Next Lesson - Human Immunodeficiency Virus (HIV)
Core
Hepatitis simply means inflammation of the liver and is by no means limited to viral infection. Other causes include:
- Viral hepatitis - the focus of this article.
- Alcoholic hepatitis - excessive consumption of alcohol resulting in an alcohol-related liver disease, which involves inflammatory changes.
- Autoimmune hepatitis - where the body attacks its own liver. This requires immunosuppression treatment. The cause of autoimmune hepatitis is unknown.
Viral hepatitis can result from infection with hepatotropic viruses or from other viral infections that involve the liver. The mechanism of liver injury varies with the virus and the host response.
- Systemic infections, such as Epstein–Barr virus (EBV), can cause hepatitis. In typical EBV hepatitis, infiltrating lymphocytes and the immune response contribute to liver injury; direct infection of hepatocytes is not the usual explanation. This should not be assumed to describe every systemic virus.
- Classical viral hepatitis is caused by hepatotropic hepatitis viruses. Infection of liver cells does not mean that injury is caused solely by viral replication: hepatitis B, for example, produces predominantly immune-mediated liver damage.
The five main hepatitis viruses are designated A to E. Types A and E usually cause acute infection, while B and C can cause chronic infection. Hepatitis D occurs only with hepatitis B. These viruses differ in their biology and in the immune responses responsible for liver injury.
Hepatitis B and Hepatitis C are the more common causes of viral hepatitis. Approximately 240 million people worldwide are infected with hepatitis B (acute or chronic) and it is the leading cause globally of liver cirrhosis.
Looking at the UK, the British Liver Trust website estimates that 180,000 people are living with a chronic hepatitis B infection and in certain areas, 1 in 60 pregnant women may be affected (figures from https://www.britishlivertrust.org.uk/liver-information/liver-conditions/hepatitis-b/)
The WHO hepatitis C fact sheet updated on 28 July 2026 estimates that 47 million people worldwide live with chronic hepatitis C. WHO estimates that hepatitis C caused approximately 239,000 deaths in 2024, mainly from cirrhosis and hepatocellular carcinoma.
Hepatitis B virus (HBV) is a partially double-stranded enveloped DNA virus. Transmission of HBV is via blood, sexual intercourse and vertical transmission. Once an individual has been infected with HBV, it can take 6 weeks to 6 months for the virus to incubate and begin to cause damage the individual’s liver.
Up to 50% of people with HBV infections will have vague symptoms or be asymptomatic, but those that do experience symptoms will most likely have jaundice, fever, nausea, vomiting and arthralgia (joint pain).
Most immunocompetent adults will clear the infection themselves within around 6 months. Approximately 5-10% will progress from an acute to a chronic infection. In countries such as China and parts of Asia, there is a high infancy HBV infection rate and 90% of these cases will progress to a chronic infection.
The most important test for hepatitis B is serology. This is the analysis of blood serum (blood without cells or clotting factors) to see what immune response has occurred and look for the presence of extra substances. The serology of hepatitis B involves three antigens and three antibodies.
The first antigen detectable is HBsAg which is the hepatitis B (HB) surface (s) antigen (Ag). The matching antibody produced is HBsAb, hepatitis B (HB) surface (s) antibody (Ab). This can be detected in the blood and indicates immunity due to past infection or vaccination. It is normally found in the blood after around 6 weeks.
HBeAg is hepatitis B e antigen, a secreted protein derived from the viral core; the “e” does not stand for envelope. Its presence generally suggests active viral replication and greater infectivity. HBV DNA measures viral replication more directly. Some HBV variants replicate without producing HBeAg, so a negative HBeAg result does not exclude infectivity. The corresponding antibody is anti-HBe.
The third antigen is HBcAg and its matching antibody, HBcAb (although only the Ab is detected). Here the “c” stands for core. IgM is the first antibody encountered unless the patient has had a previous HBV infection in which case it is IgG.
Although the antigens appear in the order above, the antibodies actually appear in the reverse order. So, for a patient that hasn’t had a hepatitis B infection before, their timeline would look like:
- Contract the virus through unprotected sex on a holiday in sub-Saharan Africa
- After 6 weeks the HBsAg is detectable in blood serum and there is a corresponding rise in ALT on liver function tests. They would now be considered infected
- Symptoms start to appear at this point
- HBeAg may appear and generally indicates greater viral replication and infectivity; transmission is not restricted to the HBeAg-positive stage.
- HBcAg is present within infected hepatocytes and is not detectable in serum by routine serology
- HBcAb appears in the form of IgM (as it is an acute infection)
- HBeAb appears and after HBeAg has been cleared infectivity usually falls, although viral replication can still persist in some cases
- HBsAb appears and the virus is completely cleared from the body
- IgM then converts to IgG and persists in the body
Diagram - Hepatitis B virion. HBsAg is in the envelope and HBcAg forms the core. The full-length minus DNA strand is pink and carries the polymerase; the incomplete plus strand is cyan. HBeAg is secreted and is not part of the virion.
