How do hepatitis A, B, C, D and E viruses differ?
Hepatitis is acute if inflammation lasts less than 6 months and chronic if it lasts longer. Five classic viruses cause it. A useful split: the enteric viruses (A and E) are spread by the faeco-oral route and are self-limited, while the parenteral viruses (B, C and D) spread through blood, sex and birth and can become chronic, leading to cirrhosis and hepatocellular carcinoma.
| Virus | Family / genome | Spread | Incubation | Chronicity / key fact |
|---|---|---|---|---|
| HAV | Picornaviridae, RNA | Faeco-oral | ≈ 4 weeks | Never chronic; fulminant failure in < 1% |
| HBV | Hepadnaviridae, DNA | Blood, sexual, perinatal | ≈ 12 weeks | Up to 90% of infected newborns become chronic; most adults clear it |
| HCV | Flaviviridae, RNA | Blood (injecting drugs), sexual, perinatal | ≈ 8 weeks | 55–85% become chronic; about 30% of these progress to cirrhosis |
| HDV | Deltaviridae, RNA (defective) | Like HBV | ≈ 13 weeks | Needs HBsAg as its envelope |
| HEV | Hepeviridae, RNA | Faeco-oral (contaminated water) | 2–10 weeks | 15–25% maternal mortality in pregnancy; chronic only in immunosuppressed |
What are the high-yield features of hepatitis A and E?
Hepatitis A is shed in stool in the highest amounts at the end of the incubation period, so patients are most infectious before jaundice appears. The illness (fatigue, nausea, vomiting, fever, jaundice, dark urine) lasts about 8 weeks, is more severe in adults than children, and never becomes chronic. In highly endemic regions most children are infected early, usually without symptoms.
Hepatitis E belongs to the genus Orthohepevirus (family Hepeviridae). Genotypes 1 and 2 are waterborne and cause large outbreaks in Asia and Africa; genotypes 3 and 4 are zoonotic, spread by undercooked pork or deer meat, and cause sporadic cases in developed countries. HEV can become chronic in organ-transplant and other immunosuppressed patients.
How do you interpret hepatitis B serology?
Six markers are tested: HBsAg, anti-HBs, anti-HBc IgM, anti-HBc IgG, HBeAg and anti-HBe. HBsAg is the first marker to appear (1–12 weeks after infection). Its persistence for more than 6 months defines chronic infection. The gap between disappearance of HBsAg and appearance of anti-HBs is the window period, when anti-HBc IgM is the only positive marker.
| Marker | Meaning |
|---|---|
| HBsAg | Current infection — acute (< 6 months) or chronic (> 6 months) |
| Anti-HBs | Immunity — recovery from infection or vaccination |
| Anti-HBc IgM | Acute infection; only marker in the window period; may reappear in a chronic flare |
| Anti-HBc IgG | Past or ongoing exposure — chronic if with HBsAg, recovered if with anti-HBs |
| HBeAg | Active viral replication, high viral load, high infectivity |
| Anti-HBe | Seroconversion towards an inactive phase |
| HBsAg | Anti-HBc | Anti-HBs | Interpretation |
|---|---|---|---|
| − | − | − | Never infected, not immune (susceptible) |
| − | − | + | Immune after vaccination |
| − | + (IgG) | + | Immune after natural infection (recovered) |
| + | + (IgM) | − | Acute hepatitis B |
| + | + (IgG) | − | Chronic hepatitis B (HBsAg > 6 months) |
| − | + (IgM) | − | Window period of acute infection |
| − | + (IgG only) | − | Isolated anti-HBc — possible occult infection |
What is the difference between HDV coinfection and superinfection?
HDV uses HBsAg as its envelope protein and cannot replicate without HBV. It is found in an estimated 4–8% of acute HBV cases and about 5% of chronic HBV carriers worldwide.
| Feature | Coinfection | Superinfection |
|---|---|---|
| Timing | HBV and HDV acquired together | HDV infects a chronic HBV carrier |
| Anti-HBc IgM | Positive | Negative (HBV is already chronic) |
| Course | Usually self-limited | More severe; most become chronic HDV |
| Outcome | Recovery common | Faster progression to cirrhosis; risk of fulminant failure |
How are hepatitis B and C prevented, confirmed and treated?
- Perinatal HBV: babies of HBeAg-positive mothers have a 70–90% chance of infection, and up to 90% of infected infants stay chronically infected — so all pregnant women and all infants of HBsAg-positive mothers are screened.
- HBV vaccine: recombinant HBsAg; produces protective anti-HBs, with seroconversion in more than 95% of recipients.
- Chronic HBV drugs: oral nucleos(t)ide analogues suppress replication. Lamivudine was the first but has high resistance; entecavir gives a better virological response than lamivudine. Tenofovir in HBsAg/HBeAg-positive mothers reduced infant infection in trials.
- Treatment goal in HBV: loss of HBsAg and HBeAg with seroconversion to anti-HBs and anti-HBe. Patients in the immune-tolerant phase (normal transaminases) are generally not treated.
- HCV diagnosis: a positive HCV antibody must be confirmed with HCV RNA, the most specific test; RNA is detectable even before antibodies develop. About 80% of acute HCV infections are asymptomatic and do not cause jaundice.
