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Advances in Bioinformatics
Volume 2015, Article ID 678587, 14 pages
http://dx.doi.org/10.1155/2015/678587
Research Article

Local Mutational Pressures in Genomes of Zaire Ebolavirus and Marburg Virus

1Department of General Chemistry, Belarusian State Medical University, Dzerzinskogo 83, 220116 Minsk, Belarus
2Laboratory of Cellular Technologies, Institute of Physiology of the National Academy of Sciences of Belarus, Academicheskaya 28, 220072 Minsk, Belarus

Received 29 July 2015; Revised 30 October 2015; Accepted 3 November 2015

Academic Editor: Huixiao Hong

Copyright © 2015 Vladislav Victorovich Khrustalev 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.

Abstract

Heterogeneities in nucleotide content distribution along the length of Zaire ebolavirus and Marburg virus genomes have been analyzed. Results showed that there is asymmetric mutational A-pressure in the majority of Zaire ebolavirus genes; there is mutational AC-pressure in the coding region of the matrix protein VP40, probably, caused by its high expression at the end of the infection process; there is also AC-pressure in the 3′-part of the nucleoprotein (NP) coding gene associated with low amount of secondary structure formed by the 3′-part of its mRNA; in the middle of the glycoprotein (GP) coding gene that kind of mutational bias is linked with the high amount of secondary structure formed by the corresponding fragment of RNA negative (−) strand; there is relatively symmetric mutational AU-pressure in the polymerase (Pol) coding gene caused by its low expression level. In Marburg virus all genes, including C-rich fragment of GP coding region, demonstrate asymmetric mutational A-bias, while the last gene (Pol) demonstrates more symmetric mutational AU-pressure. The hypothesis of a newly synthesized RNA negative (−) strand shielding by complementary fragments of mRNAs has been described in this work: shielded fragments of RNA negative (−) strand should be better protected from oxidative damage and prone to ADAR-editing.