Our objective was to evaluate the shifting burden of hepatitis E virus (HEV) across age groups and geographical scopes from 1990 to 2021 and to predict incidence rates for 2030. Leveraging data from the Global Burden of Diseases 2021, we examined HEV incidence and disability-adjusted life years, calculated average annual percentage changes (AAPCs) and identified pivotal years for incidence trends. We stratified our analysis by age, sex, and sociodemographic index and employed the Bayesian age-period-cohort model to predict future incidence. HEV incidence decreased from 269.68 per 100,000 in 1990 to 260.41 per 100,000 in 2021, with an AAPC of -0.1. Notably, the incidence significantly decreased in 1995, 2006, 2009, and 2014. Southern sub-Saharan Africa presented the most notable increase in HEV infection incidence, increasing from 218.59 per 100,000 individuals (95% [UI] 181.36 to 262.28) to 232.25 per 100,000 individuals (191.9 to 279.82), with an AAPC of 0.2 (95% [CI] 0.2 to 0.2). The 2030 incidence is projected to be 267.44 per 100,000 (95% UI, 235.27 to 299.6). Despite a general decline in HEV incidence associated with health interventions, some regions still report annual increases, underscoring the need for intensified disease management to meet the 2030 goals.

Hepatitis B virus (HBV) infection remains a major public health problem, causing nearly one million deaths annually. Nucleoporin 153 (NUP153) is known to facilitate the nuclear entry of the human immunodeficiency virus (HIV) nucleocapsids, and recent studies suggest it also plays a role in HBV nucleocapsids nuclear import. We aimed to investigate the impact of NUP153 on HBV replication and its underlying mechanism. NUP153 was knocked down by RNA interference or CRISPR/Cas9-mediated gene disruption, or overexpressed using an expression plasmid in HBV-replicating cells and animal model. Luciferase reporter assays were employed to assess the activities of viral or host factor promoters. Cytoplasmic and nuclear fractionation experiments were conducted to analyze the subcellular distribution of proteins and HBV RNA. In the present study, we found that knockdown of NUP153 significantly inhibited HBV replication without affecting the levels of covalently closed circular DNA (cccDNA) in both the prcccDNA/Cre recombinant plasmid system and HepG2-NTCP cells. Consistent results were observed in a mouse model hydrodynamically injected (HDI) with 1.2 × HBV plasmid. Conversely, NUP153 overexpression markedly increased cccDNA transcription and progeny virus production. Further study revealed that NUP153 enhanced HBV core promoter activity, likely through a hepatocyte nuclear factor 4α (HNF4α)-dependent mechanism. Mechanistically, ERK signaling was essential for NUP153-mediated promotion of HNF4α and HBV replication. Additionally, HBV replication significantly upregulated NUP153 mRNA and protein levels in both HBV cell models and HBV-infected patients. Together, we identify NUP153 as a novel host factor that promotes HBV replication by enhancing cccDNA transcription through the upregulation of HNF4α, suggesting a potential therapeutic strategy for HBV replication.

BK polyomavirus reactivation is a common complication after kidney transplantation, affecting the long-term survival of the transplanted kidney. However, it is unclear whether iron levels affect BKPyV reactivation after kidney transplantation. We first found that preoperative transferrin saturation levels in renal transplant recipients were closely associated with post-transplant BK virus reactivation and progression.

Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA virus belonging to the γ-herpesvirus subfamily. KSHV is the causative agent of Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), multicentric Castleman's disease (MCD), and KSHV inflammatory cytokine syndrome (KICS). Since its discovery, research on KSHV has rapidly progressed, but existing information platforms relatively lack comprehensiveness and do not provide efficient analysis tools tailored for KSHV. To further promote the research on KSHV more effectively, we have developed KSHVbook (http://www.kshvbook.com), a specialized information-sharing database dedicated to KSHV. This platform offers extensive information on genes, coding sequences, proteins, and the gene regulatory region. Besides, the KSHVbook includes about 35 010 transcription factor binding sites (TFBSs), 342 010 pairs of KSHV miRNA-host target gene relationships, protein structures predicted by AlphaFold3, qPCR primers, and so on. We also develop analytical tools for viral genome regions, TFBSs, and KSHV miRNA target genes to discover previously unknown biological functions of KSHV. These analytical tools can effectively identify the potential regulatory relationships between host transcription factors and viral genes. Overall, this platform provides a centralized data resource for KSHV research by integrating multiple databases, offering accessible analysis tools, and simplifying data acquisition. The KSHVbook will continue to be updated, and more features can be found on the website.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by SFTS virus (SFTSV). Shandong province is one of the epidemic regions with high incidence rate of SFTS. To investigate phylogenetical and genetic evolution characteristics of SFTSV in Shandong province, we isolated SFTSV from suspected patients between April 2023 and October 2024, and then whole SFTSV genomes were amplified and sequenced in this study. A total of 25 new strains were analyzed together 56 strains submitted in Genbank from Shandong province. Phylogenetical and genetic analyses of the data set revealed that four genotypes were co-circulating in Shandong province. C3 genotype was the most common genotype in each year with lower genetic divergence. 298 amino acid substitutions were detected in the four proteins of SFTSV, but only two substitutions (Arg624Lys and Arg962Ser) had been proven to have potential impacts on biological functions. In addition, one reassortment strain (C3/C4/C4 for L, M and S segments) and three recombinant strains were identified. Analysis of selection pressure at the level of amino acid substitutions indicated genes within the four ORFs of SFTSV were all subjected to negative selection. In conclusion, the genetic characteristics and evolutionary mechanism of SFTSV was complex in Shandong province. It is necessary to conduct continuous surveillance to grasp the genetic evolution patterns, and to discover novel prevalent variants in a timely manner.

Epstein-Barr virus (EBV) is associated with cancers, including lymphomas and nasopharyngeal carcinoma (NPC). To date, risk variants for NPC were mainly identified from Chinese populations, which dominated the world's total number of cases. Although Southeast Asia (SEA) countries have among the world's top yet intriguingly diverse NPC age-standardized incidence rates across subpopulations, data on EBV from SEA remains scarce. In this study, we examined 83 NPC patients of different ancestries for the presence of risk haplotypes associated with the Southern Chinese NPC and generated and analyzed 67 EBV sequences (from tissue, patient-derived xenografts and lymphoblastoid cell lines of 60 NPC patients) together with 838 published EBV genomes. Our study revealed that NPC patients of non-Chinese ancestry had fewer risk variants and haplotypes that are associated with Southern Chinese NPC and clustered distinctly from lymphomas, Southern Chinese NPC, and non-cancer controls. The distribution of non-synonymous variants was similar among NPC patients of Chinese ancestry, irrespective of geographical location. Meanwhile, non-synonymous variants in genes related to packaging, latency, and structural proteins such as BPLF1, LF3, and LMP1 varied across different ancestries. Our findings suggest possibilities of EBV adaptation to host genetics for NPC pathogenesis and warrant further research for the understudied NPC subpopulations.

Mayaro virus (MAYV) is an arthritogenic arbovirus that causes a debilitating illness that can progress to a chronic rheumatic disease characterized by persistent viral replication in macrophages within joint tissues. Here, we report that MAYV-infected macrophages release decondensed DNA traps (DNA extracellular traps, DETs) through a mechanism driven by the production of reactive oxygen species and peptidyl arginine deiminase activation, resembling the classical mechanism of pathogen clearance by activated neutrophils. Unlike traditional pathogen clearance observed for NETs released by neutrophils, MAYV-induced DETs did not inactivate the virus. Instead, DET-ensnared viruses are internalized by neighboring uninfected macrophages, increasing the number of infected cells. Collectively, these findings suggest that MAYV-containing DETs act as a "Trojan horse" that facilitates viral dissemination within inflamed tissues, connecting macrophage-mediated inflammatory response to viral persistence in the articular tissue in chronic MAYV disease.

