ALSO SEE IVMS-Hepatitis and HBV Interactive Tutorial

1. HEPATITIS B SERODIAGNOSIS ESSENTIALS /mic 09-13
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HEPATITIS B SERODIAGNOSIS ESSENTIALS
A supplement to IVMS-Hepatitis and HBV Interactive Tutorial
|http://www.slideshare.net/drimhotep/hepatitis-and-hbv-tutorial|
Serologic testing in HBV|
Also see HBV Antibody-Viral Test
1. HBsAg—The appearance of HBsAg in serum is the first evidence of infection,
appearing before biochemical evidence of liver disease, and persists throughout the
clinical illness. Persistence of HBsAg more than 6 months after the acute illness
signifies chronic hepatitis B.
2. Anti-HBs—Specific antibody to HBsAg (anti-HBs) appears in most individuals after
clearance of HBsAg and after successful vaccination against hepatitis B.
Disappearance of HBsAg and the appearance of anti-HBs signal recovery from HBV
infection, noninfectivity, and immunity.
3. Anti-HBc—IgM anti-HBc appears shortly after HBsAg is detected. (HBcAg alone
does not appear in serum.) In the setting of acute hepatitis, IgM anti-HBc indicates a
diagnosis of acute hepatitis B, and it fills the serologic gap in rare patients who have
cleared HBsAg but do not yet have detectable anti-HBs. IgM anti-HBc can persist for 3-
6 months or longer. IgM anti-HBc may also reappear during flares of previously inactive
From: Cecil Essentials of Medicine Andreoli and Carpenter's 8th.Ed

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chronic hepatitis B (see later). IgG anti-HBc also appears during acute hepatitis B but
persists indefinitely, whether the patient recovers (with the appearance of anti-HBs in
serum) or chronic hepatitis B develops (with persistence of HBsAg). In asymptomatic
blood donors, an isolated anti-HBc with no other positive HBV serologic results may
represent a falsely positive result or latent infection in which HBV DNA is detectable in
serum only by polymerase chain reaction testing
4. HBeAg—HBeAg is a secretory form of HBcAg that appears in serum during the
incubation period shortly after the detection of HBsAg. HBeAg indicates viral replication
and infectivity. Persistence of HBeAg beyond 3 months indicates an increased
likelihood of chronic hepatitis B. Its disappearance is often followed by the appearance
of anti-HBe, generally signifying diminished viral replication and decreased infectivity.
5. HBV DNA—The presence of HBV DNA in serum generally parallels the presence of
HBeAg, although HBV DNA is a more sensitive and precise marker of viral replication
and infectivity. Very low levels of HBV DNA, detectable only by polymerase chain
reaction testing, may persist in serum and liver long after a patient has recovered from
acute hepatitis B, but the HBV DNA in serum is bound to IgG and is rarely infectious. In
some patients with chronic hepatitis B, HBV DNA is present at high levels without
HBeAg in serum because of development of a mutation in the core promoter or precore
region of the gene that codes HBcAg; these mutations prevent synthesis of HBeAg in
infected hepato-cytes. When additional mutations in the core gene are present, the pre-
core mutant enhances the severity of HBV infection and increases the risk of cirrhosis
(see later).

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Table from: Cecil Essentials of Medicine Andreoli and Carpenter's 8th.Ed

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