Test Catalog

Interpretive Handbook

Test 200905 :
Hepatitis B Profile, Serum

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

Hepatitis B 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 has been known to be spread through oral and genital contact. Hepatitis B virus (HBV) can be transmitted from mother to child during delivery through contact with blood and vaginal secretions; it is not commonly transmitted transplacentally.

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

Determining whether a patient has been exposed to hepatitis B virus (HBV)


Monitoring patients recovering from HBV infection


Diagnosis of HBV infection, although HBIS / Hepatitis B Immune Status Profile, Serum may be more conclusive

Interpretation Provides information to assist in interpretation of the test results

Presence of hepatitis B surface antigen (HBsAg) in serum may indicate acute hepatitis B virus (HBV) infection, chronic HBV infection, or asymptomatic carrier state. The significance of HBsAg in serum is determined by evaluating it in relationship to the presence or absence of the other HBV markers and the clinical presentation and history of the patient.


Before the onset of clinical illness, HBsAg is detectable in the serum and its presence persists through the symptomatic phase of illness. Following clinical illness, the titer of HBsAg begins to decline and eventually falls below a detectable level. After HBsAg disappears, hepatitis B surface antibody (anti-HBs) appears in the serum, although there is often a gap called the "window period" between the disappearance of HBsAg and the appearance of anti-HBs. In approximately 10% of patients, HBsAg persists indefinitely in the serum, indicating a chronic carrier state, and anti-HBs does not appear.


During the course of a typical case of acute hepatitis B infection, hepatitis B core antibody (anti-HBc) is present in the serum shortly before clinical symptoms appear. It is detectable during prodromal, acute, and early convalescent phases where it exists as immunoglobulin M (IgM) anti-HBc. Total anti-HBc (IgG and IgM) rises in titer and is present during the "window period," ie, after HBsAg disappears and before anti-HBs appears. For this reason, in the absence of other HBV markers, total anti-HBc is considered a reliable indicator of ongoing infection. It is also an accurate serological marker of previous HBV infection, as it appears in all patients infected with the HBV and may persist in individuals at low titer (as IgG anti-HBc) long after HBV exposure. Although total anti-HBc is a long-lived antibody, in some cases total anti-HBc titers, along with total anti-HBs, may fall into the undetectable range.


In subclinical asymptomatic HBV infection, HBsAg and hepatitis Be antigen (HBeAg) are present for a brief period or may not be detectable and are followed by the appearance of anti-HBc and anti-HBs. In these patients, detection of total anti-HBc and total anti-HBs must be relied on as evidence of previous HBV infection.


In chronic HBV, HBsAg appears during the incubation phase of the disease and may persist for years and possibly for life. Total anti-HBc also appears during this early phase and rises in titer. The highest titers of total anti-HBc are found in the chronic HBsAg carrier state. Total anti-HBc may be negative or undetectable in serum or plasma during the early acute phase of HBV infection and long after infection resolution, when titers may fall.


The presence of anti-HBs in serum indicates previous exposure to HBV and acquired immunity. Low titers of anti-HBs in serum, however, can signal a lack of immunity to future HBV infection. The clinical relevance of anti-HBs detection is in establishing complete resolution of the infection and the acquisition of immunity, whether acquired as a result of natural HBV infection or vaccination. 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 result should be reported by the attending physician to the State Department of Health as required by law in some states.


A weakly positive anti-hepatitis B core (HBc) test result unaccompanied by other hepatitis B serologic markers, elevated liver enzymes, or a history of risk factors may be a false-positive result.


Passively acquired anti-hepatitis B surface (HBs) (ie, transfusion, recent immune globulin treatment, etc) does not signify immunity.


Anti-HBs may fall below detectable levels with time.


Assay performance characteristics have not been established for:

-Grossly icteric (total bilirubin level of >20 mg/dL)

-Grossly lipemic (triolein level of >800 mg/dL)

-Grossly hemolyzed (hemoglobin level of >500 mg/dL)

-Cadaveric specimens

-Those that contain particulate matter

-Heat-inactivated specimens

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

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