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Hepatitis B virus (HBV) infection is a major public health problem, with an estimated 296 million people chronically infected and 820 000 deaths worldwide in 2019. Diagnosis of HBV infection requires serological testing for HBsAg and for acute infection additional testing for IgM hepatitis B core antibody (IgM anti-HBc, for the window period when neither HBsAg nor anti-HBs is detected). Assessment of HBV replication status to guide treatment decisions involves testing for HBV DNA, whereas assessment of liver disease activity and staging is mainly based on aminotransferases, platelet count, and elastography. Universal infant immunisation, including birth dose vaccination is the most effective means to prevent chronic HBV infection. Two vaccines with improved immunogenicity have recently been approved for adults in the USA and EU, with availability expected to expand. Current therapies, pegylated interferon, and nucleos(t)ide analogues can prevent development of cirrhosis and hepatocellular carcinoma, but do not eradicate the virus and rarely clear HBsAg. Treatment is recommended for patients with cirrhosis or with high HBV DNA levels and active or advanced liver disease. New antiviral and immunomodulatory therapies aiming to achieve functional cure (ie, clearance of HBsAg) are in clinical development. Improved vaccination coverage, increased screening, diagnosis and linkage to care, development of curative therapies, and removal of stigma are important in achieving WHO's goal of eliminating HBV infection by 2030. [ABSTRACT FROM AUTHOR]

Background and Aim: In HBeAg negative chronic hepatitis B (CHB) patients, clinical relapse (CR) occurs more frequently, much earlier and often more severely after stopping tenofovir (TDF) and other nucleos(t)ide analogues (Nucs) than after stopping entecavir (ETV). It is unknown whether off‐Nuc hepatitis flare can be alleviated by switching from one Nuc to another. Methods: HBeAg‐negative CHB patients who had stopped Nuc according to the APASL stopping rule and had been followed‐up for > 48 weeks after Nuc cessation were recruited. Patients were classified as four groups: ETV monotherapy (mono‐ETV), TDF monotherapy (mono‐TDF), switched to ETV (switch‐ETV), and switched to TDF (switch‐TDF). Both switch groups had switched to the replacement Nuc > 12 weeks prior to end of therapy. Propensity score matching (PSM) was performed to minimize confounders among groups. Cox regression analysis was used to identify risks factors for off‐Nuc CR and flares. Results: A total of 1309 patients (1022 mono‐ETV, 219 mono‐TDF, 40 switch‐ETV and 28 switch‐TDF) were enrolled. The median time to CR was 39, 13, 38 and 14 weeks in mono‐ETV, mono‐TDF, switch‐ETV and switch‐TDF respectively (P < 0.001). After PSM, the mono‐ETV (adjusted HR: 0.39, P < 0.001) and switch‐ETV patients (adjusted HR: 0.41, P = 0.003) had both significantly later occurrence and lower rates of CR and flare. Conclusion: In summary, the incidence and timing of CR was determined by ETV or TDF in the last 3 months prior to end of treatment. Patients treated with non‐ETV‐Nuc switched to ETV > 12 weeks before end of the original Nuc therapy may reduce/defer CR. [ABSTRACT FROM AUTHOR]

Background: Off-therapy hepatitis flare may be detrimental or, conversely, facilitate hepatitis B surface antigen (HBsAg) decline. Retreatment decisions are crucial.Methods: HBsAg was quantified before and during flares, at peak/retreatment start and at Months 6 and 12 in 336 entecavir/tenofovir-retreated and 105 non-retreated hepatitis B e antigen (HBeAg)-negative patients. Increasing HBsAg during ALT flare defined a 'virus-dominating flare' and decreasing HBsAg a 'host-dominating flare'.Results: Two hundred and eighty-eight retreated patients with a virus-dominating flare showed greater 1 year HBsAg decline (-1.0 versus -0.01 log10 IU/mL; P < 0.0001), more frequent rapid decline (69.8% versus 8.3%; P < 0001) and higher 3 year incidence of HBsAg < 100 IU/mL (32% versus 12%; P = 0.026) than 48 patients with a host-dominating flare, of whom 16 (33.3%) showed 3.8-fold (2 to 52-fold) HBsAg rebound on retreatment (versus 2/288; P < 0.0001). Compared with non-retreated controls, 1 year HBsAg decline was greater (-1.0 versus -0.47 log10 IU/mL; P < 0.0001) and faster (69.8% versus 42.5%; P < 0.0001) in patients with a virus-dominating flare, whereas 1 year HBsAg decline (-0.01 versus -0.16 log10 IU/mL) and 3 year HBsAg loss rate (0% versus 21%; P = 0.009) were lower in patients with a host-dominating flare.Conclusions: Entecavir/tenofovir retreatment effectively decreases HBsAg level in patients with a virus-dominating flare but is ineffective/worse in patients with a host-dominating flare. These results support the use of combined HBsAg/ALT kinetics for the decision to retreat patients with a virus-dominating flare and withhold retreatment for patients with a host-dominating flare. [ABSTRACT FROM AUTHOR]

