Hepatitis B virus (HBV) is a small DNA virus with features similar to retroviruses, belonging to the *Hepadnaviridae* family. It infects over 300 million people globally and is a major cause of liver disease and liver cancer. HBV replicates through an RNA intermediate and can integrate into the host genome, allowing persistent infection. The virus has a complex replication cycle involving the formation of infectious virions (Dane particles) and the production of various viral proteins, including HBsAg, HBeAg, and HBxAg. The HBV genome consists of four overlapping open reading frames (S, C, P, and X), which encode different viral proteins. The S ORF encodes the viral surface envelope proteins, while the C ORF encodes the core protein and HBeAg. The P ORF encodes the polymerase, which is essential for viral replication, and the X ORF encodes HBxAg, a multifunctional protein involved in viral replication and oncogenesis. HBV infection leads to a wide spectrum of liver disease, ranging from acute hepatitis to chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). Acute HBV infection is often asymptomatic in adults, with most recovering, but 5–10% develop chronic infection. Chronic HBV infection can result in severe liver disease, requiring monitoring and treatment. Extrahepatic manifestations of HBV infection, such as serum-sickness-like syndrome, acute necrotizing vasculitis, membranous glomerulonephritis, and Gianotti-Crosti syndrome, are rare but can be difficult to diagnose and manage. HBV diagnosis involves serological and virological markers, including HBsAg, HBeAg, anti-HBe, and HBV DNA. HBV DNA testing is crucial for assessing viral replication and guiding treatment decisions. Acute liver failure due to HBV is rare but can be severe, requiring immediate medical intervention. Chronic HBV infection has a variable course, with some patients progressing to cirrhosis and HCC. The prognosis of chronic HBV infection depends on factors such as viral load, genotype, and host immune response. Future research is needed to understand the mechanisms of HBV infection, the immune response to chronic infection, and the genetic basis of disease outcomes. These areas are critical for developing better diagnostic tools, treatments, and prevention strategies for HBV infection.Hepatitis B virus (HBV) is a small DNA virus with features similar to retroviruses, belonging to the *Hepadnaviridae* family. It infects over 300 million people globally and is a major cause of liver disease and liver cancer. HBV replicates through an RNA intermediate and can integrate into the host genome, allowing persistent infection. The virus has a complex replication cycle involving the formation of infectious virions (Dane particles) and the production of various viral proteins, including HBsAg, HBeAg, and HBxAg. The HBV genome consists of four overlapping open reading frames (S, C, P, and X), which encode different viral proteins. The S ORF encodes the viral surface envelope proteins, while the C ORF encodes the core protein and HBeAg. The P ORF encodes the polymerase, which is essential for viral replication, and the X ORF encodes HBxAg, a multifunctional protein involved in viral replication and oncogenesis. HBV infection leads to a wide spectrum of liver disease, ranging from acute hepatitis to chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). Acute HBV infection is often asymptomatic in adults, with most recovering, but 5–10% develop chronic infection. Chronic HBV infection can result in severe liver disease, requiring monitoring and treatment. Extrahepatic manifestations of HBV infection, such as serum-sickness-like syndrome, acute necrotizing vasculitis, membranous glomerulonephritis, and Gianotti-Crosti syndrome, are rare but can be difficult to diagnose and manage. HBV diagnosis involves serological and virological markers, including HBsAg, HBeAg, anti-HBe, and HBV DNA. HBV DNA testing is crucial for assessing viral replication and guiding treatment decisions. Acute liver failure due to HBV is rare but can be severe, requiring immediate medical intervention. Chronic HBV infection has a variable course, with some patients progressing to cirrhosis and HCC. The prognosis of chronic HBV infection depends on factors such as viral load, genotype, and host immune response. Future research is needed to understand the mechanisms of HBV infection, the immune response to chronic infection, and the genetic basis of disease outcomes. These areas are critical for developing better diagnostic tools, treatments, and prevention strategies for HBV infection.