41. The causative agents of viral hepatitis (HAV, HBV, HCV, HDV, HEV). Characteristics. Pathogenesis and immunity. Specific prophylaxis.

Hepatitis A Virus (HAV)

• RNA virus, non-enveloped, from Picornaviridae
• Stable in environment; resistant to heat and acid
• Transmitted via fecal-oral route (contaminated water/food)
• Short incubation: 2–6 weeks
• Clinical course:
• Self-limiting acute hepatitis
• No chronicity
• Fever, malaise, anorexia → jaundice, hepatomegaly
• Diagnosis: anti-HAV IgM (acute), IgG (past infection or vaccine)
• Prevention: Inactivated vaccine, hygiene

Hepatitis B Virus (HBV)

• Partially double-stranded DNA virus, enveloped
• Unique reverse transcriptase activity (but is a DNA virus)
• Transmission: blood, sexual contact, perinatal
• Incubation: 4–12 weeks
• Pathogenesis:
• Damage is immune-mediated (CD8+ T cells attacking infected hepatocytes)
• Can cause chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC)
• Serology:
• HBsAg = infection
• anti-HBs = immunity
• anti-HBc IgM = acute infection
• anti-HBc IgG = prior exposure
• HBeAg = active replication/high infectivity
• Prevention:
• Recombinant vaccine (HBsAg)
• Neonatal prophylaxis: vaccine + HBIG
• Treatment: Tenofovir, Entecavir, Peg-IFN-α

Hepatitis C Virus (HCV)

• RNA virus, enveloped, from Flaviviridae
• High genetic variability → no vaccine
• Transmission: bloodborne (transfusions, IVDU, less sexual)
• Incubation: 6–12 weeks
• Frequently asymptomatic, but >80% become chronic
• Long-term risks: chronic hepatitis, cirrhosis, HCC
• Diagnosis: Anti-HCV Ab (screening), HCV RNA (confirmatory)
• Treatment:
• Direct-acting antivirals (DAAs) – e.g., Sofosbuvir + Velpatasvir
• Curative in >95% cases