The article presents a review of the article, "``The role of quantitative hepatitis B surface antigen revisited," along with a discussion on the role played by Serum HBsAG in the clinical prediction of Hepatitis B virus. Details related to the medical studies used, along with the findings of the study are discussed.

Background/Aims: Novel agents acting against hepatitis B virus (HBV) are needed to improve HBsAg seroclearance or termed as 'functional cure'. Inarigivir (retinoic acid‐inducible gene I agonist) has immunomodulatory and direct antiviral actions against HBV. We aimed to determine the safety and efficacy of Inarigivir for the treatment of HBV infection. Patients/Methods: 80 treatment‐naïve patients were randomized in 4 ascending dose cohorts to receive 12 weeks of Inarigivir 25, 50, 100, 200 mg or placebo in a ratio of 4:1. All patients were then given tenofovir for another 12 weeks. Results: Least squares (LS) mean reductions in HBV DNA from baseline increased with higher doses of Inarigivir (0.6116 in 25 mg and 1.5774 in 200 mg groups vs. 0.0352 in placebo group) (95% CI 0.9518–0.2011 and 1.921–1.1634 respectively). LS mean changes in HBV RNA and HBsAg from baseline ranged from −0.3856 to −0.5794 versus −0.1474 and −0.0956 to −0.1818 versus +0.0026 in Inarigivir‐treated versus placebo groups respectively. During the tenofovir‐treated period, LS mean reductions in HBsAg in the Inarigivir‐treated groups ranged from 0.1709 to 0.3529 versus 0.1984 in the placebo group. Inarigivir‐treated groups showed mean reductions in ALT from baseline between 23.3 and 33.8 versus 0.7 U/L in the placebo group. Treatment‐emergent adverse events related to Inarigivir and placebo occurred in 4.7% and 6.3% patients respectively. Conclusions: Twelve‐week Inarigivir up to 200 mg dose was associated with a reduction of HBV DNA, HBV RNA and antigen levels. A trend for greater HBsAg reduction was observed in Inarigivir pre‐treated patients after switching to tenofovir. [ABSTRACT FROM AUTHOR]

Introduction: High sustained virological response (SVR) rate (>95%) and liver stiffness regression can be achieved with direct acting antivirals treatment (DAA) in patients with chronic hepatitis C virus (CHC) infection. Reactivation of hepatitis B virus (HBV) was reported during DAA treatment in patients co-infected with HBV, although its impact on liver stiffness remains unknown. This study aims to investigate whether the liver stiffness (LSM) regression is different between HBV/HCV co-infected and mono-HCV-infected patients. Materials and Methods: CHC patients with/without HBV co-infection who received DAA treatment and achieved SVR12 between March 2015 and December 2019 in Chang Gung Memorial Hospital, Linkou branch were prospectively enrolled. LSM was assessed by transient elastography (TE, Fibroscan) at baseline and after SVR. Propensity score matching (PSM) at 3:1 ratio, adjusted for age, gender, pre-DAA alanine aminotransferase (ALT), platelet count, and LSM, between CHC with and without HBV co-infection, was performed before further analysis. Results: Among 906 CHC patients enrolled, 52 (5.7%) patients had HBV/HCV co-infection. Patients with HBV/HCV co-infection were of younger age (61.8 vs. 63.2, p = 0.31), with a higher proportion of males (53.8% vs. 38.9%, p = 0.03), and lower pretreatment LSM level (8.15 vs. 10.2 kPa, p = 0.09), while other features were comparable. After PSM, patients with HBV/HCV co-infection had insignificantly lower LSM regression compared to mono-HCV-infected patients (−0.85 kPa vs. −1.65 kPa, p = 0.250). Conclusions: The co-infection of HBV among CHC patients has limited impact on liver stiffness regression after successful DAA treatment. [ABSTRACT FROM AUTHOR]