Hepatitis Viruses

At least five hepatitis viruses (A, B, C, D, and E) infect hepatocytes, causing inflammation of the liver. Despite belonging to different families with distinct genomes, all share common clinical features: nausea, vomiting, fever, abdominal pain, dark urine, and jaundice. Clinical diagnosis alone is unreliable; laboratory testing is essential. An estimated 354 million people worldwide live with chronic HBV or HCV infection.

Hepatitis A (HAV) and E (HEV) cause acute self-limiting disease only, transmitted via the faecal-oral route. HAV is a picornavirus with a linear RNA genome. Vaccines are available for HAV. Hepatitis D (HDV) is a satellite virus requiring the HBV envelope for transmission; it exists only in HBV-infected individuals.

Hepatitis B virus (HBV) is an enveloped hepadnavirus with a partially double-stranded circular DNA genome. HBV replicates through reverse transcription. Most adults clear acute HBV infection; 90% of perinatally infected neonates develop chronic infection. Chronic HBV leads to a cycle of inflammation, cirrhosis, and hepatocellular carcinoma (HCC). Antiviral treatment includes bulevirtide (Myrucludex B / Hepcludex), which blocks HBV entry into hepatocytes, and nucleoside/nucleotide analogues (e.g., tenofovir, entecavir) targeting reverse transcriptase. Vaccines against HBV (and thus HDV) are highly effective.

Hepatitis C virus (HCV) is an enveloped flavivirus with a positive-sense, single-stranded RNA genome. HCV encodes a single polyprotein cleaved by host and viral proteases (NS3/4A) into functional proteins; NS5B is the RNA-dependent RNA polymerase; NS5A is involved in viral assembly. Approximately 75 to 85% of acute HCV infections become chronic. Combination direct-acting antivirals (DAAs) such as glecaprevir/pibrentasvir (Maviret) achieve cure rates exceeding 95% across all HCV genotypes. Drug name suffixes: -previr (NS3/4A protease inhibitors), -buvir (NS5B polymerase inhibitors), -tasvir (NS5A inhibitors). No vaccine is available for HCV.