The importance of hepatitis B virus (HBV) genotype and mutations has been increasingly recognized. We aimed to determine HBV genotype, precore (PC), and basal core promoter region (BCP) mutations in a HBV multiethnic South Florida population.
Samples from 213 patients were tested for HBV-DNA using Abbott RealTime HBV IUO assay, and for mutations using INNO-LiPA assay.
Patients were predominantly male (67%); 61 (31%) were African American, 60 (28%) Hispanic, 37 (17%) Haitian, 27 (19%) white non-Hispanic, and 14 (6.6%) Asian. Genotype A was found in 101 (69%), D in 25 (17%), F in 9 (6%), G in 7 (5%), C and E in 6 (4%) each, B in 4 (3%), and H in 2 (1%) patients. Mixed genotypes were detected in 11 patients. Genotype A was more prevalent in all ethnicities except for Asian. Among hepatitis B e antigen (HBeAg)-negative patients (59%), BCP, PC, and combined BCP/PC mutations were found in 30 (37.5%), 13 (16.3%), and 14 (17.5%), respectively. Genotype D was associated with higher frequency of HBeAg-negative status [18/24 (75%) vs. 62/121 (51%) P=0.03] and mutations [16/19 (84%) vs. 40/67 (60%) P=0.04] compared with others. Genotype A was negatively associated with mutations [26/31 (84%) vs. 30/55 (55%), P=0.009]. PC mutations were more common in genotype D (14/19, 73%) compared with genotype A (7/54, 13%, P<0.0001). One-hundred percent and 79% of Asians and Haitians had spontaneous mutations, respectively. All Haitians with genotype D had PC mutations and 3 (50%) had BCP/PC.
The present study shows that HBeAg-negative status and spontaneous mutations were more common with genotype D; the presence of genotype D in Haitians was always associated with spontaneous mutations.
*Department of Internal Medicine and Alfa Gastroenterology Institute, School of Medicine, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil
†Division of Hepatology, Center for Liver Diseases, University of Miami, Leonard M. Miller School of Medicine, Miami, FL
‡Abbott Molecular, DesPlaines, IL
Supported in part by Abbott Molecular, Grant number UM 20080863.
M.d.M.: participated in the Advisory Board meeting October 28, 2010; M.R.S.: Abbott Molecular employee and shareholder; G.A.C.: Abbott Molecular employee and shareholder; P.M.: Abbott consultant. The remaining authors declare that they have nothing to disclose.
Reprints: Paul Martin, MD, Division of Hepatology, Center for Liver Diseases, University of Miami Leonard M. Miller School of Medicine, 1500 NW, 12th Avenue, suite 1101, Miami, FL 33136 (e-mail: firstname.lastname@example.org).
Received January 17, 2012
Accepted July 3, 2012