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Related Concept Videos

Mutations01:39

Mutations

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Overview
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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...
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What is Natural Selection?01:32

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Natural selection is an evolutionary process in which individuals with survival-promoting traits reproduce at higher rates. These favorable traits become more common within a population or species. Naturally selected traits initially arise via random genetic mutations. In order for selection to occur, there must be variation within a population, the trait controlling the variation must be heritable, and there must be an evolutionary advantage for variation in the trait.
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Naturalistic Observations02:30

Naturalistic Observations

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If you want to understand how behavior occurs, one of the best ways to gain information is to simply observe the behavior in its natural context. However, people might change their behavior in unexpected ways if they know they are being observed. How do researchers obtain accurate information when people tend to hide their natural behavior? As an example, imagine that your professor asks everyone in your class to raise their hand if they always wash their hands after using the restroom. Chances...
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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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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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Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes
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Naturally Occurring Single Mutations in Ebola Virus Observably Impact Infectivity.

Gary Wong1,2,3,4, Shihua He1, Anders Leung1

  • 1Special Pathogens Program, Public Health Agency of Canada, Winnipeg, Manitoba, Canada.

Journal of Virology
|October 19, 2018
PubMed
Summary

Single Ebola virus (EBOV) mutations in glycoprotein (GP), nucleoprotein (NP), and RNA-dependent RNA polymerase (L) were studied. NP and L mutations decreased virulence, while GP altered tropism, impacting EBOV pathogenicity.

Keywords:
Ebola virusferretsmicemutationspathogenicity

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Area of Science:

  • Virology and Molecular Biology
  • Pathogen Evolution and Adaptation

Background:

  • The 2014-2016 Ebola virus (EBOV) epidemic revealed prevalent mutations potentially affecting viral virulence and tropism.
  • Understanding the impact of these naturally occurring mutations is crucial for predicting viral behavior and developing interventions.

Purpose of the Study:

  • To characterize the functional impact of three dominant EBOV mutations: A82V in glycoprotein (GP), R111C in nucleoprotein (NP), and D759G in RNA-dependent RNA polymerase (L).
  • To assess the effects of these mutations on viral replication in various cell lines and pathogenicity in animal models.

Main Methods:

  • Generation of recombinant EBOV strains carrying single point mutations (GP A82V, NP R111C, L D759G) based on a wild-type (WT) EBOV C07 isolate.
  • Assessment of viral replication efficiency in Vero E6, A549, Tb1.Lu, and Huh7 cell lines.
  • Evaluation of pathogenicity in mouse and ferret models, including survival rates, time to death, and viral shedding.

Main Results:

  • NP and L mutants showed enhanced replication in Vero E6, A549, and Tb1.Lu cells, but L mutants had reduced replication in Huh7 cells.
  • The GP mutant exhibited delayed replication in Tb1.Lu cells, with WT-like replication in other cell lines.
  • The L mutant displayed reduced virulence in animal models, indicated by increased mouse survival and delayed ferret mortality, but potentially prolonged shedding.

Conclusions:

  • Single amino acid substitutions in EBOV can significantly alter viral replication dynamics and pathogenicity.
  • The NP and L mutations appear to decrease virulence, while the GP mutation may influence viral tropism.
  • These findings provide a basis for studying EBOV mutation impacts and designing targeted antiviral therapies.