Step 1: Read the serology. HBsAg is positive, HBeAg is negative, anti-HBe is positive, the HBV DNA is high at 100,000 copies/ml, and the liver enzymes are up to 6 times normal.
Step 2: Spot the paradox. Normally a negative HBeAg with positive anti-HBe suggests seroconversion to a quiet, low-replicative state. But here the virus is replicating strongly (high DNA) and the liver is inflamed (enzymes 6 times normal). That mismatch is the whole point of the question.
Step 3: Explain the mismatch. A precore (or core promoter) mutant of HBV cannot make HBeAg because of a stop-codon mutation in the precore region. So the patient is HBeAg negative yet keeps replicating actively and damaging the liver. This is HBeAg-negative chronic hepatitis B caused by the precore mutant.
Step 4: Rule out the rest. A surface (escape) mutant alters HBsAg so it evades vaccine-induced antibody, which does not explain the HBeAg and DNA pattern here. Wild-type HBV with active disease would usually be HBeAg positive. An inactive carrier would have low DNA and normal enzymes, the opposite of this case.
The answer is option B, HBV precore mutant.