Mutaciones en el marco de lectura abierto de la polimerasa del virus de la hepatitis B en muestras de pacientes con infección crónica

Introduction. Antiviral therapy for hepatitis B virus infection controls replication but does not achieve viral clearance. Long-term treatment is generally required, with the potential emergence of viral genome mutations associated with drug resistance. Objective. To identify mutations in the hepatitis B virus polymerase open reading frame in samples from patients with chronic hepatitis B, with or without prior antiviral therapy. Materials and methods. Samples from 26 patients diagnosed with chronic hepatitis B and treated in hospitals across different regions of Colombia were analyzed. The polymerase open reading frame was amplified, sequenced, and examined using BioEdit, MEGA 11, and Geno2Pheno.Results. Amplification of the hepatitis B virus polymerase open reading frame was successful in 4 of 26 samples (15.4%), all from treatment-naïve individuals. No primary or secondary mutations associated with resistance to entecavir were detected. However, 10 amino acid substitutions were identified in the RT domain of the polymerase open Reading frame: rtH35Q, rtT38A, rt126Y, rtD134Y, rtN139H, rtF151Y, rtR153W, rtS259A, rtE271H,and rtC332S.Conclusions. This exploratory study did not reveal primary mutations linked to entecavir resistance in Colombian patients with chronic hepatitis B who were treatment-naïve. Ten amino acid changes were observed in the RT region of the polymerase open reading frame, none within the YMDD motif, a conserved sequence of the viral polymerase catalytic site. Further studies are required to estimate the prevalence and clinical significance of antiviralresistance mutations in Colombian patients with hepatitis B virus.