Question:hard
A male patient is observed to be HBsAg positive, HBeAg negative, and anti-HBe antibody positive. HBV DNA copies are observed to be 100,000/ml, while SGOT and SGPT are elevated to 6 times the upper limit of normal. What is the likely diagnosis?
A male patient is observed to be HBsAg positive, HBeAg negative, and anti-HBe antibody positive. HBV DNA copies are observed to be 100,000/ml, while SGOT and SGPT are elevated to 6 times the upper limit of normal. What is the likely diagnosis?
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HBeAg negative but high DNA and raised enzymes equals the precore mutant that cannot make e antigen.
Updated On: Jun 24, 2026
- HBV surface mutant
- HBV precore mutant
- Wild HBsAg
- Inactive HBV carrier
Show Solution
The Correct Option is B
Solution and Explanation
This vignette sets a trap by pairing a reassuring serology with alarming activity. The patient has lost HBeAg and gained anti-HBe, which usually signals a calm, low-replicative phase. Yet his HBV DNA sits at 100,000 copies per ml and his transaminases are six times normal, both pointing to aggressive, ongoing disease.
To reconcile this, ask how a virus can replicate hard while making no e antigen. The answer is a $precore$ mutant. A point mutation in the precore region introduces a stop codon, so the virus can no longer synthesise HBeAg, even though it copies its DNA briskly and keeps inflaming the liver. This produces the classic HBeAg-negative chronic hepatitis B picture: HBeAg absent, anti-HBe present, high viral load, and raised enzymes.
The other options do not fit. A surface mutant changes the HBsAg epitope to dodge neutralising antibody and is a vaccine-escape issue, not an HBeAg-DNA story. Wild-type virus in an actively replicating, enzyme-raising state is typically still HBeAg positive. An inactive carrier would show low DNA and normal enzymes, which is the exact opposite of this active disease.
The combination of no e antigen yet high replication and liver damage is the fingerprint of the precore mutant.
\[\boxed{\text{HBV precore mutant}}\]
To reconcile this, ask how a virus can replicate hard while making no e antigen. The answer is a $precore$ mutant. A point mutation in the precore region introduces a stop codon, so the virus can no longer synthesise HBeAg, even though it copies its DNA briskly and keeps inflaming the liver. This produces the classic HBeAg-negative chronic hepatitis B picture: HBeAg absent, anti-HBe present, high viral load, and raised enzymes.
The other options do not fit. A surface mutant changes the HBsAg epitope to dodge neutralising antibody and is a vaccine-escape issue, not an HBeAg-DNA story. Wild-type virus in an actively replicating, enzyme-raising state is typically still HBeAg positive. An inactive carrier would show low DNA and normal enzymes, which is the exact opposite of this active disease.
The combination of no e antigen yet high replication and liver damage is the fingerprint of the precore mutant.
\[\boxed{\text{HBV precore mutant}}\]
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