Molecular Mechanisms of Poxvirus Evolution
Poxviruses are often thought to evolve relatively slowly because they are double-stranded DNA pathogens with proofreading polymerases. However, poxviruses have highly adaptable genomes and can undergo relatively rapid genotypic and phenotypic change, as illustrated by the recent increase in human-to...
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Published in | mBio Vol. 14; no. 1; p. e0152622 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Society for Microbiology
28.02.2023
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Subjects | |
Online Access | Get full text |
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Summary: | Poxviruses are often thought to evolve relatively slowly because they are double-stranded DNA pathogens with proofreading polymerases. However, poxviruses have highly adaptable genomes and can undergo relatively rapid genotypic and phenotypic change, as illustrated by the recent increase in human-to-human transmission of monkeypox virus.
Poxviruses are often thought to evolve relatively slowly because they are double-stranded DNA pathogens with proofreading polymerases. However, poxviruses have highly adaptable genomes and can undergo relatively rapid genotypic and phenotypic change, as illustrated by the recent increase in human-to-human transmission of monkeypox virus. Advances in deep sequencing technologies have demonstrated standing nucleotide variation in poxvirus populations, which has been underappreciated. There is also an emerging understanding of the role genomic architectural changes play in shaping poxvirus evolution. These mechanisms include homologous and nonhomologous recombination, gene duplications, gene loss, and the acquisition of new genes through horizontal gene transfer. In this review, we discuss these evolutionary mechanisms and their potential roles for adaption to novel host species and modulating virulence. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Present address: Chorong Park, Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. Present address: Shefali Banerjee, Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA. The authors declare no conflict of interest. Present address: M. Julhasur Rahman, Analytical Sciences, BioMarin Pharmaceutical Inc., Novato, California, USA. Present address: Huibin Yu, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. |
ISSN: | 2150-7511 2150-7511 |
DOI: | 10.1128/mbio.01526-22 |