Emerging treatments
Experimental therapies
Several novel treatments are in development including small molecule drugs, next-generation nucleoside/nucleotide analogues with reduced toxicity and higher barriers to resistance, direct-acting antivirals (e.g., core inhibitors, entry inhibitors, nucleic acid polymers, capsid assembly modulators, translation inhibitors), and therapeutic vaccines.[144] Gene therapy has also shown promise, and different strategies have been used including gene editing, hepatitis B virus-specific gene silencing, and nucleic acid-based vaccination.[145] New drug classes such as entry inhibitors (e.g., bulevirtide), prenylation inhibitors (e.g., lonafarnib), and nucleic acid polymers show promise for the treatment of hepatitis B/hepatitis D co-infection.[146] Other drugs in development include REP 2139 (hepatitis B surface antigen inhibitor); selgantolimod, CB06, and GSK 5251738 (toll-like receptor-8 agonists); ruzotolimod and PRTX007 (toll-like receptor-7 agonists); xalnesiran, imdurisan, BW-20507, ALG-125755, BB-103, JNJ-3989, and VIR-2218 (RNAi gene silencers); cledvudine 3 (HBV polymerase inhibitor); ZM-H1505R, ALG-000184, ABI-H4334, and EDP-514 (capsid or core inhibitors); bepirovirsen and AHB-137 (antisense molecules); envafolimab, RG6084, and AB-101 (checkpoint inhibitors); and VIR-3434, burfiralimab, BJT-778, and RG6449VIR-3434, burfiralimab, BJT-778, and RG6449 (monoclonal antibody).[147]
Statins
Statin use has been associated with a decreased incidence of cirrhosis and hepatocellular carcinoma (HCC) in patients with viral hepatitis. One systematic review found that use of statins was associated with a 42% reduction in the risk of cirrhosis, with the protective effect more pronounced in Asian countries.[148] A Swedish cohort study of over 16,000 patients found that patients who used lipophilic statins (e.g., atorvastatin, simvastatin, fluvastatin, lovastatin) had a lower 10-year cumulative incidence of hepatocellular carcinoma (3.3%) compared to patients who do not take statins (8.1%). However, the same effect was not seen with hydrophilic statins. Ten-year mortality rates were significantly lower with both types of statins.[149] A large meta-analysis including over 195,000 patients with chronic viral hepatitis found that the risk of HCC, fibrosis, and cirrhosis decreased by 53%, 45%, and 41% respectively, in statin users compared with those not using statins. Overall mortality rates did not differ between groups, although there was a 39% reduction in mortality in statin users who were followed up for more than 3 years. The review found no significant reduction in liver function related to statin therapy.[150] Other meta-analyses also support the finding that statins reduce the risk of HCC in patients with HBV infection.[151]
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