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Double-stranded linear DNA (dslDNA), considered to serve as a major precursor to integrated HBV DNA (iDNA), is generally located in the livers of patients with chronic HBV infection. Prior research has primarily focused on the role and mechanisms of HBV integration in the progression of hepatocellular carcinoma (HCC), demonstrating that iDNA can lead to genomic instability in the host and induce aberrant expression of host tumor-related genes around the integration sites, while viral proteins expressed by iDNA exhibit tumor-promoting effects. In recent years, the impact of iDNA-derived hepatitis B surface antigen on antiviral therapy in patients with chronic hepatitis B has received increasing attention with a deeper understanding of integrated HBV DNA. Consequently, the field has become a research hotspot and challenge in determining how to eliminate or silence iDNA to improve functional cure in patients with chronic hepatitis B. This paper aims to provide new sights to the clinical significance of iDNA and a theoretical basis for optimizing antiviral therapy strategies by summarizing the occurrence mechanisms of iDNA and its impact on the onset and progression of hepatocellular carcinoma and antiviral therapy for patients with chronic hepatitis B.