Mem Inst Oswaldo Cruz, Rio de Janeiro, 112(9) September 2017
Basal core promoter and precore mutations among hepatitis B virus circulating in Brazil and its association with severe forms of hepatic diseases
1Universidade Federal de São Carlos, Departamento de Medicina, São Carlos, SP, Brasil
2Universidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Departamento de Clínica Médica, Divisão de Gastroenterologia, Ribeirão Preto, SP, Brasil
3Faculdade de Medicina da Universidade de São Paulo, Instituto de Medicina Tropical, Departamento de Gastroenterologia, Laboratório de Gastroenterologia e Hepatologia Tropical, São Paulo, SP, Brasil
4Universidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Departamento de Medicina Social, Ribeirão Preto, SP, Brasil
5Hospital Israelita Albert Einstein, São Paulo, SP, Brasil
BACKGROUND In Brazil, few studies have investigated the prevalence of infection with the precore (PC) and basal core promoter (BCP) mutants of the hepatitis B virus (HBV).
OBJECTIVES This study aimed to analyse the frequency of PC and BCP mutations among patients infected with HBV and to evaluate the association between the variants and advanced hepatic disease.
METHODS A total of 161 patients infected with HBV were studied. To identify PC and BCP mutations, a 501-bp fragment of HBV DNA was amplified and sequenced.
FINDINGS PC and BCP regions from HBV strains were successfully amplified and sequenced in 129 and 118 cases, respectively. PC and BCP mutations were detected in 61.0% and 80.6% of the cases, respectively. The A1762T/G1764A variant was identified in 36.7% of the patients with grade 1 and 2 liver fibrosis (29/79) and in 81.8% of the patients with grade 3 and 4 liver fibrosis (9/11) (p < 0.01); in 76.9% of the patients with cirrhosis (10/13) and in 38.1% of the patients without cirrhosis (40/105) (p = 0.01); and in 77.8% of the patients with hepatocellular carcinoma (HCC) (7/9) and in 39.4% of the patients without HCC (43/109) (p = 0.03).
MAIN CONCLUSIONS A high prevalence of HBV PC and BCP mutants was found. The A1762T/G1764A variant was independently associated with advanced forms of liver fibrosis, hepatic cirrhosis, and HCC.