In this report, the clinical performance of Liferiver HarmoniaHPV and Liferiver VenusHPV was evaluated under the VALHUDES framework. Five hundred and twenty-three women collected first-void urine (FVU) with Colli-Pee and vaginal samples with Evalyn Brush or Qvintip. Cervical samples were taken with the Cervex Brush by a clinician. Both vaginal and cervical samples were resuspended in 20 mL ThinPrep. Triplet samples from 499 women were tested with HarmoniaHPV and VenusHPV tests. The clinical accuracy of HarmoniaHPV did not differ in FVU and vaginal self-samples versus cervical samples. The relative sensitivity for CIN2+ on FVU and vaginal samples was 0.95 [95% CI 0.89-1.02] and 0.95 [95% CI 0.88-1.02], respectively. Relative specificity for < CIN2 was 0.95 [0.86-1.04] on FVU and 0.93 [0.86-1.01] on vaginal samples. VenusHPV demonstrated lower sensitivity on both self-sample types, whereas the specificity was similar to cervical samples. Post-hoc adjustment of the VenusHPV C-values improved sensitivity (ratio FVU/cervical = 0.94 [95% CI 0.88-1.00]; ratio vaginal/cervical = 0.96 [95% CI 0.92-1.01]) without compromising specificity (ratio FVU/cervical = 1.00 [0.92-1.09]; ratio vaginal/cervical = 0.95 [95% CI 0.88-1.02]) on both self-samples. In conclusion, HarmoniaHPV and VenusHPV tests demonstrated similar clinical accuracy on FVU and vaginal self- versus cervical samples, although VenusHPV test required cut-off optimization.

Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS), syphilis, hepatitis B and hepatitis C are the four major Mother-to-child transmission (MTCT) diseases, represent a significant public health challenge worldwide. Understanding the disease burden among women of child-bearing age (WCBA) helps to implement effective screening and treatment programs to control the MTCT diseases globally. Data on HIV/AIDS, syphilis, hepatitis B, and hepatitis C was collected from the Global Burden of Disease (GBD) 2021 database spanning 1992-2021. We analyzed the temporal trends of four MTCT diseases with joinpoint regression and further evaluated age-period-cohort effects using the age-period-cohort model. The age-standardized incidence rates per 100,000 population for HIV/AIDS, syphilis, hepatitis B, and hepatitis C in 2021 were 34.73 (95% uncertainty interval [UI]: 30.03, 40.54), 279.19 (95% UI: 174.59, 459.54), 908.39 (95% UI: 494.99, 1640.44), and 77.44 (95% UI: 41.57, 126.12). Joinpoint regression revealed ongoing declines in HIV/AIDS and hepatitis B rates among WCBA, contrasting with increasing trends for hepatitis C and syphilis post-2012. Age effects for HIV/AIDS, syphilis, and hepatitis B peaked in the 15-29 age group, while hepatitis C peaked in the 45-49 age group. Period effects showed increased incidence rates for syphilis and hepatitis C since 2012, peaking between 2017-2021, while HIV/AIDS and hepatitis B showed a general decline. Cohort effects for all four diseases generally followed a fluctuating downward trend. For hepatitis B, the incidence rate is declining in all 21 GBD regions. At national level, only the United Kingdom and Greece have seen a slight increase in incidence rates compared to 30 years ago, but the increase is minimal. For other MTCT diseases, Eastern Europe has the highest increase in incidence rates of HIV/AIDS and hepatitis C among WCBA, which requires special attention. Tropical Latin America is the region with the greatest increase in syphilis incidence rates. Specifically, at the national level, the countries with the highest increase in incidence rates for HIV/AIDS, syphilis, and hepatitis C are Pakistan, Greece, and Ukraine, respectively. Globally, while HIV/AIDS and hepatitis B incidence in WCBA has decreased, negative age, period, and cohort effects persist in certain countries. Post-2012, hepatitis C and syphilis incidence in WCBA has risen, underscoring the need to refine management strategies against MTCT diseases.

Congenital cytomegalovirus (cCMV) infection is diagnosed by positive urine or saliva testing within 21 days after birth. Beyond this age, newborn dried blood spot (DBS) PCR can retrospectively diagnose cCMV infection but has lower sensitivity than urine or saliva PCR testing. The DBS PCR may be negative due to the absence of blood DNAemia at birth or to the technical limit of detection for DBS PCR. The objective of this study was to distinguish these two possibilities by determining agreement between DBS and plasma CMV PCR tests among cCMV-infected infants. This single center retrospective cohort study evaluated 70 cCMV-infected infants diagnosed by a positive urine CMV PCR, who had a CMV DBS at birth and a plasma PCR test within 31 days after birth. Clinical characteristics and viral loads were compared between groups according to paired DBS and plasma PCR results. Test agreement was calculated using Cohen's kappa coefficient. The DBS PCR sensitivity was 71% compared to urine PCR. Of the 70 subjects, 49 (70%) subjects were DBS+ /plasma+ , 1 (1.4%) were DBS+ /plasma-, 14 (20%) were DBS-/plasma+ , and 6 (9%) were DBS-/plasma-. Agreement between the tests was fair (κ = 0.348, 95% CI 0.115-0.581). Of the 20 subjects with DBS- tests, 6 (30%) had undetectable plasma DNAemia. Of the infants with DBS-/plasma+ PCR, plasma viral loads were significantly lower than infants with DBS+ /plasma+ PCR testing. Nearly a third of cCMV infected infants may be missed by DBS testing due to both biological and technical limitations of this method.

