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Hepatitis B Surface Antibody (Hbsab) - Quantitative

Principle

Viral hepatitis remains a major global public health concern, with an estimated 300 million chronic carriers of hepatitis B virus (HBV) worldwide. HBV infection can lead to a wide spectrum of acute and chronic liver diseases, including cirrhosis and hepatocellular carcinoma. HBV infection produces a series of viral antigens and corresponding antibody responses that follow characteristic serologic patterns. Hepatitis B surface antigen (HBsAg), derived from the viral envelope, is the first antigen detected after infection. Neutralizing antibodies to HBsAg (anti-HBs) develop in approximately 90% of HBV-infected individuals and are associated with recovery from infection and the establishment of protective immunity. Individuals who have resolved HBV infection typically have both anti-HBs and antibody to hepatitis B core antigen (anti-HBc) detectable in serum. The absence of both anti-HBs and anti-HBc indicates susceptibility to HBV infection and identifies those who may benefit from vaccination. Both plasma-derived and recombinant protein–based hepatitis B vaccines are effective in inducing protective immunity through the production of anti-HBs. Quantitative anti-HBs testing is useful for determining susceptibility to HBV and for evaluating immune response in pre- and post-vaccination screening programs.

Specimen Requirements

Specimen

Serum

Collection

Collect 2 mL of serum in a red-top tube (no additives) or a serum separator tube (gel barrier).

Processing

Separate serum from the clot as soon as possible to prevent hemolysis.

Storage and Transport

  • 2–8 °C: stable for up to 48 hours
  • −20 °C or below: required if testing is delayed beyond 48 hours
  • Avoid repeated freeze–thaw cycles

Method

Enzyme-Linked Immunosorbent Assay (ELISA).

Turnaround Time

One Week.

Clinical Interpretation of Immune Status

< 9.0 mIU/mL — Non-Reactive
Patient is considered not immune to HBV infection.

> 9.0 mIU/mL and < 12.0 mIU/mL — Borderline
Unable to determine if antibody levels are

References

  1. Maynard JE. et al. In Zuckerman AJ. (ed), Viral Hepatitis and Liver Disease. New York: Alan R. Liss Inc; 967-969; 1988.
  2. Beasley RP, Hwang L. In Vyas GN. (ed), Viral Hepatitis and Liver Disease. New York: Grune & S

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