Hepatitis A to E: How the Viruses Differ
Hepatitis means inflammation of the liver. The word describes what is happening in the organ, not what caused it.
Viruses are one important cause. Hepatitis A, B, C, D and E all involve the liver, but they are different viruses with different routes of transmission, different chances of becoming chronic and very different treatment pathways.
The common thread is liver injury. Hepatocytes become inflamed, liver enzymes may rise, bilirubin handling can be disturbed and, if inflammation persists, scar tissue can accumulate. The important clinical question is therefore not simply “Which hepatitis is this?” but also “Is this an acute infection that will resolve, or a persistent infection that can keep damaging the liver over time?”
What viral hepatitis does to the liver
The liver receives nutrient-rich blood from the gastrointestinal tract, metabolises drugs and hormones, produces bile, stores glycogen, processes bilirubin and synthesises proteins including albumin and many clotting factors. Viral hepatitis can disturb several of these functions, but the pattern depends on how much hepatocyte injury has occurred and whether the disease is acute or chronic.
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) rise when hepatocytes are injured and release intracellular enzymes into the blood. They are therefore markers of cell injury rather than direct measurements of liver function.
Bilirubin may rise if the liver cannot process and excrete it effectively. That can produce jaundice, dark urine and pale stools. Cholestasis can also contribute to pruritus.
Albumin and clotting measurements such as the international normalised ratio (INR) tell a different story because they reflect hepatic synthetic function. In severe acute hepatitis or advanced chronic liver disease, impaired synthesis can become clinically important even if transaminase levels are not especially high.
Another useful distinction is that the virus does not always injure hepatocytes in the same way. In hepatitis B, much of the liver damage is driven by the immune response against infected hepatocytes rather than by direct viral destruction alone. Persistent immune-mediated injury can then drive fibrosis over many years.
This is why the same patient may move from a phase of active inflammation to a quieter period with relatively few symptoms, while still needing specialist monitoring.
Acute and chronic infection are the key dividing line
Hepatitis A and hepatitis E are usually acute infections. The immune system clears the virus and chronic infection does not normally develop, although hepatitis E can persist in a small number of immunosuppressed people.
Hepatitis B and hepatitis C can become chronic. Hepatitis D can also become chronic, but only in someone who also has hepatitis B because HDV depends on HBV for its life cycle.
| Virus | Main transmission pattern | Can become chronic? | Vaccine? |
|---|---|---|---|
| Hepatitis A | Faecal-oral, including contaminated food or water and close contact | No | Yes |
| Hepatitis B | Blood and body fluids, sexual transmission and transmission around birth | Yes | Yes |
| Hepatitis C | Blood-to-blood exposure | Yes | No |
| Hepatitis D | Blood and body fluids, only in someone with hepatitis B | Yes | No separate vaccine, but hepatitis B vaccination prevents it |
| Hepatitis E | Faecal-oral; in the UK, zoonotic food-borne transmission is important | Usually no, but possible in immunosuppressed people | No routinely available UK vaccine |
The transmission route is important because it determines both prevention and the questions you ask in a history. Hepatitis A and E require attention to food, water, sanitation and travel. Hepatitis B, C and D require careful assessment of blood and body-fluid exposure, injecting equipment, sexual exposure, birth history, previous transfusion or healthcare exposure, and occupational risk.
Hepatitis A and E usually cause acute enteric hepatitis
Hepatitis A virus (HAV) is transmitted by the faecal-oral route. Infection can follow contaminated food or water or close contact with an infected person. Symptoms can include fever, fatigue, nausea, abdominal discomfort, dark urine, pale stools and jaundice, but many infections are mild or asymptomatic, particularly in children.
HAV does not establish chronic infection. Most people recover completely, although acute illness can still be severe, especially in older adults or in people who already have liver disease.
There is no specific antiviral treatment for uncomplicated hepatitis A. Management is mainly supportive, with hydration, symptom control and monitoring where clinically indicated. Vaccination is available for people at increased risk and may also be used as part of public-health management after exposure.
Hepatitis E virus (HEV) also commonly causes an acute hepatitis, but its epidemiology is more complex. Globally, genotypes 1 and 2 are associated with faecal-oral spread through contaminated water, particularly in areas with poor sanitation.
In the UK and other parts of Europe, genotype 3 is more important. These infections are usually zoonotic, and undercooked pork products are a recognised exposure route. This means hepatitis E should not be dismissed simply because a patient has not travelled abroad.
Most HEV infections resolve spontaneously. Chronic infection can occur in some immunosuppressed people, particularly organ-transplant recipients. Severe acute disease is also recognised in pregnancy, especially with genotypes 1 and 2 circulating in endemic regions.
For both HAV and HEV, the clinical picture may resemble other causes of acute hepatitis. Jaundice alone cannot tell you which virus is responsible.
