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Interpretive Handbook

Test 209102 :
Hepatitis B Immune Status Profile, Serum

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Hepatitis B virus (HBV) is a DNA virus that is endemic throughout the world. The infection is spread primarily through percutaneous contact with infected blood products, eg, blood transfusion, sharing of needles by drug addicts. The virus is also found in virtually every type of human body fluid and is known to be spread through oral and genital contact. HBV can be transmitted from mother to child during delivery through contact with blood and vaginal secretions; it is not commonly transmitted transplacentally. After a course of acute illness, HBV persists in approximately 10% of patients; some of these chronic carriers are asymptomatic.

Useful For Suggests clinical disorders or settings where the test may be helpful

Determining stage of disease, degree of infectivity, prognosis, and immune status of patients exposed to hepatitis B virus

Interpretation Provides information to assist in interpretation of the test results

In a normal course of hepatitis B virus (HBV) infection, hepatitis Be antigen (HBeAg) along with hepatitis B surface antigen (HBsAg) become detectable in a patient's serum during the incubation period, before the onset of clinical symptoms. Once clinical symptoms appear, HBeAg and HBsAg peak and then start to decline. The presence of HBeAg and/or HBsAg indicates active replication of HBV and positive results indicate patients are highly infectious for hepatitis B. HBV carriers usually carry HBsAg, and possibly HBeAg, indefinitely in the serum.


Hepatitis Be antibody (anti-HBe) begins to appear after HBeAg has disappeared and may be detectable for several years after a patient's recovery. Detectable anti-HBe in a patient who is an HBV carrier may indicate inactivity of the virus and low infectivity of the patient. However, the absence or disappearance of HBeAg or anti-HBe does not rule out chronic hepatitis B carrier state and/or infectivity.


Production of hepatitis B core antibody (anti-HBc) begins in the window period after HBsAg disappears and before anti-HBs appears. Anti-HBc is present shortly after the onset of symptoms and can remain present for years after HBV infection. Anti-HBc IgM is elevated during the acute phase of hepatitis B but will become negative within 6 months.


The presence of hepatitis B surface antibody (anti-HBs) usually indicates resolution of the HBV infection and acquired immunity to the virus. Anti-HBs may fall below detectable levels with time.


See Viral Hepatitis Serologic Profiles in Special Instructions.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

Positive hepatitis B surface antigen (HBsAg) test results should be reported by the attending physician to the State Department of Health as required by law in some states.


Consider administration of hepatitis B immune globulin (HBIG) and hepatitis B vaccine to individuals exposed to the patient's blood and/or body fluids.


Performance characteristics have not been established for heat-inactivated specimens or specimens containing particulate matter.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.














Unvaccinated: negative

Vaccinated: positive



Unvaccinated: <5.0 mIU/mL

Vaccinated: > or =12.0 mIU/mL


Interpretation depends on clinical setting.

See Viral Hepatitis Serologic Profiles in Special Instructions.

Clinical References Provides recommendations for further in-depth reading of a clinical nature

1. Kubo S, Nishiguchi S, Hirohashi K, et al: Clinical significance of prior hepatitis B virus infection in patients with hepatitis C virus-related hepatocellular carcinoma. Cancer 1999 September 1;86(5):793-798

2. Farrell G: Hepatitis Be antigen seroconversion: effects of lamivudine alone on in combination with interferon alpha. J Med Virol 2000 July; 61(3):374-379

3. Schiff ER: Lamivudine for hepatitis B in clinical practice. J Med Virol 2000 July;61(3):386-391

4. Sherlock S: Hepatitis B: the disease. Vaccine 1990;8 Suppl:S6-S9