Autoimmune liver diseases (AILD) constitute a spectrum of distinct chronic liver disorders characterized by the generation of reactive cells and antibodies, leading to progressive and irreversible hepatic tissue damage (Dyson et al., 2015; Horst et al., 2021). The principal subcategories of AILD comprise primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and autoimmune hepatitis (AIH) (Floreani et al., 2019; Horst et al., 2021). AILD typically manifests with a subtle onset and inconspicuous morbidity features, presenting clinical manifestations such as jaundice, pruritus, and malaise. Additionally, approximately one-third of AILD patients manifest extrahepatic autoimmune conditions, encompassing rheumatic and gastrointestinal disorders (Biewenga et al., 2020). The etiology of AILD remains elusive, implicating potential contributions from genetic factors, environmental influences, and immune responses (Ellinghaus, 2022). Among environmental determinants, viral infections have been implicated in the modification of autoantigens, thereby inciting an autoimmune response that ultimately precipitates the development of AILD.

Hepatitis B virus (HBV) infection poses a substantial global health challenge, representing a pervasive epidemic. According to the World Health Organization (WHO), the worldwide prevalence of HBsAg in the general population was 3.8% in 2019, yielding approximately 1.5 million new HBV infections, 296 million cases of chronic hepatitis B (CHB), and 820,000 fatalities attributed to liver failure, cirrhosis, hepatocellular carcinoma, and other consequential conditions stemming from HBV infection. The WHO has articulated an ambitious global elimination strategy for viral hepatitis, with the aim of eradicating viral hepatitis as a public health concern by 2030 (Jeng et al., 2023). A substantial body of literature has explored the nexus between AILD and viral infections, with observational investigations linking Epstein-Barr virus to AILD (Bolia and Srivastava, 2022; Nayagam et al., 2022). Moreover, AILD has been intimately associated with hepatotropic viruses. Some observational studies have suggested that HBV infection may confer a protective role in certain autoimmune diseases (Ram et al., 2008). Multiple studies have demonstrated a reduction in HBV infection among patients with AIH (Czaja et al., 1993; Maya et al., 2008). Relevant instances where HBV infection and AIH intersect are scant (Maya et al., 2008; Murakami et al., 1996; Tseng et al., 2008). In hence, there is insufficient evidence to elucidate the role of HBV infection in the pathogenesis of AILD. In summary, the causal relationship between AILD and HBV remains unclear.

The Mendelian randomization (MR) approach is an invaluable methodology for assessing potential causal relationships between exposures and outcomes. This technique remains impervious to confounding factors, as the instrumental variables (IVs) selected are exclusively associated with the outcomes. MR finds application in estimating causal associations in medical domains such as neoplasms, cardiovascular diseases, and psychiatry where randomized controlled trials are impractical (Emdin et al., 2017; Hólm et al., 2020; Papiol et al., 2021). In this investigation, a two-sample MR was employed to scrutinize the causal connection between AILD and CHB, incorporating a series of sensitivity analyses.