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Viral hepatitis is an infection caused by hepatotropic viruses that leads to liver inflammation and may progress from a prolonged asymptomatic phase to decompensated liver disease. Among the main types, hepatitis A (HAV), B (HBV), and C(HCV) are most common, with HBV being the most widespread worldwide. Both HBV and HCV contribute substantially to global morbidity and mortality. However, HBV accounts for the most significant burden of chronic infections and associated complications, including cirrhosis and hepatocellular carcinoma (HCC). HBV infection is one of the leading causes of HCC globally. The chronically infected individuals face a lifetime risk of up to 25% of developing liver cancer, which progresses from cirrhosis and is affected by many comorbidities. Clinical and epidemiological studies, including research from our group, have shown that alcohol consumption in HBV-infected people speeds up disease progression, increases viral replication, and worsens liver damage. Heavy alcohol use is a major cofactor that significantly raises the risk of HCC in patients with HBV-related cirrhosis. Despite this well-established link, the safe level of alcohol consumption for HBV-infected patients remains unclear. Additionally, other cofactors such as viral co-infections, metabolic disorders, genetic predisposition, demographic factors, and environmental exposures interact with alcohol to influence HBV-related disease outcomes. Understanding the systemic effects of alcohol and its underlying mechanisms in HBV development is essential to defining its role as a comorbid factor in liver disease progression. This brief review highlights current knowledge and mechanistic insights into how alcohol influences HBV infection, contributes to HCC development, and acts as a comorbid factor that worsens disease severity.
Pathania et al. (Wed,) studied this question.