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Related Concept Videos

Viral Mutations00:36

Viral Mutations

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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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Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency
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Mutations in chikungunya virus nsP4 decrease viral fitness and sensitivity to the broad-spectrum antiviral

Peiqi Yin1, Elizabeth B Sobolik2, Nicholas A May3

  • 1Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, United States of America.

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The antiviral 4'-fluorouridine (4'-FlU) shows promise against Chikungunya virus (CHIKV). Resistance mutations were identified but did not compromise CHIKV replication, supporting 4'-FlU

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Area of Science:

  • Virology
  • Drug Discovery
  • Infectious Diseases

Background:

  • Chikungunya virus (CHIKV) causes widespread human infections, with no current approved antiviral treatments.
  • The ribonucleoside analog 4 -fluorouridine (4 -FlU) effectively inhibits CHIKV replication by targeting the viral RNA-dependent RNA polymerase (nsP4).
  • Previous studies demonstrated 4 -FlU's efficacy in reducing viral loads and disease signs in mouse models.

Purpose of the Study:

  • To assess the potential of 4 -FlU as a Chikungunya virus antiviral.
  • To identify and characterize CHIKV variants with reduced sensitivity to 4 -FlU.

Main Methods:

  • Selection of CHIKV variants resistant to 4 -FlU.
  • Identification of mutations in viral proteins nsP2 and nsP4.
  • Assessment of 4 -FlU sensitivity, viral fitness (in vitro and in vivo), and nsP4 fidelity.
  • Pathogenesis studies in mouse models using identified CHIKV variants.

Main Results:

  • Two pairs of mutations in nsP2 and nsP4 conferred decreased 4 -FlU sensitivity, with nsP4 mutations Q192L and C483Y being primarily responsible.
  • Resistant variants remained susceptible to higher concentrations of 4 -FlU.
  • Identified mutations did not affect nsP4 fidelity or confer a viral fitness advantage.
  • The nsP4-C483Y variant exhibited similar pathogenesis to wild-type CHIKV, while the nsP4-Q192L variant was attenuated in mice.

Conclusions:

  • The identified resistance mutations do not fully abrogate 4 -FlU's antiviral activity.
  • The study supports the potential of 4 -FlU as a viable antiviral therapeutic for Chikungunya virus infections.
  • Further investigation into 4 -FlU's efficacy and resistance profile is warranted.