This study aims to assess the impact of recombinant zoster vaccine (RZV) on the risk of major cardiovascular events (MACE) in patients with rheumatoid arthritis (RA), spondyloarthritis (SpA), or psoriatic diseases who are receiving Janus kinase inhibitors (JAKi). We conducted a new user design study utilizing the TriNetX database. We identified patients diagnosed with RA, SpA, or psoriatic diseases receiving JAKi. Two cohorts were constructed based on RZV vaccination status. Propensity score matching was performed. The primary outcome was MACE, analyzed using Cox regression with hazard ratios (HR) and Kaplan-Meier plots. Subgroup analyses were performed by age, sex, race, and zoster history. Sensitivity analyses were conducted with different follow-up periods and diseases. Of the 1 528 771 eligible patients initially included, each cohort included 1756 patients after propensity score matching. No significant difference in MACE risk was observed between the two cohorts (HR 1.121, 95% CI: 0.901-1.395). Subgroup and sensitivity analyses were consistent with the main findings. However, RZV vaccination was associated with a significant reduction in all-cause mortality (HR 0.610, 95% CI: 0.427-0.870). Subgroup analyses indicated that the mortality benefit was particularly evident in females (HR 0.585, 95% CI: 0.379-0.901) and those aged 65 years and older (HR 0.500, 95% CI: 0.301-0.806). In patients with immune-mediated inflammatory diseases receiving JAKi, RZV vaccination is associated with a 39% reduction in all-cause mortality compared to unvaccinated individuals. RZV vaccination should be considered for this high-risk population.

A large spectrum of viruses can infect the male reproductive system (MRS). Although the MRS adopts the local antiviral defense, it has also been considered as a potential viral reservoir. We hypothesize that tissue-specific cells may eliminate invading viruses and harbor viral replication in the MRS. We herein aimed to identify viral eliminators and potential reservoirs in the MRS using mumps virus (MuV) and mouse models. Primary cells, mainly consisting of epithelial cells, stromal cells, and macrophages, were isolated from the epididymis, seminal vesicle, and prostate of mice. MuV infection and replication were analyzed by determining MuV nucleoprotein (MuV-NP) in the primary cells. We demonstrated that a subset of resident macrophages efficiently took up and eliminated MuV, which should be involved in the antiviral defense in the MRS. However, a small subset of epithelial and stromal cells in these organs harbored MuV replication, and these cells could be viral reservoirs. Furthermore, interferon-β (IFN-β) inhibited MuV replication in MuV-replicating cells, suggesting that IFN-β administration may limit viral reservoirs. The results of the present study provide novel insights into the antiviral defense and viral reservoirs in the MRS, which can aid in the development of preventive and therapeutic approaches for viral infection of the MRS.

