Precore G1896A mutation of hepatitis B virus in patients with chronic hepatitis B, hepatic cirrhosis, and hepatocellular carcinoma in Burkina Faso.

Background: Hepatitis B virus (HBV) infection, which can progress to liver cancer and even death, remains a public health problem. The high variability of HBV leading to the accumulation of mutations influences the natural history of this infection. Mutations in the precore/core region, in particular the G1896A mutation, have been associated with severe forms of liver disease in certain populations around the world. The aim of this study was to determine the molecular epidemiology of the HBV precore G1896A mutation and its relationship to hepatic complications in HBV chronically infected patients.

Methods: Classical nested PCR was used to amplify the HBV precore region. A total of 97 samples consisting of 53 cases of chronic hepatitis B (CHB), 18 cases of hepatic cirrhosis (HC) and 26 cases of hepatocellular carcinoma (HCC) were amplified. The G1896A mutation was determined by enzymatic digestion on 81 samples using the restriction enzyme Bsu36I. Serological (HBeAg, anti-HBe Ac), biochemical (ALT) and virological (HBV-DNA viral load) tests were performed.

Results: The frequency of the G1896A mutation was 44.44% in our study population. It was 56.82% in CHB cases, 28.57% in HC cases and 30.43% in HCC. The G1896A mutation was found more in subjects with a negative HBeAg status than in those with a positive HBeAg (p = 0.05) in the CHB subgroup. The DNA level was higher in subjects carrying wild-type strains for the G1896A mutation (p > 0.05). ALT levels were lower in subjects carrying the G1896A mutation than in those infected with wild-type strains (p = 0.006) in the HBC subgroup.

Conclusion: This study, conducted on patients with chronic hepatitis B, cirrhosis, and hepatocellular carcinoma (HCC), showed that the frequency of the precore G1896A mutation was 44.44%. We found no correlation between this mutation and cirrhosis and HCC. However, it was more found in subjects with chronic hepatitis B and was associated with HBeAg negativity in the latter. It would therefore be involved in the elimination of this protein partly responsible for the persistence of HBV infection and could be a molecular marker for clinicians in the management of patients infected with HBV with negative HBeAg and positive anti-HBe antibodies. However, studies on other mutations of the precore gene would be necessary to obtain more conclusive results in terms of effective treatment.