Abstract
The genetic diversity of orthohepadnaviruses is not yet fully understood. This study was conducted to investigate the role of structural variations (SVs) in their diversity. Genetic sequences of orthohepadnaviruses were retrieved from databases. The positions of sequence gaps were investigated, since they were found to be related to SVs, and they were further used to search for SVs. Then, a combination of pair-wise and multiple alignment analyses was performed to analyze the genomic structure. Unique patterns of SVs were observed; genetic sequences at certain genomic positions could be separated into multiple patterns, such as no SV, SV pattern 1, SV pattern 2, and SV pattern 3, which were observed as polymorphic changes. We provisionally referred to these genetic changes as SV polymorphisms. Our data showed that higher frequency of sequence gaps and lower genetic identity were observed in the pre-S1-S2 region of various types of HBVs. Detailed examination of the genetic structure in the pre-S region by a combination of pair-wise and multiple alignment analyses showed that the genetic diversity of orthohepadnaviruses in the pre-S1 region could have been also induced by SV polymorphisms. Our data showed that novel genetic rearrangements provisionally termed SV polymorphisms were observed in various orthohepadnaviruses.
Highlights
Hepatitis B virus (HBV) infection is an important global health issue and can cause acute and chronic liver diseases
Together with wooly monkey Hepatitis B virus (WMHBV) and rodent HBVs (WHV, GSHV, and ASHV), bat HBVs (TBHBV, PBHBV, BHBV-C, LBHBV, HBHBV, and RBHBV) and species of primate HBVs were analyzed in this study (Table S1)
We found that complex structural variations (SVs) tended to accompany sequence gaps [21,22,23], the positions and lengths of sequence gaps in bat and rodent HBVs were analyzed using WMHBV as a reference sequence in order to investigate the presence of SVs in their genomes
Summary
Hepatitis B virus (HBV) infection is an important global health issue and can cause acute and chronic liver diseases. An estimated 257 million people are deemed to be infected with HBV as they are positive for hepatitis B surface antigen (HBs-Ag), and HBV infection causes approximately. Fatal liver failure caused by reactivation of occult HBV in HBs-Ag-negative patients, who were considered as cured of a previous infection, by treatment with anti-cancer and immune-modulating drugs is a serious clinical problem [2,3]. HBV infection is a lifelong threat even after clinical cure of chronic infection. HBV is a member of the hepadnaviridae family, which is composed of two genera—the genus. Orthohepadnavirus infects mammals, and the genus Avihepadnavirus infects birds [4]. Bat HBVs (tent-making bat HBV (TBHBV), Pomona bat HBV (PBHBV), unspecified bat HBV from China (BHBV-C), long-fingered bat HBV (LBHBV), Viruses 2019, 11, 871; doi:10.3390/v11090871 www.mdpi.com/journal/viruses
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