-glycerol rose with the progression from CHB to LC to HCC, whereas levels of 5-hydroxy-6E,8Z,11Z,14Z,17Z-eicosapentaenoic acid, and glycyrrhizic acid were gradually reduced with liver disease progression in these groups. The ROC analysis showed that taurodeoxy cholic acid (TCA), 1,2-diacyl-3-β-d-galactosyl-sn-glycerol, 5-hydroxy-6E,8Z,11Z,14Z,17Z-eicosapentaenoic acid, and glycyrrhizic acid had a diagnosis performance with liver disease progression. These four metabolites have a significant correlation with alpha fetal protein (AFP) level and age. Our results highlight novel metabolic biomarkers that have the potential to be used for differentiating between CHB, LC, and HCC patients, thereby facilitating the identification and treatment of patients with early-stage HCC.

Recently, more and more attention has been paid on adult hemophagocytic lymphohistiocytosis (HLH), a disease with complicated symptoms and high mortality. In order to analyze the clinical characteristics and prediction risk factors of mortality, we designed a retrospective study with 1-year follow-up and included 155 patients admitted to Tongji Hospital diagnosed as HLH. One hundred seven patients formed the training cohort for nomogram development, and 48 patients formed the validation cohort to confirm the model’s performance. All patients’ clinical characteristics, laboratory results, medical records, and prognosis were analyzed. Among all the 107 patients in the training cohort, 46 were male and 61 were female, with the median age of 49.0 (IQR 31.0–63.0). The 1-year mortality rate was 43.9% (47/107) and 45.8% (22/48) in the training and validation cohort, respectively. And further multivariate logistic regression analysis in the training cohort showed that male (odds ratio 5.534, 95% CI 1.507–20.318, p = 0.010), altered mental status (11.876, 1.882–74.947, p = 0.008), serum ferritin ≥ 31,381 μg/L (8.273, 1.855–36.883, p = 0.006), and IL-6 ≥ 18.59 pg/mL (19.446, 1.527–247.642, p = 0.022) were independent risk factor of mortality. A nomogram included the four prediction factors mentioned above was also tabled to help clinicians evaluate the probability of poor outcome. Area under the receiver operating characteristic curve (AUROC) analysis, calibration curves, and decision curve analysis (DCA) certify the accuracy and the clinical usefulness of the nomogram. Our research reveals that male, altered mental status, serum ferritin ≥ 31,381 µg/L, and IL-6 ≥ 18.59 pg/mL are four independent predictors for poor prognosis. Doctors should pay more attention to patients with altered mental status, high serum ferritin, and IL-6 level, who have a higher risk of death.

Abstract Background: Hepatitis B virus (HBV) infection is still a public issue in the world. Hepatitis B vaccination is widely used as an effective measure to prevent HBV infection. This large-sample study aimed to evaluate the positive rates of hepatitis B surface antibody (anti-HBs) in youth after booster vaccination. Methods: A total of 37788 participants were divided into two groups according to the baseline levels of anti-HBs before booster vaccination: the negative group (anti-HBs(−)) and the positive group (anti-HBs(+)). Participants were tested for anti-HBs levels after receiving a booster vaccine at 1 and 4 years. Results: The positive rates of anti-HBs were 34.50%, 73.80% and 67.32% before booster vaccination at 1 and 4 years after vaccination, respectively. At 4 years after the booster vaccination, the positive rates of 13–18 years were 47.54%, which was the lowest level among all youth age groups. In the anti-HBs(−) group, the positive conversion rates of anti-HBs were 74.62% at 1 year after receiving a booster vaccine, and 67.66% at 4 years after vaccination. In the anti-HBs(+) group, the positive maintenance rates of anti-HBs were 70.16% after 1 year, and 66.66% after 4 years. Compared with the baseline anti-HBs (+) group, the positive rates of the baseline anti-HBs(−) group were higher at 1 and 4 years after receiving the booster vaccine. Conclusion: The positive rates of anti-HBs declined over time, especially the positive maintenance rates were the lowest at age of 13–18 years.