Hepatitis A

Shah fahad paul02592 sunny4822137 178 Users are discussing this topic

PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Hepatitis A written for patients
This disease is notifiable in the UK, see NOIDs article for more detail.

Hepatitis A virus (HAV) is a small, unenveloped, symmetrical RNA virus (picornavirus). The HAV was first isolated by Purcell in 1973. Since the 1980s specific antibody tests have helped reveal the epidemiology, clinical manifestations, and natural history of HAV infection. Infection with the virus ranges from mild symptoms of nausea to, in very rare cases, liver failure. Symptoms are usually worse and the illness more often severe in older patients.

Spread is normally by the faecal-oral route although there are occasional outbreaks through food sources.[1] Hand washing and good hygiene around food and drink prevent spread of infection. Active and passive immunisation are used in those at risk of infection. Travellers to certain countries, injecting drug users and those in contact with infected individuals are at risk of infection.

The most important determinant of illness severity is age and there is a direct correlation between increasing age and morbidity and mortality. Most deaths from acute HAV infection occur in those over the age of 50, even though infection is uncommon in this age group.

  • Humans appear to be the only reservoir for the HAV.
  • The incubation period usually lasts 2-6 weeks. The time to onset of symptoms may be dose-related.
  • Viral replication depends on hepatocyte uptake.
  • After uptake, the viral RNA is uncoated, and host ribosomes bind to form polysomes.
  • Viral proteins can then be synthesised with the viral genome being copied by a viral RNA polymerase.
  • Assembled virus particles are then shed through the biliary tree into the faeces.
  • Shedding of the HAV is greatest during the anicteric prodrome of infection (between 14 and 21 days after infection). This corresponds to the time when transmission is highest.

NEW - log your activity

  • Notes
    Add notes to any clinical page and create a reflective diary
  • Track
    Automatically track and log every page you have viewed
  • Print
    Print and export a summary to use in your appraisal
Click to find out more »
  • The anti-HAV seroprevalence rate is presently decreasing in many parts of the world, but in less developed regions and in several developing countries, HAV infection is still very common in the first years of life and seroprevalence rates approach 100%.[2] 
  • Hepatitis A is the most common form of acute viral hepatitis worldwide.
  • The highest risk areas of the world for hepatitis A infection include: the Indian subcontinent (in particular India, Pakistan, Bangladesh, and Nepal), Africa, parts of the Far East (except Japan), South and Central America, and the Middle East.
  • Approximately 1.5 million clinical cases of hepatitis A occur worldwide annually but the rate of infection is probably as much as ten times higher.[2] 
  • The incidence rate is strongly related to socio-economic indicators and access to safe drinking water.
  • There was a peak in incidence in the early 1990s in the UK and numbers have been reducing since this time.[3] 
  • In developed countries, reduced encounters with HAV in the young have resulted in a decline in herd immunity.

Most people acquiring HAV infection do not have risk factors but these include:

  • Personal contact.
  • Certain occupations (for example, staff of large residential institutions, sewage workers).
  • Travel to high-risk areas.
  • Male homosexuality with multiple partners.
  • Intravenous drug abuse.
  • People with clotting factor disorders who are receiving factor VIII and factor IX concentrates.
  • The incubation period is 2-6 weeks with a mean of 4 weeks.
  • There is a prodrome of mild flu-like symptoms (anorexia, nausea, fatigue, malaise and joint pain) preceding the jaundice. Smokers often lose their taste for tobacco. Diarrhoea can occur, particularly in children.
  • Fever is not usually common.
  • This can progress to the icteric phase with:
    • Dark urine (appears first).
    • Pale stools (not always).
    • Jaundice occurring in 70-85% of adults with acute HAV infection.
    • Abdominal pain occurring in 40% of patients.
    • Itch or pruritus (usually with jaundice but can occur without).
    • Arthralgias and skin rash. These occur less often (lower limbs and with a vasculitic appearance).
  • Tender hepatomegaly, splenomegaly, and lymphadenopathy may occur.
  • Young children are usually asymptomatic and the likelihood of symptoms tends to increase with age.[1] 
  • Complete clinical recovery may take up to six months after the onset of the illness.
  • Anorexia, malaise, and weakness may persist for some weeks after biochemical recovery.

