Background and Aims The safety and antibody responses of coronavirus disease 2019 (COVID‐19) vaccination in patients with chronic hepatitis B (CHB) virus infection is still unclear, and exploration in safety and antibody responses of COVID‐19 vaccination in CHB patients is significant in clinical practice. Methods 362 adult CHB patients and 87 healthy controls at an interval of at least 21 days after a full‐course vaccination (21–105 days) were enrolled. Adverse events (AEs) were collected by questionnaire. The antibody profiles at 1, 2 and 3 months were elucidated by determination of anti‐spike IgG, anti‐receptor‐binding domain (RBD) IgG, and RBD‐angiotensin‐converting enzyme 2 blocking antibody. SARS‐CoV‐2 specific B cells were also analysed. Results All AEs were mild and self‐limiting, and the incidence was similar between CHB patients and controls. Seropositivity rates of three antibodies were similar between CHB patients and healthy controls at 1, 2 and 3 months, but CHB patients had lower titers of three antibodies at 1 month. Compared to healthy controls, HBeAg‐positive CHB patients had higher titers of three antibodies at 3 months (all P < .05) and a slower decline in antibody titers. Frequency of RBD‐specific B cells was positively correlated with titers of anti‐RBD IgG (OR = 1.067, P = .004), while liver cirrhosis, antiviral treatment, levels of HBV DNA, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and total bilirubin (TB) were not correlated with titers of anti‐RBD IgG. Conclusions Inactivated COVID‐19 vaccines were well tolerated, and induced effective antibody response against SARS‐CoV‐2 in CHB patients.

Introduction The Female Sexual Function Index (FSFI) remains the most widely used scale for screening female sexual dysfunction (FSD), and the Chinese Version of the FSFI (CVFSFI) has been validated, but cutoff scores for the CVFSFI to distinguish between cases and noncases have not been developed, so the real prevalence of FSD in China is unknown. Aim To establish clinical cutoff scores for the CVFSFI and to evaluate the prevalence of FSD in urban Chinese women. Methods A cross-sectional study was conducted between June and December 2011. A total of 586 (age range of 22–60 years) women participated in the study. Receiving operating characteristic curve and classification and regression trees methodology were combined to establish clinical cutoff scores for the CVFSFI. The cutoff scores we developed were used to determine the prevalence of FSD in urban Chinese women. Main Outcome Measures The prevalence of FSD based on cutoff scores developed herein. Results The optimal CVFSFI cutoff score for the FSFI total score was 23.45 (sensitivity = 66.9%; specificity = 72.7%; area under curve [AUC] = 0.75). The cutoff score for each domain was also established as follows: ≤2.7 low desire (sensitivity = 55.2%; specificity = 78.3%; AUC = 0.73); ≤3.15 arousal disorder (sensitivity = 62.1%; specificity = 76.9%; AUC = 0.74); ≤4.05 lubrication disorder (sensitivity = 86.4%; specificity = 69.8%; AUC = 0.85); ≤3.8 orgasm disorder (sensitivity = 83.3%; specificity = 74.2%; AUC = 0.85); and ≤3.8 sexual pain (sensitivity = 65.4%; specificity = 80.6%; AUC = 0.79). Using these cutoff scores, we determined the prevalence for FSD, low desire, arousal disorder, lubrication disorder, orgasm disorder, and sexual pain to be 37.6%, 23.6%, 25.4%, 36.8%, 30.6%, and 21.8% in urban Chinese women, respectively. Conclusions The present data may suggest that urban Chinese women might have a lower FSD prevalence than women from some other countries; however, further study to achieve a better understanding of its epidemiology in China is a high necessity.

Hepatitis B virus (HBV) is considered a “metabolic virus” and affects many hepatic metabolic pathways. However, how HBV affects lipid metabolism in hepatocytes remains uncertain yet. Accumulating clinical studies suggested that compared to non-HBV-infected controls, chronic HBV infection was associated with lower levels of serum total cholesterol and triglycerides and a lower prevalence of hepatic steatosis. In patients with chronic HBV infection, high ALT level, high body mass index, male gender, or old age was found to be positively correlated with hepatic steatosis. Furthermore, mechanisms of how HBV infection affected hepatic lipid metabolism had also been explored in a number of studies based on cell lines and mouse models. These results demonstrated that HBV replication or expression induced extensive and diverse changes in hepatic lipid metabolism, by not only activating expression of some critical lipogenesis and cholesterolgenesis-related proteins but also upregulating fatty acid oxidation and bile acid synthesis. Moreover, increasing studies found some potential targets to inhibit HBV replication or expression by decreasing or enhancing certain lipid metabolism-related proteins or metabolites. Therefore, in this article, we comprehensively reviewed these publications and revealed the connections between clinical observations and experimental findings to better understand the interaction between hepatic lipid metabolism and HBV infection. However, the available data are far from conclusive, and there is still a long way to go before clarifying the complex interaction between HBV infection and hepatic lipid metabolism.

α-Galactosylceramide (α-GalCer)-activated natural killer T (NKT) cells have antiviral properties against hepatitis B virus (HBV). However, α-GalCer activation of NKT cells can induce anergy. We hypothesized that this effect may be overcome by a treatment strategy that includes manipulation of CD28/CD80 costimulatory and PD-1/PDL1 coinhibitory signals of NKT cells, thereby enhancing the anti-HBV effect of α-GalCer. We established a transgenic mouse model of chronic HBV infection and investigated hepatic NKT cell frequencies, functions and expression of immunomodulatory factors. Our results showed that compared with uninfected control mice, hepatic NKT cells from HBV transgenic mice displayed lower frequencies (7.91% vs 16.74%, P < 0.05), impaired capabilities to produce interferon (IFN)-γ (5.6% vs 1.4%, P < 0.05) and interleukin (IL)-4 (6.8% vs 0.3%, P < 0.05), higher expression of PD-1 (9.64% vs 6.36%, P < 0.05) and lower expression of CD28 (5.05% vs 28.88%, P < 0.05). However, when hepatic mononuclear cells (MNCs) were isolated from HBV transgenic mice, α-GalCer exposure in culture remarkably upregulated both PD-1(+) NKT cells (P < 0.05) and CD28(+) NKT cells (P < 0.05). Furthermore, when HBV transgenic mice were treated with combination therapies consisting of α-GalCer and anti-PDL1 monoclonal antibody (mAb) and/or anti-CD80/anti-CD28 mAbs, IFN-γ(+) NKT cell frequency was selectively increased (P < 0.05) and HBV replication was suppressed; these effects were accompanied by varying degrees and types of liver damage. Surprisingly, activating CD28/CD80 signal in HBV transgenic mice was more effective but caused less liver injury than blocking PD-1/PDL1 signal in modulating αGalCer-activated NKT cell function to inhibit HBV infection. Our findings also show that combined therapy with blocking PD-1/PDL1 and activating CD28/CD80 signal in the presence of aGalCer cannot superimpose the effect of antivirus. α-GalCer combination therapy that modulates the CD28/CD80 pathways of NKT cells may represent a promising approach to inhibit HBV replication in chronically infected patients.

These results suggest that γδ T cells might participate in liver injury in HBV-ACLF patients by producing increased amounts of inflammatory cytokines and/or cytotoxicity ability. These findings provide novel information regarding the pathogenesis of HBV-ACLF.