Arthritogenic alphaviruses such as chikungunya (CHIKV) and o'nyong-nyong (ONNV) viruses have shown capacity to cause widespread epidemics, with recurrent and sporadic outbreaks occurring throughout sub-Saharan Africa. We analyzed the seroprevalence for CHIKV and ONNV in 470 non-febrile subjects from three regions in Senegal (Sindia, 2018; Thies, 2018; and Kedougou, 2022/2023) using retrospective samples. We assessed the presence of anti-CHIKV IgG and neutralizing antibody titers against CHIKV and ONNV via enzyme-linked immunosorbent assay (ELISA) and microneutralization tests, respectively, and determined risk factors of CHIKV and ONNV exposure by binary logistic regression. The overall alphavirus seroprevalence based on an anti-CHIKV virus like particle (VLP) IgG ELISA was 38.5%, with rates varying geographically: Kedougou (48.6%), Thies (31.9%), and Sindia (14.9%). Neutralizing antibody titers revealed CHIKV and ONNV seroprevalence rates of 7.4% and 9.8%, respectively, with significant variations by region and age group. Cross-reactivity analysis showed that 82.9% of CHIKV cases exhibited a neutralizing response to ONNV, while 71.7% of ONNV cases cross-neutralized CHIKV. Residents of Thies had significantly higher odds of CHIKV infection (aOR, 3.147; 95% CI: 1.164-8.510) while ONNV infection was more likely in Kedougou (aOR, 3.888; 95% CI: 1.319-11.466). Furthermore, older age (> 40 years) was a significant risk factor both CHIKV (aOR, 2.094; 95% CI: 0.846-5.185) and ONNV infection (aOR, 2.745; 95% CI: 1.212-6.216). Our study confirms the co-circulation of CHIKV and ONNV in Senegal, highlighting their geographic and demographic distribution. These findings underscore the need for continued surveillance, alphavirus testing, and tailored public health strategies to mitigate their impact in Senegal.

The lymphocytic choriomeningitis virus (LCMV) is a widespread pathogen that causes mild-to-severe infections to severe outcomes. In this study, we explored the potential of trametinib, a mitogen-activated protein kinase (MAPK) inhibitor, as an antiviral agent against LCMV. Trametinib demonstrated significant antiviral activity against two distinct LCMV strains, Armstrong and Cl13, with promising half-maximal inhibitory concentrations (IC) and selectivity indices (SI) indicating its potency and safety profile. Mechanistic investigations revealed that trametinib interfered with multiple stages of the LCMV life cycle, including membrane fusion and genomic replication, leading to the robust inhibition of viral proliferation. Furthermore, trametinib disrupted the MEK/ERK signaling pathway, which is crucial for LCMV infection. In both in vitro and in vivo experiments, trametinib effectively reduced viral loads and mitigated pathological damage to the spleen and liver tissues. Overall, our findings suggest that trametinib is a promising novel therapeutic option for combating LCMV infection by targeting key stages of the viral life cycle and disrupting host cellular signaling pathways. Further exploration of the antiviral properties of trametinib is likely to pave the way for its clinical development as a treatment for LCMV infections.

Long COVID represents a significant global health challenge with an unclear etiology. Alongside accumulating evidence of mitochondrial dysfunction in patients with acute SARS-CoV-2 infection, a symptomatic overlap exists between long COVID and mitochondrial disorders. However, the genetic underpinnings of mitochondrial dysfunction in long COVID have not been previously explored. We employed whole genome sequencing to analyze 13 patients with severe long COVID to identify genetic defects related to mitochondrial function. We performed extracellular bioenergetics flux analysis on peripheral blood mononuclear cells and proteomics to evaluate cellular bioenergetics and compared the results to those of healthy controls. Our investigation identified 10 variants classified as pathogenic or likely pathogenic and 83 variants of unknown significance affecting a wide range of mitochondria-associated biological functions. Bioenergetics flux analysis in peripheral blood mononuclear cells revealed an altered ATP production rate in four long COVID patients compared to healthy controls. This study presents initial evidence of a potential underlying genetic predisposition to mitochondrial dysfunction in long COVID while demonstrating altered cellular energy capacity in a subset of these patients. These findings open avenues for further research into the role of mitochondrial dysfunction and pathology in patients suffering from long COVID and may pave the way for targeted therapeutic strategies aimed at mitigating mitochondrial dysfunction.

To examine the relationship between autoantibodies, inflammatory cytokines, and coagulation abnormalities in patients with severe fever with thrombocytopenia syndrome (SFTS) and assess their potential as prognostic markers. A total of 105 SFTS patients and 85 healthy controls (HCs) were included. Serum levels of antinuclear antibodies (ANAs), anti-neutrophil cytoplasmic antibodies (ANCAs), anti-endothelial cell antibodies (AECAs), antiphospholipid antibodies (aPLs), as well as inflammatory cytokines and chemokines were measured to evaluate their correlation with prognosis. AECA positivity was found in over 50% of SFTS patients, with higher titers correlating with poor prognosis. AECA levels were associated with hypertension, consciousness disorder, and advanced age. Elevated aPLs were observed and associated with coagulation dysfunction, including prolonged activated partial thromboplastin time (APTT) and thrombin time (TT). Serum levels of inflammatory cytokines and chemokines (IL-1β, IL-6, IL-8, CCL2, and CXCL10) were significantly higher in SFTS patients compared to HCs. Elevated AECA and aPLs, along with a dysregulated cytokine/chemokine profile, were identified as significant prognostic indicators in SFTS, offering potential biomarkers for disease severity. Further research is needed to explore the mechanistic roles of these immune responses and to develop targeted therapies.