Specific antibody tests

  • IgM antibody to HAV is positive with onset of symptoms (usually about 3 to 4 weeks after exposure but up to 6 weeks). The test is sensitive and specific. It remains positive for between 3 and 6 months (up to 12 months). It remains positive in relapsing hepatitis.
  • IgG antibody to HAV appears soon after IgM and persists for many years. In the absence of IgM it indicates past infection or vaccination rather than acute infection. IgG remains detectable for life.

Liver enzymes

  • Alanine aminotransferase (ALT) rises more than aspartate aminotransferase (AST) again with onset of symptoms, about 4 weeks after exposure. Levels usually return to reference ranges over several weeks but can remain elevated for months.
  • Alkaline phosphatase rises with ALT and AST.

Other test results

  • Bilirubin rises soon after rises in ALT and AST levels. Levels may be very high and remain elevated for several months. Older patients have higher bilirubin levels.
  • Modest falls in serum albumin level may occur.
  • Prothrombin time usually remains normal and estimation is necessary only in unusual cases or with complications.
  • Indices of low-grade haemolysis may be detected.
  • Mild lymphocytosis is common.
  • Pure red cell aplasia and pancytopenia may very rarely occur.


  • Ultrasound may, rarely, be needed to exclude other diseases.
  • Mainly supportive with treatment of symptoms (fluids, antiemetics, rest).
  • Avoid alcohol until liver enzymes are normal.
  • Admit patients with severe systemic upset or intractable vomiting for rehydration and observation.

These rarely occur but include:

  • Cholestatic hepatitis. This can occur in around 8% of people. Features may include severe pruritus, diarrhoea, weight loss, and malabsorption. However, they usually fully recover.
  • Death (mortality 0.2%)
  • Fulminant liver failure. This occurs in less than 0.4% of people and usually manifests during the first four weeks of illness. It is more common in those with concurrent chronic hepatitis B or C.
  • Autoimmune hepatitis (AIH). This may lead to anti-HAV IgM positivity detection for a prolonged time. However, hepatitis A infection may actually trigger AIH.[4] 
  • Relapsing HAV infection can occur in up to 15% of people, at an interval of 4-15 weeks after the original illness. It can occur more than once.
  • Other very rare complications (for example, acute kidney injury, red cell aplasia, Guillain-Barré syndrome, pancreatitis).

Hepatitis A is the most frequent vaccine-preventable disease in travellers. 

It can be a serious illness, particularly in the elderly. With proven means of prevention, it is important to pursue prevention actively. After infection and active immunisation, immunity is probably lifelong.

  • Control of infection at source is needed. This requires notification and contact tracing.
  • Good hygiene and sanitation are of fundamental importance. Tap water should be avoided in high-risk areas.
  • Public education about transmission and prevention are needed, particularly in communities where HAV is endemic.
  • Immunisation is effective and should be appropriately used. This is covered in the separate article Hepatitis A Vaccination.
  • Excellent. It is usually self-limiting with no long-term sequelae.
  • There is no carrier state and chronic liver disease does not occur.

Further reading & references

  1. Matheny SC, Kingery JE; Hepatitis A. Am Fam Physician. 2012 Dec 1;86(11):1027-34; quiz 1010-2.
  2. Franco E, Meleleo C, Serino L, et al; Hepatitis A: Epidemiology and prevention in developing countries. World J Hepatol. 2012 Mar 27;4(3):68-73. doi: 10.4254/wjh.v4.i3.68.
  3. Hepatitis A - Epidemiological Data; Public Health England
  4. Tabak F, Ozdemir F, Tabak O, et al; Autoimmune hepatitis induced by the prolonged hepatitis A virus infection. Ann Hepatol. 2008 Apr-Jun;7(2):177-9.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Richard Draper
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
12440 (v3)
Last Checked:
Next Review:

Did you find this health information useful?

Yes No

Thank you for your feedback!

Subcribe to the Patient newsletter for healthcare and news updates.

We would love to hear your feedback!

Patient Access app - find out more Patient facebook page - Like our page