Hepatitis B, C and D can produce persistent liver injury
Hepatitis B virus (HBV) is transmitted through infected blood and body fluids. Important routes include sexual transmission, shared injecting equipment, occupational exposure and transmission around the time of birth.
The risk of chronic infection is strongly influenced by age. Immunocompetent adults usually clear acute HBV, whereas infection acquired in infancy or early childhood is much more likely to persist.
Chronic hepatitis B is not one fixed disease state. Viral replication, immune activity and liver inflammation can change over time. Some people have little active inflammation for long periods, while others develop progressive fibrosis. Chronic HBV also increases the risk of hepatocellular carcinoma, including in some people who have not yet developed cirrhosis.
Vaccination is central to prevention. Hepatitis B vaccination is included in the UK childhood immunisation programme and is also recommended for people at increased risk, including healthcare workers with occupational exposure.
Specialist treatment for chronic HBV aims to suppress viral replication, reduce liver inflammation and lower the risk of cirrhosis and liver cancer. Nucleoside or nucleotide analogues such as tenofovir or entecavir are used in appropriate patients, but treatment does not usually eradicate chronic HBV completely.
Hepatitis C virus (HCV) is primarily blood-borne. In the UK, past or current injecting drug use remains an important risk factor. Historical exposure through unscreened blood or blood products is also relevant, particularly for people treated before modern screening was introduced.
HCV often causes few or no symptoms for years. That makes chronic infection particularly easy to miss while fibrosis is developing. The absence of jaundice or abdominal pain does not mean the liver is unaffected.
Treatment has changed dramatically. Direct-acting antiviral tablets are usually taken for 8 to 12 weeks and cure more than 95% of treated infections. There is no hepatitis C vaccine.
After virological cure, ongoing liver injury from HCV stops, but established cirrhosis does not disappear immediately. People with advanced fibrosis or cirrhosis may still need long-term surveillance, particularly for hepatocellular carcinoma.
Hepatitis D virus (HDV) is unusual because it cannot complete its life cycle without hepatitis B. HDV uses hepatitis B surface antigen to assemble infectious particles, so hepatitis D only occurs in someone who is also infected with HBV.
HBV and HDV may be acquired at the same time, known as coinfection, or HDV may infect someone who already has chronic hepatitis B, known as superinfection.
Chronic HBV/HDV infection can be more aggressive than HBV alone, with faster progression towards cirrhosis, liver failure and hepatocellular carcinoma. Vaccination against hepatitis B therefore also prevents hepatitis D.
Specialist treatment options for chronic hepatitis D now include bulevirtide for selected adults under NICE guidance in England and Wales. Eligibility depends on disease stage and previous or unsuitable interferon therapy, and treatment pathways differ across UK nations.
Diagnosis depends on virus-specific testing
Raised liver enzymes can suggest hepatitis, but they cannot identify the cause. Viral hepatitis requires specific serological and molecular testing.
In suspected acute hepatitis A, HAV-specific IgM supports a diagnosis of recent infection.
For hepatitis B, hepatitis B surface antigen (HBsAg) indicates current infection. Antibody to hepatitis B core antigen, particularly anti-HBc IgM, helps identify acute or recent infection. Hepatitis B DNA testing measures viral replication and is important in specialist assessment.
Hepatitis B serology can be confusing because vaccination and previous infection produce different antibody patterns. A person vaccinated against HBV develops anti-HBs without anti-HBc, because the vaccine contains surface antigen rather than whole virus.
For hepatitis C, a positive anti-HCV antibody shows that the person has been exposed to the virus at some point. It does not prove that current infection is still present. Active infection is confirmed using HCV RNA or, in some pathways, HCV core antigen.
This distinction remains important after treatment. HCV antibody often stays positive even after successful cure, so someone with ongoing risk of reinfection needs RNA or core-antigen testing rather than repeat antibody testing alone.
Hepatitis D testing is only relevant in someone with hepatitis B infection. Specialist assessment may include anti-HDV followed by HDV RNA to confirm active infection.
For suspected hepatitis E, testing can include anti-HEV IgM and HEV RNA. Molecular testing becomes particularly important in immunosuppressed people, where antibody responses may be less reliable and persistent infection is possible.
In acute hepatitis, severity assessment also matters. Liver function tests are interpreted alongside clotting, bilirubin, renal function, clinical state and signs of hepatic failure. A patient with worsening coagulopathy, confusion, hypoglycaemia or rapidly deteriorating liver function needs urgent specialist assessment.
Chronic hepatitis can progress from inflammation to fibrosis and cirrhosis
Persistent hepatocyte injury activates hepatic stellate cells and promotes deposition of collagen and other extracellular matrix. This is the basis of fibrosis.