Rhinovirus (RV), classified into RV-A, RV-B, and RV-C, is a prevalent cause of respiratory tract infections (RTIs). Here, we analysed RV infection and its clinical implications among outpatients with acute upper RTIs. Demographic data, baseline comorbidities, clinical symptoms, and health outcomes of RV-infected patients (n = 849) were compared with influenza (n = 417). Multivariable logistic regression was employed to evaluate predictors and health outcomes over a 1-year follow-up period. RV infections predominantly presented with cough, nasal discharge, and sore throat, whereas fever was more prevalent in influenza cases. RV-C-infected individuals with diabetes mellitus (adjusted odds ratio [aOR] 3.6; 95% CI 1.7-7.2; p = 0.001) and asthma (aOR 1.9; 95% CI 1.0-3.5; p = 0.047) showed a higher likelihood of experiencing severe acute respiratory symptoms. RV-C patients with comorbidities were twice more likely to have primary care visits due to RTIs within 1 year (aOR 2.4; 95% CI 1.4-4.4; p = 0.003). Asthma (aOR 3.8; 95% CI 1.9-7.2; p < 0.0001) and allergic rhinitis (aOR 2.9; 95% CI 1.0-8.0; p = 0.042) were key predictors of increased RTI-related primary care visits. RV infection, particularly in individuals with asthma, allergic rhinitis and diabetes, poses a significant disease burden similar to that of influenza.

Congenital cytomegalovirus infections (cCMV) are an important cause of childhood neurodevelopmental deficits. Most cCMV are the result of maternal non-primary infections during pregnancy, which can be due to reactivation or reinfection. To identify the rate of CMV reinfection during pregnancy and its risk factors. We performed a secondary analysis of CMV seropositive participants from two prospective cohort studies in Quebec, Canada. Antibody responses to four strain-specific CMV epitopes located in glycoproteins B and H were measured by enzyme-linked immunosorbent assay. CMV reinfection was defined as the appearance of an antibody response to a new epitope in the third compared to the first trimester. Risk factors for reinfection were assessed. Among 1614 participants, CMV reinfection was identified in 2.7% of participants, representing an incidence of 54.99 per 1000 person-years at risk (95% confidence interval 39.95-73.82). Age, marital status, household income, continent of birth or ethnicity were not associated with reinfection during pregnancy. The incidence of CMV reinfection during pregnancy is like what has been reported for primary infection in Quebec. A greater understanding of the patterns of reinfection is needed to inform strategies to reduce the burden of disease from cCMV.

Dendritic cells and the exosomes they secrete play a crucial role in the immune system, and studies have shown that dendritic cell function is dramatically reduced in patients with chronic hepatitis B. Alcohol could stimulate dendritic cell maturation. Consequently, the present work explored the therapeutic effect of alcohol-induced dendritic cells and their exosomes in hepatitis B virus (HBV) infection. We systematically investigated the functional effects of alcohol stimulation and HBV infection on dendritic cells and their exosomes, as well as cocultured alcohol-induced dendritic cells and exosomes with lymphocytes from HBV transgenic mice and chronic hepatitis B patients to study the T cell immune response. Our findings revealed that alcohol significantly accelerated the maturation of bone marrow-derived dendritic cells in mice and dendritic cells in patients with chronic hepatitis B, but had no effect on the DC2.4 cell line. Simultaneously, HBV infection was demonstrated to inhibit dendritic cell activation and maturation, as well as exosomes. More importantly, alcohol-induced dendritic cells enhanced T-cell immunity in HBV transgenic mice and chronic hepatitis B patients, and their exosomes had the same impact. The maturation of dendritic cells and their exosomes can be effectively induced by alcohol. Meanwhile, alcohol-induced maturation of dendritic cells and exosomes can significantly repair the poor T-cell immunity caused by HBV infection, making it a promising novel treatment for chronic hepatitis B patients in the future.