The Analysis of Mutation Profile on Pre-S1 and Pre-S2 Region of Hepatitif B Virus in Chronic Liver Disease

• Main Authors: Citrawati Dyah Kencono Wungu, Mochamad Amin, Ulfa Kholili, Gwenny Ichsan Prabowo, Poernomo Boedi Setiawan, Soetjipto, Retno Handajani
• Format: Article PeerReviewed
• Language: English; English; English
• Published: Malaysian Society for Biochemistry & Molecular Biology 2018
• Subjects: R Medicine (General); RA Public aspects of medicine
• Online Access: http://repository.unair.ac.id/91382/1/The%20Analysis%20of%20Mutation%20Profile%20on%20Pre-S1%20and%20Pre-S2%20Region%20of%20Hepatitis%20B%20Virus%20in%20Chronic%20Liver%20Disease.pdf; http://repository.unair.ac.id/91382/3/The%20Analysis%20of%20Mutation%20Profile%20on%20Pre-S1%20and%20Pre-S2%20Region%20of%20Hepatitis%20B%20Virus%20in%20Chronic%20Liver%20Disease.pdf; http://repository.unair.ac.id/91382/7/The%20Analysis%20of%20Mutation%20.pdf; http://repository.unair.ac.id/91382/; https://msbmb2010.wixsite.com/mjbmb/copy-of-home-4
• Institution: Universitas Airlangga

Objective: The purpose of this study was to complete the data frequency and mutation profile of Hepatitis B Virus (HBV) pre-S1 and pre-S2 in Indonesia. Methods: This cross-sectional study was used 32 blood serum samples of Chronic Liver Disease (CLD) patients with Hepatitis B surface antigen (HbsAg) at Endoscopy Outpatient Clinic, RSUD Dr. Soetomo Hospital, Surabaya. Polymerase Chain Reaction (PCR) of HBV DNA was performed on the samples based on pre-S1 and pre-S2 region. Then, electrophoresis was performed on the PCR product and followed by sequencing on samples with positive electrophoresis result. The sequencing results were analyzed by comparing them with the published sequences of HBV nucleotide. Results: The amplification results of nested PCR DNA HBV with primers based on HBV pre-S1 and pre-S2 region were positive at 21 serums. In patients with CLD in this study, pre-S1 and / or pre-S2 HBV mutations were found in 11 (84.62%) chronically infected HBV patients, 4 (100%) patients with liver cirrhosis, and 4 (100%) HCC patients. Dominant mutations were L101V (16.57%), M120I / T or pre-S2 start codon (10.82%), and F141L (10.81%). M120 and F141L mutations have been previously reported to be associated with CLD, while the dominant L101V mutation in this study as well as several other mutations has not been reported in previous studies. Conclusions: Mutations of pre-S1 and pre-S2 HBV regions were obtained in 90.48% of CLD patients in the form of substitution and deletion of amino acids.