The mutations frequency of enhancer II/ HBx regions of hepatitis B virus in acutely infected Iranian patients: a cross-sectional study

Chiman Karami; Hamidreza Mollaei; Seyed Alimohammad Arabzadeh; Kamyar Mazloum Jalali; Saman Amerkani; Salar Pashangzadeh; Najmeh Nikpour

doi:10.18502/ijm.v14i4.10242

Chiman Karami Department of Microbiology, Parasitology and Immunology, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran
Hamidreza Mollaei Department of Microbiology and Medical Virology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran
Seyed Alimohammad Arabzadeh Department of Microbiology and Medical Virology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran
Kamyar Mazloum Jalali Department of Microbiology and Medical Virology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran
Saman Amerkani Department of Microbiology and Medical Virology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran
Salar Pashangzadeh Iranian Research Center for HIV/AIDS, Iranian Institute for Reduction of High Risk Behaviors, Tehran University of Medical Sciences, Tehran, Iran
Najmeh Nikpour Department of Microbiology and Medical Virology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran

DOI: https://doi.org/10.18502/ijm.v14i4.10242

Keywords: Hepatitis B virus; X protein; Infections; Enhancer II; Mutation; Liver diseases

Abstract

Background and Objectives: The viral transactivator HBx protein affect cellular, viral and pregenomic factors pathway. Mutations in this protein can produce new viruses with new antigenic determinants that are generally related to developing cancerous.

Materials and Methods: In this cross-sectional study, 33 serum samples of patients diagnosed with acute HBV infection were investigated for HBeAg and HBV DNA viral load and HBx gene mutations. mutation in the HBx protein detected by sequencing analysis.

Results: Out of the 33 samples, 19 samples were males (57.6%), and 14 samples were females. 15 (45.5%) were positive for HBx DNA and 18 patients were negative for HBx DNA (54.5%). After sequencing, three mutations were recognized in HBx at nucleotide positions 147, 148, and 391 that were stationed to G1524A, G1525A, and G1767C mutations.

Conclusion: The analysis result of this study shows G1524A and G1525A mutations that an important role in altering the inhibition function of the HBx activity domain. The G1767C mutation inactivates HBx transactivation activity. These muta- tions have a critical role in the pathogenicity of the virus, and the intensity of hepatic tissue demolition and the development of cirrhosis or carcinoma in patients can be understood.