Adapted for SimpleMed (2026) from Hepatitis B virus v2.png, created by Graham Colm and originally uploaded by TimVickers; the source bitmap is released into the public domain. Changes: HBeAg removed from the particle, genome polarity corrected, and labels revised.
Another test that can be done is a HBV DNA PCR test to see how much viral DNA is in the body.
If HBV infection doesn't resolve, then a patient can develop a chronic HBV infection. Chronic HBV is a lifelong chronic infection that is defined by HBsAg staying in the body for longer than 6 months. Of the chronically infected patients, 25% will go on to develop cirrhosis and 5% will develop hepatocellular carcinoma.
Chronic HBV cannot currently be cured, but antivirals are used to suppress viral replication in selected patients and treatment is not always lifelong. Most acute HBV infections are managed supportively, with antivirals reserved for severe or fulminant disease.
There is a vaccine for HBV. It involves injecting the patient with a genetically engineered surface antigen for HBV (HBsAg) that is harmless and allows the body to develop HBsAb so it can fight off a HBV infection. The target for long term protection is an anti-HBs level of at least 10 mIU/mL. There are three doses and any boosters, which is effective for most people. The WHO recommends that all babies are vaccinated preferably within 24 hours of birth (the NHS offers it as part of their vaccination schedule at 8, 12 and 16 weeks old).
Hepatitis C virus (HCV) is a single-stranded RNA virus that is enveloped and icosahedral in shape. Transmission of HCV is primarily blood-borne, with sexual transmission occurring less commonly. Those at most risk of HCV are those that come in contact with needles including; intravenous drug users and healthcare workers (needlestick injury). Others at risk include infants born to HCV positive mothers and those who had blood transfusions before 1991. Incubation is much faster with HCV compared to HBV at around 6 to 12 weeks.
Around 80% of acute HCV infections are asymptomatic. When symptoms present, they include fatigue, decreased appetite, nausea, vomiting, abdominal pain, dark coloured urine, grey faeces, arthralgia and jaundice. The WHO estimates between 15-45% of adults can clear the HCV infection within about 6 months. 80% of HCV patients will develop a chronic infection.
Testing and detecting HCV is different to HBV. The only serological test is for the anti-hepatitis C antibody which will detect whether people have been infected by HCV or if they have been infected before. This antibody is not protective and is only really of diagnostic value.
As the anti-hepatitis C antibody remains after clearance, the next step is to do a viral PCR to look for HCV RNA to confirm if the patient has a chronic infection. For those that can clear HCV, they will still be positive for anti-hepatitis C antibody. Once a patient is confirmed to have a chronic infection, the degree of cirrhosis and variation of HCV needs to be ascertained to guide the patient’s treatment will be.
HCV does not have a vaccine so to prevent infection so prevention is limited to exposure limitation. However, an antiviral combination can be used to treat and cure HCV. The combination is 95% effective. The treatment of HCV lasts about 8-12 weeks and costs between £20,000 to £60,000.
A needlestick exposure requires prompt assessment. Transmission risk depends on the infection, whether the source has transmissible virus, the depth and type of injury, the amount of blood transferred, and the exposed person’s hepatitis B immunity. The figures below are not universal probabilities for every injury.
- HIV: risk depends on the source’s infection and viral suppression and on the exposure. Seek urgent assessment for post-exposure prophylaxis.
- Hepatitis B: a susceptible worker can face a substantial risk after exposure to infectious blood. Documented vaccine-induced protection changes that risk markedly; source infectivity and injury characteristics also matter.
- Hepatitis C: risk depends on exposure to blood containing HCV RNA. CDC estimates an average risk of about 0.2% after percutaneous exposure in the studies informing its guidance; this is not a prediction for an individual injury.
Report the exposure immediately for urgent occupational health or emergency assessment. HIV post-exposure prophylaxis, when indicated, should start as soon as possible and within 72 hours. Hepatitis B management depends on vaccination, documented antibody response and source status, and may include vaccine and hepatitis B immunoglobulin. There is no recommended routine antiviral post-exposure prophylaxis for hepatitis C; arrange testing and follow-up, with treatment if infection is detected.
- The PEP treatment for HIV consists of 3 different antivirals (ARVs) for 28 days and then re-tests at 1 and 3 months.
- The hepatitis B vaccine is very effective as post-exposure prophylaxis for a potential needlestick injury.
- If the individual tests are negative for HBsAg and positive for HBsAb then you do not need to give a booster, otherwise give the booster or start the vaccination if they haven’t had it already.
If someone has received a needlestick injury, they should wash the area with soap and water without squeezing the wound, cover it, and report to occupational health as soon as possible. After this, they should be referred from counselling and advised to use condoms until they have received the all clear.
Edited by: Dr. Thomas Burnell and Dr. Ben Appleby
Reviewed by: Dr. Marcus Judge
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