These findings, and the evidence in the adults that after HBeAg to anti-HBe seroconversion, a dominant G1896A precore mutant population was more frequent in patients with CHB (44.4%) than in HBeAg-negative infection carriers (19.6%), suggest that the faster and stronger the immune control of HBV replication is, the lower the selection of HBeAg defective variants [72,73,74,75]. This evidence concerns the gene HBE1 and infection.