Anti-HBs (Hepatitis B immune

status/Anti-Hepatitis B surface
antibody)
Useful For

Detection of antibody to Hepatitis B surface antigen as a measure of vaccine-induced immunity and immunity due
to infection.

Testing Algorithm
Available Always
Reporting Name separately performed

Anti-HBs YES YES

Indications for Testing

Anti-HBs should be ordered to determine immune status to HBV and is included as part of the following
investigations/orders (see Special Instructions):

Acute Hepatitis B Follow-up

Chronic Hepatitis Screen (unknown etiology)
Previous Hepatitis Exposure

Clinical Information

Anti-HBs is a key serological marker for both vaccine-induced immunity and immunity due to infection. Anti-HBs is
also used to monitor the convalescence and recovery of HBV infected individuials. The presence of anti-HBs after
acute HBV infection and loss of Hepatitis B virus surface antigen (HBsAg) can be a useful indicator of disease
resolution. Detection of of anti-HBs in an asymptomatic individual may indicate previous exposure to HBV.

Postvaccination testing for the presence of anti-HBs is not recommended for infants, children, and most adults.
Exceptions to this rule are infants born to mothers who are HBsAg-positive, immunocompromised patients, dialysis
patients, and helathcare workers whose successful vaccination needs to be confirmed. Infants born to HBV-positive
mothers should be testing for anti-HBs after reaching 2 years of age due to passive antibody from the mother.

HBV “escape” mutants in which the HBsAg is altered can result in HBV infections without detectable anti-HBs.
 Typical sequence of serologic markers in patients with acute HBV infection with resolution of symptoms (Horvat,
R. T., and Tegtmeier, G. E. 2007).

Typical sequence of serologic markers in patients with HBV infection that progresses to chronicity. In patients with
chronic HBV infection, both HBsAg and IgG anti-HBc remain persistently detectable, generally for life. HBeAg is
variably present in these patients (Horvat, R. T., and Tegtmeier, G. E. 2007).

Hepatitis B virus (HBV) causes a wide spectrum of manifestations ranging from asymptomatic seroconversion, sub-
acute illness with non-specific symptoms (e.g. anorexia, nausea, or malaise) or extrahepatic symptoms, and clinical
hepatitis with jaundice, to fuliminant fatal hepatitis. Only 10% of children and 50% of adults will exhibit symptoms.
An acute illness may last up to three months with a fatality of 1-2%. In most acute cases HBsAg serum levels are
positive initially, resolve and the individual develops anti-HBs which confers immunity.

HBV occurs worldwide, and is endemic in some Asian countries. In Canada the incidence of acute hepatitis B is
estimated to be 2.3 per 100,000. In developed countries exposure to HBV may be common in certain high-risk
groups such as injection drug users, person who have multiple sex partners, men who have sex with men, sex with
HBV-infected persons and having a hepatitis B carrier in the family. The prevalence of chronic hepatitis B varies in
different populations.

Chronic HBV infection is found in 0.5 % of adults in North America. After acute HBV infection, the risk of developing
chronic infection varies with age; infants infected at birth have a 90% chance of becoming a chronic carrier. A
chronic carrier is one who retains HBsAg positivity six months after the initial infection. These individuals are always
infectious. Hepatocellular carcinoma and hepatic cirrhosis is likely to result in the premature death of 15-25% of
those who have chronic HBV.

Reference Values

Vaccinated individuals
Anti-HBs: ≥ 10 mIU/ml

Non-vaccinated individuals
Anti-HBs: 0 mIU/ml

Interpretation

For diagnostic purposes, and to stage the disease, results should be used in conjunction with patient history and
other hepatitis markers for diagnosis of acute or chronic infection (see special instructions).
For determination of immunity the World Health Organization (WHO) recognizes a level of 10 mIU/ml of anti-HBs
as protective.
See Special Instructions for PHL recommended diagnostic approach to hepatitis.

Clinical Reference

Curry, M. P., and Chopra, S. 2010. Acute Viral Hepatitis, p. 1577-1592. In Mandell, D., Bennett, J. E., and Dolin, R.
Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone, Elsevier, Philadelphia, PA.

Horvat, R. T., and Tegtmeier, G. E. 2007. Hepatitis B and D Viruses, p. 1641-1659. In Murray, P. R., Baron, E. J.,
Jorgensen, J. H., Landry, M. L., and Pfaller, M. A. Manual of Clinical Microbiology, 9th ed., vol. 2. ASM Press, American
Society for Microbiology, Washington, DC.

James Koziel, M., and Thio, C. L. 2010. Hepatitis B Virus and Hepatitis Delta Virus, p. 2059-2086. InMandell, D.,
Bennett, J. E., and Dolin, R. Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone,
Elsevier, Philadelphia, PA.

Abbott. 2008. Architect System Anti-HBs: package insert. Abbott Ireland, Diagnostics Division. Ireland.