- HCV screening (CDC 2020): one-time testing for all adults aged 18 and over and for pregnant women in every pregnancy.
What are the histological hallmarks of viral hepatitis?
- Councilman (acidophil) bodies: cytotoxic T cells make infected hepatocytes undergo apoptosis, leaving shrunken, eosinophilic bodies — characteristic of acute viral hepatitis.
- Ground-glass hepatocytes: finely granular, pale eosinophilic cytoplasm from proliferated smooth endoplasmic reticulum that harbours HBsAg — a clue to chronic hepatitis B.
- Chronic hepatitis: chronic inflammation in portal tracts that progresses to fibrosis and, finally, cirrhosis.
- Liver injury in HBV is mainly immune-mediated, not directly cytopathic — T cells attack hepatocytes that display viral antigens.
What is cirrhosis and how is it classified?
Cirrhosis is diffuse fibrosis with regenerative nodules that destroys the normal lobular architecture after chronic injury. The key cell is the hepatic stellate (Ito) cell, which normally stores vitamin A; inflammatory cytokines activate it into a myofibroblast that lays down collagen. In the developing world the commonest causes are HBV and HCV; in the developed world they are HCV, alcohol and non-alcoholic steatohepatitis.
| Type | Nodule size | Typical causes |
|---|---|---|
| Micronodular | Uniform, < 3 mm | Alcohol, haemochromatosis, hepatic venous outflow obstruction, chronic biliary obstruction, Indian childhood cirrhosis |
| Macronodular | Irregular, > 3 mm | Hepatitis B and C, alpha-1 antitrypsin deficiency, primary biliary cholangitis |
| Mixed | Both | Micronodular often progresses to macronodular with time |
How are Child-Pugh and MELD scores calculated?
The Child-Pugh (Child-Turcotte-Pugh) score adds 1–3 points for each of five items. It was designed to predict mortality in cirrhosis and still guides surgical risk.
| Parameter | 1 point | 2 points | 3 points |
|---|---|---|---|
| Bilirubin (mg/dL) | < 2 | 2–3 | > 3 |
| Albumin (g/dL) | > 3.5 | 2.8–3.5 | < 2.8 |
| INR (or PT prolonged) | < 1.7 (< 4 s) | 1.7–2.2 (4–6 s) | > 2.2 (> 6 s) |
| Ascites | None | Slight | Moderate |
| Encephalopathy | None | Grade 1–2 | Grade 3–4 |
| Class | Points | 1-year / 2-year survival | Mortality after abdominal surgery |
|---|---|---|---|
| A | 5–6 | 100% / 85% | ≈ 10% |
| B | 7–9 | 80% / 60% | ≈ 30% |
| C | 10–15 | 45% / 35% | ≈ 70–80% |
MELD (Model for End-stage Liver Disease) uses bilirubin, creatinine and INR to predict 3-month mortality; the newer MELD-Na adds sodium and is used to prioritise liver transplantation. MELD fixes the three weaknesses of Child-Pugh: subjective grading of ascites and encephalopathy, no measure of renal function, and only ten possible scores.
What are the major complications of cirrhosis?
- Portal hypertension — the main cause of illness and death; causes splenomegaly, caput medusae and collateral veins.
- Oesophageal varices — bleeding carries a mortality of at least 20% at 6 weeks.
- Ascites — SAAG ≥ 1.1 g/dL means portal hypertension (cirrhosis, Budd-Chiari, heart failure); SAAG < 1.1 g/dL points to peritoneal TB, carcinomatosis, pancreatitis or nephrotic syndrome.
- Spontaneous bacterial peritonitis — ascitic fluid neutrophil (PMN) count ≥ 250/mm³.
- Hepatorenal syndrome — splanchnic vasodilation reduces effective renal blood flow and activates the renin-angiotensin system.
- Hepatic encephalopathy — confusion, asterixis (flapping tremor) and fetor hepaticus.
- Hepatocellular carcinoma — cirrhosis from HBV or HCV is the commonest risk factor; screen with ultrasound every 6 months.
- Others — hepatopulmonary syndrome, portopulmonary hypertension, hypogonadism and gynaecomastia, anaemia and coagulopathy.
See also Wilson's disease as a metabolic cause of cirrhosis in the young, gallstones and cholecystitis for other causes of jaundice, and the national immunisation schedule for hepatitis B vaccination.
What health education should a patient with cirrhosis receive?
Lifestyle changes cannot cure cirrhosis, but they prevent or delay progression and relieve symptoms. This is the standard counselling answer in a community-medicine or medicine question.
- Eliminate alcohol — abstinence is crucial in alcoholic cirrhosis; avoid further liver injury of any kind.
- Diet — a balanced, nutritious diet; a low-sodium diet may be advised to reduce water retention; protein intake is regulated as the doctor directs; vitamin and mineral supplements are sometimes added.
- Avoid raw seafood and shellfish.
- Vaccination — against hepatitis A and B, pneumococcus and influenza.
- Weight reduction where relevant (at least 7% weight loss helps in NASH).
- Treat precipitants early — dehydration, hypotension and infections; monitor volume status, kidney function, varices and progression to HCC.
- Screen for HCC with abdominal ultrasonography at least every 6 months.