Fibrosis is not the same as cirrhosis. Early fibrosis may be limited and potentially partly reversible if the injurious stimulus is removed. With ongoing inflammation, scar tissue becomes more extensive and the normal architecture of the liver is increasingly distorted.
Cirrhosis is advanced fibrosis with structural reorganisation of the liver. Blood flow through the organ becomes abnormal, which can produce portal hypertension. Varices, splenomegaly and ascites may follow. Loss of functional hepatocyte mass can reduce albumin synthesis, impair clotting-factor production and contribute to jaundice or hepatic encephalopathy.
Chronic HBV and HCV also increase the risk of hepatocellular carcinoma. This is why treatment and surveillance continue to matter even when a patient feels well.
Viral suppression in hepatitis B and cure in hepatitis C can substantially reduce further inflammatory injury and the risk of progression, but they do not instantly erase damage that has already occurred.
What nurses need to recognise
Viral hepatitis does not always present as an obviously jaundiced patient with abdominal pain. Diagnosis may arise through antenatal screening, abnormal liver blood tests, blood-borne virus testing, assessment before immunosuppressive treatment, occupational exposure or investigation of chronic liver disease.
For blood-borne hepatitis, standard precautions and safe sharps practice remain fundamental. Healthcare workers should know their hepatitis B vaccination status and follow occupational-health pathways after significant exposure.
For hepatitis A and many hepatitis E infections, hand hygiene, food exposure, sanitation and travel history become more important.
Testing should be offered without judgement. NICE specifically emphasises confidentiality, informed consent and respectful communication because stigma can become a barrier to testing and treatment.
Risk factors such as injecting drug use, sexual exposure, migration, imprisonment or previous healthcare treatment should be discussed as clinical information, not as moral judgements.
It is also important to distinguish routine viral hepatitis from possible acute liver failure. New confusion, marked drowsiness, worsening clotting, recurrent hypoglycaemia, rapidly rising bilirubin or other evidence of deteriorating liver function should trigger urgent escalation and specialist review.
The central pattern is straightforward: identify the virus, establish whether the infection is acute or persistent, assess how much liver injury has occurred and understand whether the patient needs supportive care, antiviral treatment, public-health follow-up, vaccination of contacts or longer-term surveillance.
Summary
Hepatitis A to E are five different viral infections that all cause inflammation of the liver.
Hepatitis A and E are usually acute enteric infections. Hepatitis B, C and D are more strongly associated with blood or body-fluid exposure and can produce chronic liver disease. Hepatitis D only occurs in the presence of hepatitis B.
Hepatitis B is vaccine-preventable but may require long-term antiviral suppression when chronic. Hepatitis C has no vaccine but is now usually curable with short-course direct-acting antiviral treatment. Hepatitis A does not become chronic. Hepatitis E is usually self-limiting but can become persistent in some immunosuppressed people.
Diagnosis relies on virus-specific serology and molecular testing rather than liver enzymes alone. When infection becomes chronic, repeated hepatocyte injury can drive fibrosis, cirrhosis and hepatocellular carcinoma.
References
Garvey, L. et al. (2026) ‘British Association of Sexual Health and HIV guidelines on the management of viral hepatitis 2026’, International Journal of STD & AIDS, 37(9), pp. 939–968. Available at: https://doi.org/10.1177/09564624261440830
National Institute for Health and Care Excellence (NICE) (2012, updated) Hepatitis B and C testing: people at risk of infection (PH43). Available at: https://www.nice.org.uk/guidance/ph43
National Institute for Health and Care Excellence (NICE) (2013, updated) Hepatitis B (chronic): diagnosis and management (CG165). Available at: https://www.nice.org.uk/guidance/cg165
National Institute for Health and Care Excellence (NICE) (2023) Bulevirtide for treating chronic hepatitis D (TA896). Available at: https://www.nice.org.uk/guidance/ta896
NHS (n.d.) Hepatitis. Available at: https://www.nhs.uk/conditions/hepatitis/
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UK Health Security Agency (2026) Hepatitis. Available at: https://www.gov.uk/government/collections/hepatitis
UK Health Security Agency (2025) Hepatitis C in England 2025. Available at: https://www.gov.uk/government/publications/hepatitis-c-in-england-and-the-uk/hepatitis-c-in-england-2025
UK Health Security Agency (2025) Common animal-associated infections in England: 2025. Available at: https://www.gov.uk/government/publications/common-animal-associated-infections-2025/common-animal-associated-infections-in-england-2025
World Health Organization (2026) Hepatitis D. Available at: https://www.who.int/news-room/fact-sheets/detail/hepatitis-d
World Health Organization (2026) Hepatitis E. Available at: https://www.who.int/news-room/fact-sheets/detail/hepatitis-E