Hepatitis B Blood Tests

Hepatitis B markers explained

Interpreting hepatitis B result patterns

Who should be tested for hepatitis B?

• People born in regions with high HBV prevalence (Asia, Africa, Eastern Europe)
• Household contacts or sexual partners of HBsAg-positive people
• People with multiple sexual partners
• Healthcare workers
• People with HIV or hepatitis C
• Pregnant women (all should be screened)

Questions to ask your doctor

• Am I infected, immune, or susceptible?
• Do I need the hepatitis B vaccine?
• If I have chronic HBV, do I need antiviral treatment?
• Do I need regular liver ultrasound and AFP for liver cancer surveillance?

Frequently Asked Questions

References

The clinical information on this page is drawn from peer-reviewed sources indexed by the US National Library of Medicine. Links go to the source so you can read it yourself.

1. Hepatitis B. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK555945

References

Sources cited on this page. PubMed links open the original abstract.

1. Terrault NA, Lok ASF, McMahon BJ, et al. Update on prevention, diagnosis, and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance. Hepatology. 2018;67(4):1560–1599. PMID 29477461 · doi:10.1002/hep.29800

The hepatitis B serology puzzle – what each marker means

Hepatitis B has more serological markers than virtually any other infection, and interpreting them requires understanding what each marker represents in the viral life cycle:

• HBsAg (hepatitis B surface antigen): The virus's outer coat protein. Its presence in blood means the person is currently infected with hepatitis B – either acutely or as a chronic carrier. Persisting beyond 6 months defines chronic hepatitis B.
• Anti-HBs (antibody to HBsAg): Protective antibody. Present after successful vaccination (as the sole positive marker), or after natural infection and recovery (alongside anti-HBc). Anti-HBs above 10 mIU/mL indicates immunity.
• HBeAg (hepatitis B e-antigen): A secreted protein indicating active viral replication. HBeAg-positive chronic hepatitis B is highly infectious (serum HBV DNA typically very high) and causes more aggressive liver disease. Spontaneous HBeAg seroconversion to anti-HBe is a favourable event indicating reduction of viral replication.
• Anti-HBc (antibody to core antigen): IgM anti-HBc rises in acute infection; IgG anti-HBc persists for life and indicates past or current infection. Anti-HBc IgG positive with negative HBsAg and positive anti-HBs = resolved infection (immune). Anti-HBc IgG with negative HBsAg and negative anti-HBs = "occult" hepatitis B – low-level infection sometimes reactivated by immunosuppression.
• HBV DNA (viral load): Quantitative PCR measurement of virus in the blood. The key test for guiding treatment decisions. HBV DNA above 2000 IU/mL is the threshold above which antiviral therapy is generally considered in chronic hepatitis B with evidence of liver damage.

Chronic hepatitis B – monitoring and treatment

Chronic hepatitis B does not mean severe liver disease is inevitable. Many people have "inactive" chronic infection – normal ALT, HBV DNA below 2000 IU/mL, and minimal liver fibrosis – and can be monitored without treatment. Key monitoring schedule includes: ALT every 6 months, HBV DNA every 6–12 months, and abdominal ultrasound plus AFP (alpha-fetoprotein) every 6 months for hepatocellular carcinoma (HCC) surveillance – because HBV-related HCC can develop even without cirrhosis, unlike most other causes of liver cirrhosis. Tenofovir and entecavir are first-line antiviral agents – they suppress HBV DNA to undetectable levels, normalize ALT, and significantly reduce the risk of cirrhosis progression and HCC.