Core promoter: A critical region where the hepatitis B virus makes decisions

Table 1 More frequent basal core promoter mutations and their clinical relevance

Nucleotide position	Clinical relevance
1762T + 1764A (BCP double mutant)	Chronic HBV Fulminant hepatitis Decrease in HBeAg production and increase viral replicationDiminished binding of a liver-specific transcription factor, resulting in a decrease in HBeAg, but unchanged amounts of HBV pregenomic RNAEnhance viral replication through the combined effects of X gene mutations and the appearance of a HNF-1 transcription factor binding site Elevated ALT (diminishing circulating HBeAg levels → augment the host immune response to HBV-infected hepatocytes → increasing hepatocyte apoptosis) More often in patients with HBV genotypes that have 1858C (i.e., genotype C)
1762T	HBeAg seroconversion and histological inflammation
1764A	No suppression on HBV RNA transcription and only slightly decreases the efficiency of virus replication
1653T	Usually together with the 1762T + 1764A in patients with fulminant hepatitis and hepatocellular carcinoma
1753-1757	Together with the 1762T + 1764A mutation, have been detected in patients with fulminant hepatitis and in patients with HCCALT levels and histological changes
1764A/T + 1766A/G	Found in active and inactive disease in conjunction with 1810T + 1811T double mutation 1762A1766A mutation, together with 1762T, was found in fulminant hepatitis and HCC patients The 1764T + 1766G mutation was found in a patient with fulminant recurrent hepatitis after liver transplantation, but was absent in patients with fulminant hepatitis.
1766T + 1768A	Fulminant hepatitis Together with 1762T + 1764A, in a patient with recurrent hepatitis following liver transplantation With 1764A in a HBeAg-negative asymptomatic carrierExacerbation of HBV infection and created two overlapping low-affinity HNF1 sites

BCP: Basal core promoter; HBV: Hepatitis B virus; HNF-1: Hepatocyte nuclear factor 1; ALT: Alanine transaminase; HCC: Hepatocellular carcinoma.