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Journal of Pathogens
Volume 2017, Article ID 1231204, 6 pages
Research Article

Novel Genetic Variants of Hepatitis B Virus in Fulminant Hepatitis

1Sunway Institute for Healthcare Development (SIHD), Sunway University, 47500 Bandar Sunway, Selangor Darul Ehsan, Malaysia
2Department of Pre-Clinical Sciences, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, 43000 Selangor, Malaysia
3Department of Medical Microbiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
4Department of Medicine, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia

Correspondence should be addressed to Jack Bee Chook; ym.ude.yawnus@ceebkcaj

Received 29 August 2017; Accepted 20 November 2017; Published 19 December 2017

Academic Editor: Mario M. D’Elios

Copyright © 2017 Jack Bee Chook et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Fulminant hepatitis (FH) is a life-threatening liver disease characterised by intense immune attack and massive liver cell death. The common precore stop codon mutation of hepatitis B virus (HBV), A1896, is frequently associated with FH, but lacks specificity. This study attempts to uncover all possible viral nucleotides that are specifically associated with FH through a compiled sequence analysis of FH and non-FH cases from acute infection. We retrieved 67 FH and 280 acute non-FH cases of hepatitis B from GenBank and applied support vector machine (SVM) model to seek candidate nucleotides highly predictive of FH. Six best candidates with top predictive accuracy, 92.5%, were used to build a SVM model; they are C2129 (85.3%), T720 (83.0%), Y2131 (82.4%), T2013 (82.1%), K2048 (82.1%), and A2512 (82.1%). This model gave a high specificity (99.3%), positive predictive value (95.6%), and negative predictive value (92.1%), but only moderate sensitivity (64.2%). We successfully built a SVM model comprising six variants that are highly predictive and specific for FH: four in the core region and one each in the polymerase and the surface regions. These variants indicate that intracellular virion/core retention could play an important role in the progression to FH.