Viral Hepatitis

Overview

5 unrelated viruses, shared hepatocyte tropism. Key organizing distinction: transmission route. A+E = feco-oral, ACUTE ONLY. B+C+D = blood-borne/parenteral/sexual, CAN BE CHRONIC.

Hepatitis A (HAV)

Non-enveloped picornavirus (RNA). Feco-oral (food/water). Severity ↑ with age at infection (children often subclinical, adults more symptomatic/rarely fulminant). NEVER CHRONIC (contrast B/C/D) — robust immune clearance, no integration/persistence. Diagnosis: IgM anti-HAV (acute/recent) vs IgG anti-HAV (past infection/vaccination, lifelong immunity). Vaccine: safe, effective, inactivated, national schedules.

Hepatitis B (HBV)

Partially dsDNA hepadnavirus. Parenteral, sexual, VERTICAL (mother-child, esp. delivery). CHRONICITY RISK BY ACQUISITION AGE: Perinatal >90% chronic. Adult ~5% chronic. Paradox: MILDEST-appearing (infant, rarely symptomatic) = HIGHEST long-term risk (immature immune system can’t clear).

Serological markers (interpret TOGETHER, not alone):

• HBsAg: current infection (acute or chronic)
• Anti-HBs: immunity (resolved infection OR vaccination)
• HBcAg: NOT detectable serum (intracellular only)
• Anti-HBc IgM: recent acute infection
• Anti-HBc IgG: persists indefinitely, ANY past infection — distinguishes TRUE past infection from vaccine immunity (vaccine = HBsAg subunit only, NEVER generates anti-HBc)
• HBeAg: active replication, high infectivity
• Anti-HBe: seroconversion, lower replication/infectivity (EXCEPTION: precore mutant strains replicate actively while HBeAg-negative — diagnostic trap)
• HBV DNA (viral load): guides treatment, monitors response

Chronic HBV → cirrhosis + HCC. NOTABLE: HBV drives carcinogenesis via DIRECT GENOME INTEGRATION (not just chronic inflammation pathway other causes use).

Treatment: nucleos(t)ide analogues (tenofovir, entecavir) or peg-interferon. NO CURE eliminating cccDNA — suppression not eradication typically. Vaccine: recombinant HBsAg, universal infant immunization. BIRTH DOSE critical for perinatal transmission prevention (see NIS, Vaccines topic) + HBIG for HBsAg+ mother’s neonate (see Needle Stick Injury topic).

Hepatitis C (HCV)

Enveloped +ssRNA flavivirus. Parenteral (historically transfusion, now IDU-dominant), less-efficient sexual/vertical. DEFINING FEATURE: HIGH CHRONICITY (55-85% acute→chronic) — high mutation rate, continuous immune evasion via antigenic variation. Most acute infection SUBCLINICAL → chronic HCV often diagnosed INCIDENTALLY, years-decades later (cirrhosis/HCC already present).

Diagnosis: anti-HCV Ab (screen) → HCV RNA (confirms ACTIVE infection, distinguishes from resolved-with-persistent-Ab).

Treatment: DAAs (Direct-Acting Antivirals) — oral, >95% CURE RATE, 8-12wk. Dramatic improvement over old interferon regimens. NO VACCINE (same antigenic variation challenge drives chronicity AND blocks vaccine development).

Hepatitis D (HDV)

UNIQUE defective RNA virus — CANNOT replicate/make virions alone, needs HBsAg (borrowed from HBV) for envelope. ONLY occurs WITH HBV, never alone.

Coinfection (HBV+HDV simultaneous): follows acute HBV course, HIGHER fulminant hepatitis risk than HBV alone. Superinfection (HDV on pre-existing chronic HBV): MORE severe acute disease + SUBSTANTIALLY higher chronic HDV progression (HBsAg production already established/ongoing).

HBV VACCINATION PREVENTS HDV (elegant public health point — HDV depends entirely on HBV).

Hepatitis E (HEV)

Non-enveloped +ssRNA. Feco-oral (water = classic outbreak vehicle), ALSO ZOONOTIC (undercooked pork/game, some genotypes — distinctive among hepatitis viruses). Resembles HAV: acute-only, self-limited generally.

CRITICAL EXCEPTION: PREGNANCY → dramatically ↑ fulminant hepatic failure + maternal mortality risk (up to 20-25% 3rd trimester, some endemic series). Real specific danger NOT shared by HAV — changes counseling/risk-stratification.

Comparison Table

Five Distinct Viruses, One Shared Target Organ

“Viral hepatitis” describes liver inflammation caused by five genuinely unrelated virus families (hepatitis A through E) that share almost nothing in common except their shared tropism for hepatocytes — different genome types, different transmission routes, and dramatically different capacity to cause chronic infection. Transmission route predicts most of what matters clinically across all five: A and E are faeco-oral (acute-only, essentially never chronic), while B, C, and D are blood-borne/parenteral/sexual (all capable of chronic infection).

Hepatitis A Virus (HAV)

A non-enveloped picornavirus (RNA), transmitted faeco-orally via contaminated food/water, with disease severity rising sharply with age at infection — infection in young children is frequently subclinical, while adult infection is far more likely to be symptomatic and, rarely, fulminant. HAV causes only acute infection, never chronicity — a genuinely important point of contrast with B/C/D, reflecting the virus’s biology (it does not integrate or establish persistence, and a robust immune response typically clears it completely within weeks to a few months). Diagnosis rests on IgM anti-HAV (confirming acute/recent infection) versus IgG anti-HAV (confirming past infection or vaccination, and lifelong immunity thereafter). A safe, effective inactivated vaccine exists and is part of many national immunization schedules.

