Viral hepatitis !
Viral hepatitis is liver inflammation caused by the hepatitis A, B, C, D or E viruses; B, C and D can become chronic and lead to cirrhosis and liver cancer.
Updated 2026-10-30
Structures involved
Tap one to see what it is and open it in 3D.
In biochemistry
- Alanine aminotransferase (ALT, GPT)
- Aspartate aminotransferase (AST, GOT)
- Transamination and deamination
- Glucose–alanine cycle
- Liver function tests: reading the pattern
- Aminotransferases (ALT and AST) as lab tests
- Alpha-fetoprotein (AFP)
- Uroporphyrinogen decarboxylase
- Bilirubin
- ELISA (enzyme-linked immunosorbent assay)
- Isoenzymes
Microorganisms that cause it
In immunology
- Type I interferons (α, β)
- Colombia's PAI schedule (which vaccines, at what age)
- Passive immunization: immunoglobulins and antitoxins
- Serology: IgM vs IgG, seroconversion, avidity
In histology
In the clinical exam
- Palpation of the liver and spleen
- Pallor, cyanosis and jaundice
- Portal hypertension and the signs of chronic liver disease
- Jaundice: prehepatic, hepatic and posthepatic
In physiology
Why it happens
- Apoptosis: the intrinsic and extrinsic pathways
- Fibrosis in organs: TGF-β and the myofibroblast
- Liver regeneration
- Apoptosis vs necrosis: the comparison table
- Tissue repair: regeneration or scar; labile, stable and permanent cells
- Chronic inflammation: causes, cells and features
Show 4 more
What it is
Inflammation of the liver caused by the hepatotropic viruses A, B, C, D and E. It can be acute and self-limited or, for B, C and D, become chronic and lead to cirrhosis and liver cancer.
Who gets it
Hepatitis A and E spread where sanitation is poor; B and C are the main viral causes of cirrhosis and liver cancer worldwide. B and its dependent virus D are commoner in parts of the Amazon. Colombia vaccinates children against hepatitis B (from birth) and A. In Medellín, a small study found hepatitis E in 9 of 40 people (22.5%) with clinical viral hepatitis.
Causes
- Hepatitis A (RNA virus): faecal-oral, contaminated food and water; acute only
- Hepatitis B (DNA virus): blood, sexual and mother-to-child transmission; can become chronic
- Hepatitis C (RNA virus): mainly blood (injecting drugs, unsafe injections, transfusion before screening); often chronic
- Hepatitis D: needs hepatitis B to replicate; co-infection or superinfection
- Hepatitis E (RNA virus): faecal-oral, waterborne; also undercooked pork or game in some genotypes
Risk factors
- Poor sanitation and unsafe water (A, E)
- Unvaccinated status (A, B)
- Birth to a mother with hepatitis B
- Injection drug use, unsafe medical injections, needlestick injury
- Unprotected sex, multiple partners, HIV infection
- Haemodialysis, tattoos or piercing with unsterile equipment
Pathophysiology
The viruses infect hepatocytes, and most of the liver damage comes from the immune response that clears infected cells. Hepatitis B, C and D can persist, causing ongoing inflammation, fibrosis and cirrhosis. Hepatitis B DNA can integrate into the host genome, so it can cause liver cancer even without cirrhosis.
Classification
- Acute vs chronic (persisting more than six months)
- By virus: A, B, C, D, E
- Hepatitis D: co-infection with B vs superinfection of chronic B (more often severe)
- Fulminant hepatitis (acute liver failure)
Symptoms and signs
- Many infections, especially in children, are silent
- Prodrome: tiredness, nausea, loss of appetite, low fever, right upper quadrant ache
- Jaundice, dark urine and pale stools
- Tender enlarged liver
- Chronic infection is usually silent until cirrhosis develops
Diagnosis
- Clinical
- Exposure history (travel, water, sex, injections, vaccination), jaundice and liver tenderness; signs of chronic liver disease in long-standing infection.
- Tests
- Aminotransferases (often very high in acute disease), bilirubin, INR. Serology: anti-HAV IgM; for hepatitis B, HBsAg, anti-HBc (IgM in acute infection), anti-HBs (immunity), HBeAg and HBV DNA; anti-HCV with HCV RNA; anti-HDV in HBsAg-positive patients; anti-HEV IgM.
