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Journal ArticleDOI

Rapid genomic evolution of a non-virulent coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolates.

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TLDR
To the best of the knowledge, this is the first report of a specific nutritional deficiency driving changes in a viral genome, permitting an avirulent virus to acquire virulence due to genetic mutation.
Abstract
Previous work from our laboratory demonstrated that selenium deficiency in the mouse allows a normally benign (amyocarditic) cloned and sequenced Coxackievirus to cause significant heart damage. Furthermore, Coxsackievirus recovered from the hearts of selenium-deficient mice inoculated into selenium-adequate mice still induced significant heart damage, suggesting that the amyocarditic Coxsackievirus had mutated to a virulent phenotype. Here we report that sequence analysis revealed six nucleotide changes between the virulent virus recovered from the selenium-deficient host and the avirulent input virus. These nucleotide changes are consistent with known differences in base composition between virulent and avirulent strains of Coxsackievirus. To the best of our knowledge, this is the first report of a specific nutritional deficiency driving changes in a viral genome, permitting an avirulent virus to acquire virulence due to genetic mutation.

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Citations
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Journal ArticleDOI

Relationship between selenium status, selenoproteins and COVID-19 and other inflammatory diseases: A critical review

TL;DR: In this article , the relationship between selenium, selenoproteins, COVID-19, immune and inflammatory responses, viral infection, and aging has been reviewed.
Book ChapterDOI

Selenium-Based Drug Design

TL;DR: Improved understanding of the biology, biochemistry and pharmacology of selenium and selenoproteins is rapidly expanding, and it is anticipated that the coming years will bring further development of newSelenium-based pharmaceutical agents with therapeutic potential against human diseases.
Book ChapterDOI

Effects of Nutritional Antioxidants and Other Dietary Constituents on Coxsackievirus-Induced Myocarditis

TL;DR: The vast majority of nutrition research related to viral infection has emphasized the effect of nutrition on the host immune system, which in turn leads to a change in host susceptibility to infectious disease.
Journal ArticleDOI

Effect of gold(I) compounds on the virulence of an amyocarditic strain of coxsackievirus B3

TL;DR: Under this study, intraperitoneal administration of equal doses of ATM or ATG increased the virulence of CVB3/0, whereas ATG did not, and it is unlikely that these compounds affect virulence by acting as selenium antagonists.
References
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Journal ArticleDOI

Oxidants, antioxidants, and the degenerative diseases of aging

TL;DR: It is argued that this damage to DNA, protein, and lipid is a major contributor to aging and to degenerative diseases of aging such as cancer, cardiovascular disease, immune-system decline, brain dysfunction, and cataracts.
Journal ArticleDOI

Rapid evolution of RNA genomes

TL;DR: RNA viruses show high mutation frequencies partly because of a lack of the proofreading enzymes that assure fidelity of DNA replication, and high rates of replication reflected in rates of RNA genome evolution which can be more than a millionfold greater than the rates of the DNA chromosome evolution of their hosts.
Journal Article

Viral myocarditis. A review.

Journal ArticleDOI

Spontaneous point mutations that occur more often when advantageous than when neutral.

TL;DR: It is shown that point mutations in the trp operon reverted to trp+ more frequently under conditions of prolonged tryptophan deprivation when the reversions were advantageous, than in the presence of tryPTophan when the reversal were neutral, and a heuristic model for the molecular basis of such mutations is proposed.
Journal ArticleDOI

Complete nucleotide sequence of infectious Coxsackievirus B3 cDNA: two initial 5' uridine residues are regained during plus-strand RNA synthesis.

TL;DR: It is reported that cDNA-generated CVB3, as well asCVB3 generated by in vitro-synthesized RNA transcripts, regains the authentic initial 5' uridine residues during replication in transfected cells, indicating that the picornaviral primer molecule VPg-pUpU may be uridylylated in a template-independent fashion.
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