Hepatitis B Virus (HBV)

A partially double-stranded DNA hepadnavirus, transmitted parenterally (blood, needle-sharing), sexually, and vertically (mother-to-child, particularly efficient and clinically important at delivery) — the route and age of acquisition strongly predict chronicity risk, worth fixing precisely: perinatal infection carries a >90% risk of chronicity, while adult-acquired infection carries only a ~5% risk, reflecting the immature neonatal immune system’s inability to mount the vigorous cytotoxic T-cell response needed to clear the virus, which paradoxically means the mildest-appearing acute infections (in infants, who are rarely symptomatic) carry the highest long-term risk.

Serological markers are the cornerstone of HBV diagnosis and staging, and interpreting the pattern together (not any single marker alone) is what actually tells the clinical story: HBsAg (surface antigen) indicates current infection, acute or chronic; anti-HBs indicates immunity, either from resolved past infection or vaccination; HBcAg is not detectable in serum (intracellular only) but anti-HBc IgM indicates recent acute infection while anti-HBc IgG persists indefinitely after any past infection (a genuinely useful marker specifically because it distinguishes true past infection from vaccine-induced immunity, since vaccination — being subunit HBsAg only — never generates anti-HBc); HBeAg indicates active viral replication and high infectivity; anti-HBe indicates seroconversion toward lower replication/infectivity (though “precore mutant” strains can replicate actively while HBeAg-negative, a genuine diagnostic trap worth knowing). HBV DNA quantification (viral load) directly guides treatment decisions and monitors response.

Chronic HBV risks progression to cirrhosis and hepatocellular carcinoma — genuinely notable in that HBV can drive carcinogenesis through direct viral genome integration into the host genome, not only through the chronic-inflammation pathway most other chronic hepatic insults use. Treatment uses nucleos(t)ide analogues (tenofovir, entecavir) or pegylated interferon for eligible chronic cases; there is no cure that eliminates the integrated viral genome (covalently closed circular DNA, cccDNA) entirely, so treatment suppresses rather than eradicates in most cases. A highly effective vaccine exists (recombinant HBsAg), given as part of universal infant immunization in most countries, with a birth dose specifically critical for preventing perinatal transmission (see National Immunization Schedule under Vaccines and Immunoprophylaxis) — combined with HBIG for neonates of HBsAg-positive mothers (see Needle Stick Injury and Standard Precautions for the same immunoglobulin used in post-exposure prophylaxis more generally).

Hepatitis C Virus (HCV)

An enveloped, positive-sense ssRNA flavivirus, transmitted predominantly parenterally (historically transfusion-associated, now dominantly injection drug use in most settings), with sexual and vertical transmission occurring but considerably less efficiently than with HBV. HCV’s defining, clinically dominant feature is its high rate of chronicity — roughly 55–85% of acute infections become chronic (in sharp contrast to HAV’s zero chronicity and HBV’s age-dependent range), reflecting the virus’s high mutation rate and consequent ability to continuously evade the developing immune response through antigenic variation. Most acute infection is subclinical, which is exactly why chronic HCV is so often diagnosed only incidentally, years to decades later, once cirrhosis or hepatocellular carcinoma has already developed. Diagnosis: anti-HCV antibody as an initial screen, confirmed by HCV RNA (which also distinguishes active infection from a resolved past infection where antibody persists but the virus has cleared). Treatment has been genuinely transformed by direct-acting antivirals (DAAs) — oral regimens now achieving >95% cure rates with 8–12 week courses, a dramatic improvement over the older interferon-based regimens’ far lower efficacy and substantial side-effect burden. No vaccine exists for HCV, reflecting the same antigenic-variation challenge that drives its chronicity.

Hepatitis D Virus (HDV)

A genuinely unique, defective RNA virus — it cannot replicate or produce infectious virions on its own, requiring HBsAg specifically (borrowed from HBV) to form its own outer envelope, which is why HDV infection can only ever occur in the presence of concurrent HBV infection, never alone. Two acquisition patterns matter: coinfection (HBV and HDV acquired simultaneously, generally following the acute HBV course, though with a higher risk of fulminant hepatitis than HBV alone) and superinfection (HDV acquired on top of pre-existing chronic HBV, generally causing more severe acute disease and a substantially higher likelihood of progression to chronic HDV, since the underlying chronic HBsAg production HDV depends on is already established and ongoing). Since HDV depends entirely on HBV, HBV vaccination itself prevents HDV infection, a genuinely elegant public-health point.

Hepatitis E Virus (HEV)

A non-enveloped, positive-sense ssRNA virus, faeco-orally transmitted (contaminated water is the classic large-outbreak vehicle, and, distinctively among the hepatitis viruses, also zoonotically transmissible via undercooked pork/game meat in some genotypes), clinically resembling HAV in most respects — acute-only, self-limited in the general population. The single genuinely critical clinical exception: HEV infection in pregnancy carries a dramatically elevated risk of fulminant hepatic failure and maternal mortality (reported as high as 20–25% in the third trimester in some endemic-region series) — a real, specific danger not shared by HAV, and worth remembering precisely, since it directly changes counselling and risk-stratification for a pregnant patient with acute hepatitis in an endemic setting.

Comparative Summary

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