Báo cáo sinh học: " HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers"

HBx M130K and V131I (T-A) mutations in HBV genotype F during a follow-up study in chronic carriers | Virology Journal BioMed Central Research Open Access HBx MI30K and V131I T-A mutations in HBV genotype F during a follow-up study in chronic carriers Bernal León 1 Lizeth Taylor1 Minor Vargas2 Ronald B Luftig5 Federico Albertazzi3 Libia Herrero4 and Kirsten Visona1 Address 1International Center for Medical Research and Training Louisiana State University ICMRT-LSU San José Costa Rica 2Pathology Department San Juan de Dios Hospital CCSS Costa Rica 3Molecular Biology Center Universidad of Costa Rica 4Virology Department Microbiology School Universidad of Costa Rica and 5Microbiology Immunology Parasitology Department School of Medicine Louisiana State University USA Email Bernal León - bernalleon@ Lizeth Taylor - lizethtaylor@ Minor Vargas - Minorvargasb@ Ronald B Luftig - rlufti@ Federico Albertazzi - falbertazzi@ Libia Herrero - lherrero@ Kirsten Visona - mvisona@ Corresponding author Published 04 August 2005 Received 05 April 2005 Accepted 04 August 2005 Virology Journal 2005 2 60 doi l 743-422X-2-60 This article is available from http content 2 1 60 2005 León et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Around 400 million people worldwide are chronically infected with Hepatitis B virus HBV . An estimated 10 of these chronic patients develop progressive liver damage including cirrhosis and Hepatocellular Carcinoma HCC . The HBx gene encodes a protein of l54 amino acids which is a transactivator and has been associated with HBV pathogenesis. A change in the amino acid sequences at positions 130 and 131 in the HBV-X protein M130K and V131I produced by T-A point mutations at the nucleic acids

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