HBV

HBV is a partially double-stranded circular DNA virus with a reverse transcriptase-dependent replication cycle, making it unique among DNA viruses. It is transmitted parenterally, sexually, and vertically (mother-to-child, especially high risk with active viral replication). After exposure, HBV can cause acute hepatitis (often subclinical in adults but with higher chronicity risk in neonates and infants) or progress to chronic hepatitis (defined as HBsAg positivity >6 months), which increases risk for cirrhosis and hepatocellular carcinoma (HCC) even without cirrhosis, due to direct oncogenic integration of viral DNA into the host genome.

Key serologic markers (high-yield for boards): - HBsAg: surface antigen; indicates active infection (acute or chronic) - Anti-HBs: antibody to surface antigen; indicates immunity (from vaccination or resolved infection) - HBcAg/Anti-HBc (IgM vs IgG): core antigen not detectable in serum, but anti-HBc IgM indicates recent infection (window period marker), IgG indicates past or chronic infection - HBeAg: marker of active viral replication and high infectivity - Anti-HBe: seroconversion marker, indicates lower replication/infectivity

Clinical extrahepatic manifestations include polyarteritis nodosa, membranous glomerulonephritis, and cryoglobulinemia (immune complex-mediated).

Treatment: Nucleos(t)ide analogs (e.g., tenofovir, entecavir) or pegylated interferon-alfa for chronic HBV. Acute HBV is typically supportive care only.

Prevention: HBV vaccine (recombinant HBsAg) is part of routine childhood immunization; post-exposure prophylaxis with HBIG plus vaccine for perinatal exposure or needlestick injuries.

High-yield boards testing points: interpreting serologic panels (e.g., differentiating vaccinated vs. naturally immune vs. chronic carrier vs. window period), associations with HCC and polyarteritis nodosa, and vertical transmission risk reduction strategies.