Viruses
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Viral Hepatitis
Overview of Hepatitis Viruses
Viral hepatitis causes inflammation and injury of hepatocytes. The viruses differ in their transmission, likelihood of chronic infection and prevention.
| Virus | Main transmission | Chronic infection | Vaccine |
|---|---|---|---|
| HAV | Fecal–oral | No | Yes |
| HBV | Blood, sexual contact and perinatal exposure | Yes | Yes |
| HCV | Primarily blood-borne | Common | No |
| HDV | Blood/body fluids; requires HBV | Yes, depending on infection pattern | Prevented by HBV vaccination |
| HEV | Mainly fecal–oral, often contaminated water | Usually no; chronic infection can occur in immunocompromised patients | Limited availability in selected countries |
Hepatitis A (HAV)
- Transmitted primarily by the fecal–oral route.
- Commonly associated with contaminated food or water.
- Causes acute hepatitis but does not cause chronic infection.
- Prevention includes vaccination and safe food/water practices.
- Treatment is generally supportive.
Remember: HAV does not cause chronic hepatitis.
Hepatitis B (HBV)
HBV is a partially double-stranded DNA virus transmitted through infected blood, sexual contact and perinatal exposure.
Natural history
- Acute infection may be asymptomatic or cause acute hepatitis.
- Some patients clear the infection; others develop chronic infection.
- Chronic infection can lead to cirrhosis and hepatocellular carcinoma.
- Chronicity is more likely following perinatal or early-childhood infection than adult-acquired infection.
HBV serology
| Marker | Meaning |
|---|---|
| HBsAg | Current HBV infection |
| Anti-HBs | Immunity from vaccination or recovery |
| Total anti-HBc | Previous or current natural HBV infection; not produced by vaccination alone |
| IgM anti-HBc | Recent/acute infection; may identify the window period |
| HBeAg | Often associated with active viral replication and greater infectivity |
| HBV DNA | Direct marker of viral replication |
Common serology patterns
| Clinical state | HBsAg | Anti-HBs | Anti-HBc |
|---|---|---|---|
| Susceptible, unvaccinated | − | − | − |
| Vaccinated | − | + | − |
| Recovered from natural infection | − | + | + |
| Acute infection | + | − | +, with IgM anti-HBc |
| Chronic infection | + | − | +, usually total anti-HBc |
Window period
During the HBV window period, HBsAg may have disappeared while anti-HBs has not yet become detectable. IgM anti-HBc is the key marker.
Prevention and treatment
- Vaccination is the main prevention strategy.
- Antiviral treatment is indicated in selected patients with chronic HBV based on viral load, liver inflammation, fibrosis and other risk factors.
- Cirrhosis and hepatocellular carcinoma surveillance are important in appropriate chronic HBV populations.
Hepatitis C (HCV)
- An RNA virus transmitted primarily through blood.
- Chronic infection is common if untreated.
- Chronic HCV can lead to fibrosis, cirrhosis and hepatocellular carcinoma.
- Screening commonly uses anti-HCV antibodies; HCV RNA confirms current viremia.
- Direct-acting antiviral regimens can cure the great majority of treated patients.
- No widely available vaccine currently provides routine protection against HCV.
MCQ tip: A positive anti-HCV result indicates exposure, not necessarily active infection. HCV RNA establishes current infection.
Hepatitis D (HDV)
HDV is a defective RNA virus that requires hepatitis B surface antigen to complete its life cycle.
- Coinfection: HBV and HDV acquired together.
- Superinfection: HDV acquired in someone already infected with HBV.
- Superinfection in chronic HBV can cause severe disease and increases the risk of chronic HDV infection.
- HBV vaccination prevents HDV infection in people who are not already infected with HBV.
Hepatitis E (HEV)
- Usually transmitted through contaminated water via the fecal–oral route.
- Commonly causes acute, self-limited hepatitis.
- Severe disease can occur during pregnancy, especially in certain endemic settings.
- Chronic infection is possible in some immunocompromised patients.
Alcohol-Associated Hepatitis
Alcohol-associated hepatitis is an inflammatory liver injury associated with substantial alcohol exposure. It can range from mild disease to severe acute liver dysfunction.
Pathology and laboratory clues
- Hepatocyte ballooning and inflammatory infiltration.
- Mallory–Denk bodies may be present.
- AST is often greater than ALT, frequently with an AST:ALT ratio above 1.5–2.
- GGT may be elevated but is nonspecific.
- Bilirubin and INR help assess severity.
Exam tip: AST greater than ALT is a classic clue, but the enzyme pattern alone does not establish the diagnosis.
Severe alcohol-associated hepatitis requires specialist assessment because treatment depends on severity, contraindications, infection status and overall clinical condition.