Viral Hepatitis A, B, C, D, E: Diagnosis and Treatment

1. Comparison of hepatitis viruses

2. Hepatitis A

• Incubation period 15–50 days (average 28).
• Clinical presentation: prodrome (fever, ARVI-like symptoms, dyspepsia) → icteric phase (choluria, acholia, jaundice) → convalescence.
• In children, anicteric forms are more common.
• Diagnostics: IgM anti-HAV (acute), IgG anti-HAV (immunity/past infection).
• Treatment is supportive; does not become chronic.
• Fulminant form < 0.5%.
• Vaccine: 2 doses (0 and 6–12 months), efficacy > 95%.

3. Hepatitis B — markers

4. Hepatitis B — phases of chronic infection (EASL 2017)

• HBeAg+ chronic infection ("immune tolerant"): HBeAg+, DNA very high, ALT normal.
• HBeAg+ chronic hepatitis: HBeAg+, DNA high, ALT ↑.
• HBeAg− chronic infection ("inactive carrier"): anti-HBe+, DNA < 2000 IU/mL, ALT normal.
• HBeAg− chronic hepatitis: anti-HBe+, DNA > 2000, ALT ↑ (frequent precore mutants).
• HBsAg− ("occult"): HBsAg−, anti-HBc+, DNA in the liver.

5. Management of hepatitis B

• Indications: ALT > 2 ULN + DNA > 2000 IU/mL; F ≥ 2 by biopsy or elastography; all decompensated patients; all candidates for immunosuppression or chemotherapy.
• First-line drugs: tenofovir disoproxil (TDF), tenofovir alafenamide (TAF), entecavir (ETV) — high barrier to resistance.
• Peg-IFN-α is an alternative in young patients with HBeAg+ and low DNA, for 48 weeks.
• Cessation criteria: HBsAg seroconversion (rare) or sustained DNA suppression with HBeAg seroconversion.
• Monitoring: DNA every 3–6 months, AFP + liver ultrasound every 6 months (HCC screening).

6. Hepatitis D

• Defective virus — uses HBsAg as an envelope.
• Coinfection (simultaneous with HBV) — usually acute course.
• Superinfection (on top of chronic HBV) — rapid progression to cirrhosis (50% in 5 years).
• Diagnostics: anti-HDV IgM/IgG, HDV RNA.
• Treatment: peg-IFN-α for 48 weeks (low efficacy); bulevirtide (Hepcludex) — a novel entry inhibitor.

7. Hepatitis C — diagnostics

• Screening: anti-HCV (EIA).
• Confirmation of active infection: HCV RNA (PCR).
• Genotyping (1–6) — influences regimen selection, although its significance is decreasing with pangenotypic regimens.
• Fibrosis assessment: elastography (FibroScan), APRI, FIB-4.
• Screening: all HIV+, individuals with parenteral risk factors, born 1945–1965, before chemotherapy and immunosuppression.

8. Hepatitis C — treatment (DAAs)

• Direct-acting antivirals (DAAs).
• Pangenotypic regimens (EASL 2020, AASLD 2023):
• — Sofosbuvir + velpatasvir for 12 weeks.
• — Glecaprevir + pibrentasvir for 8 weeks (without cirrhosis) or 12 weeks (with compensated cirrhosis).
• Regimens for decompensation: sofosbuvir + velpatasvir ± ribavirin for 12–24 weeks.
• Cure criterion: SVR12 — undetectable HCV RNA at 12 weeks post-treatment.
• DAA efficacy > 95% regardless of genotype.

9. Hepatitis E

• Genotypes 1, 2 — fecal-oral, epidemic outbreaks in developing countries.
• Genotypes 3, 4 — zoonotic (pigs, deer), sporadic in Europe.
• Feature: in pregnant women (3rd trimester) — fulminant form with mortality up to 20%.
• Chronification — only in immunosuppression (transplantation, HIV).
• Diagnostics: IgM anti-HEV (acute), IgG anti-HEV, HEV RNA in serum and stool.
• Treatment of acute — symptomatic; of chronic — ribavirin for 12 weeks.

10. Complications of chronic hepatitis

• Liver cirrhosis — 20–30% after 20 years in CHC; faster with HIV, HDV coinfection.
• Hepatocellular carcinoma (HCC) — 3–5% per year in cirrhosis associated with HBV/HCV.
• Decompensation: ascites, variceal bleeding, hepatic encephalopathy.
• Extrahepatic manifestations: cryoglobulinemia (HCV), polyarteritis nodosa (HBV), membranous glomerulonephritis.
• HCC screening: AFP + ultrasound every 6 months in all patients with cirrhosis and in HBsAg+ with family history/high DNA.

11. Prevention and vaccination

• HAV vaccine: 2 doses, children from 1 year and risk groups.
• HBV vaccine: 3 doses (0-1-6 months); in Russia — universal since 2002 under the National Immunization Schedule.
• HBV post-exposure prophylaxis: HBIG immunoglobulin + vaccine; newborns of HBsAg+ mothers — within the first 12 hours.
• HCV — no vaccine available; prevention — blood transfusion safety, harm reduction in PWID.
• Screening of pregnant women for HBsAg, anti-HCV, HIV — mandatory.

12. FAQ

How to interpret simultaneous HBsAg+ and anti-HBs+?
A rare phenomenon — either an inactive infection with inadequate anti-HBs (mutation) or a false-positive test. Requires re-testing and HBV DNA.

Can hepatitis B be completely cured?
Functional cure (HBsAg loss) is achieved in 1–5% with long-term therapy; complete virus eradication (cccDNA) is nearly impossible. The goal is long-term DNA suppression.

Why was hepatitis C previously considered incurable?
Before 2014, the standard was peg-IFN + ribavirin, with 40–60% efficacy and many side effects. With the advent of DAAs, treatment became short (8–12 weeks), oral, and > 95% effective.

What to do after an accidental needlestick injury from an HCV-infected patient?
Test the exposed person for anti-HCV/HCV RNA at 0, 3, 6 weeks. In case of seroconversion — early initiation of DAAs. There is no post-exposure prophylaxis.

Why is pregnancy dangerous in hepatitis E?
Immune changes in the 3rd trimester + estrogen-dependent virus expression → fulminant course, acute liver failure, mortality up to 15–20%.

See also: Liver cirrhosis · HCC · HIV infection · Portal hypertension · Infections catalog