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Related Concept Videos

Mutations in Microorganisms01:18

Mutations in Microorganisms

Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
In-vitro Mutagenesis01:16

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
Viral Mutations00:36

Viral Mutations

A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material for adaptive...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Mismatch Repair01:36

Mismatch Repair

Overview
Mutation, Gene Flow, and Genetic Drift01:09

Mutation, Gene Flow, and Genetic Drift

In a population that is not at Hardy-Weinberg equilibrium, the frequency of alleles changes over time. Therefore, any deviations from the five conditions of Hardy-Weinberg equilibrium can alter the genetic variation of a given population. Conditions that change the genetic variability of a population include mutations, natural selection, non-random mating, gene flow, and genetic drift (small population size).

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Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency
18:10

Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency

Published on: June 16, 2011

Mutagenesis-mediated decrease of pathogenicity as a feature of the mutant spectrum of a viral population.

Marta Sanz-Ramos1, Teresa Rodríguez-Calvo, Noemí Sevilla

  • 1Centro de Investigación en Sanidad Animal, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Valdeolmos, Madrid, Spain.

Plos One
|July 5, 2012
PubMed
Summary

Mutagenizing foot-and-mouth disease virus (FMDV) with ribavirin created an attenuated viral population in mice. This mutagenized quasispecies suppressed the virulent phenotype of the original FMDV, suggesting new therapeutic strategies.

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Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • RNA virus populations exist as complex quasispecies, influencing pathogenicity.
  • Increased viral mutagenesis is hypothesized to alter pathogenic potential.
  • This study investigates mutagenized foot-and-mouth disease virus (FMDV) virulence in mice.

Purpose of the Study:

  • To determine if mutagenized FMDV populations exhibit altered virulence in a murine model.
  • To explore the impact of ribavirin-induced mutagenesis on FMDV pathogenicity.
  • To investigate the suppressive effects of mutagenized viral quasispecies.

Main Methods:

  • FMDV was passaged in cell culture with the mutagen ribavirin.
  • Viral virulence was assessed in mice using lethal dose 50 (LD50) assays.
  • Mutation frequency and infectivity were analyzed.
  • Individual viral clones and mixed populations were tested.

Main Results:

  • Ribavirin treatment led to a significant decrease in FMDV virulence in mice (LD50 >10(4) PFU vs. 50 PFU for parental virus).
  • The attenuated viral population showed a 20-fold increase in mutation frequency.
  • Individual virulent clones were isolated from the attenuated population.
  • The mutagenized population suppressed the virulence of the parental FMDV in mixed infections.

Conclusions:

  • Ribavirin-induced mutagenesis attenuates FMDV populations in vivo.
  • Mutagenized viral quasispecies can exert a suppressive effect on virulent viral phenotypes.
  • These findings suggest novel strategies for viral disease treatment and prevention.