- Imaging
- Ultrasound excludes biliary obstruction and assesses the liver and spleen. Elastography stages fibrosis in chronic hepatitis.
Differential diagnosis
- Drug- or toxin-induced liver injury (including paracetamol)
- Alcohol-related hepatitis
- Autoimmune hepatitis
- Biliary obstruction (choledocholithiasis)
- Ischaemic hepatitis
- Leptospirosis, yellow fever, dengue or malaria with liver involvement
Goal of treatment
Support recovery in acute hepatitis, detect acute liver failure early, and in chronic infection suppress or cure the virus to prevent cirrhosis and liver cancer.
Treatment
- Conservative
- Acute hepatitis A and E and most acute hepatitis B: supportive care, avoidance of alcohol and hepatotoxic drugs, and monitoring.
- Acute
- Acute liver failure: hospital care, intensive support and early contact with a transplant centre.
- Medical
- Chronic hepatitis B: nucleoside or nucleotide analogues for long-term suppression, or interferon in selected patients, based on viral load, enzymes and fibrosis.
- Medical
- Chronic hepatitis C: oral direct-acting antivirals, which cure most patients after a short course.
- Medical
- Hepatitis D: interferon-based therapy; newer entry inhibitors exist in some countries. Hepatitis B treatment continues.
- Follow-up
- Chronic B and C: follow-up of liver tests, viral load and fibrosis; ultrasound surveillance for liver cancer in cirrhosis and in selected hepatitis B carriers.
Drugs for this condition
- Lamivudine
- Tenofovir disoproxil
- Tenofovir alafenamide
- Dolutegravir + lamivudine + tenofovir disoproxil (TLD)
- Entecavir
- Ribavirin
- Sofosbuvir
- Sofosbuvir + velpatasvir
- Ledipasvir + sofosbuvir
- Glecaprevir + pibrentasvir
- Interferon alfa
- Hepatitis B vaccine
- Hepatitis A vaccine
Complications
- Acute liver failure
- Chronic hepatitis, cirrhosis and portal hypertension
- Hepatocellular carcinoma
- Extrahepatic disease: glomerulonephritis, cryoglobulinaemia, polyarteritis nodosa
- Severe hepatitis E in pregnancy
Prognosis
Hepatitis A and E usually resolve fully. Most adults clear hepatitis B, but most infected newborns develop chronic infection. Hepatitis C is now curable in most patients; superinfection with hepatitis D speeds progression to cirrhosis.
Prevention
- Hepatitis B vaccination from birth, with immunoglobulin for babies of infected mothers
- Hepatitis A vaccination; safe water, sanitation and hand hygiene
- Screening of blood donors, safe injections and needle exchange
- Condom use; screening in pregnancy
- Hepatitis B vaccination also prevents hepatitis D
Test yourself
Think of the answer, then tap the question to see it.
Which hepatitis B marker pattern indicates immunity from vaccination only?
Anti-HBs positive with HBsAg and anti-HBc negative; anti-HBc is positive only after natural infection.
Which serological marker shows acute hepatitis B, including during the window period?
IgM anti-HBc, which can be the only positive marker after HBsAg clears and before anti-HBs appears.
Which hepatitis virus needs hepatitis B to replicate?
Hepatitis D (delta), which uses the hepatitis B surface antigen as its envelope; hepatitis B vaccination also prevents it.
Which viral hepatitis is especially dangerous in pregnancy?
Hepatitis E, which can cause fulminant hepatitis, particularly in the third trimester.
Which drug class cures most patients with chronic hepatitis C?
Oral direct-acting antivirals, given for a short course of several weeks.
Related conditions
- Cirrhosis
- Hepatocellular carcinoma
- Portal hypertension
- HIV infection and AIDS
- Leptospirosis
- Amoebic liver abscess
- Malaria
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Viral Hepatitis (StatPearls (NCBI Bookshelf), 2024); Hepatitis E Virus Genotype 3 in Colombia: Survey in Patients with Clinical Diagnosis of Viral Hepatitis (PloS one, 2016) · adapted, CC BY 4.0.
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