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Related Experiment Videos

Human rhinovirus mutants resistant to low pH.

T Skern1, H Torgersen, H Auer

  • 1Institute of Biochemistry, University of Vienna, Austria.

Virology
|August 1, 1991
PubMed
Summary

Human rhinovirus 14 (HRV14) mutants show enhanced stability at low pH. Specific mutations in the VP1 protein significantly increase viral resistance to acid treatment, impacting capsid structure.

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Area of Science:

  • Virology
  • Structural Biology
  • Molecular Biology

Background:

  • Human rhinovirus serotype 14 (HRV14) is a common human pathogen.
  • Viral stability at low pH is crucial for infectivity and transmission.
  • Understanding capsid protein mutations can reveal mechanisms of viral stability.

Purpose of the Study:

  • To isolate and characterize HRV14 mutants with increased resistance to low pH.
  • To identify the specific mutations responsible for enhanced acid stability.
  • To investigate the structural implications of these mutations on the viral capsid.

Main Methods:

  • Repeated exposure of wild-type HRV14 to low pH (4.5) and propagation in HeLa cells to generate resistant mutants.
  • Assessing viral infectivity and conformational changes (hydrophobicity) at low pH.
  • Determining the capsid protein sequences of resistant isolates.
  • Introducing identified mutations into wild-type HRV14 cDNA clones to confirm their role in stability.

Main Results:

  • Three HRV14 mutants resistant to low pH were isolated.
  • Mutants retained infectivity at pH 4.3, unlike wild-type HRV14.
  • Mutations identified in VP1 and VP2 capsid proteins.
  • VP1 mutations alone were sufficient to confer increased stability at low pH.
  • Mutations altered the pH threshold for viral capsid conformational changes.

Conclusions:

  • Specific mutations in the VP1 capsid protein of HRV14 are critical for conferring resistance to low pH.
  • These mutations likely stabilize the viral capsid structure, preventing conformational changes at acidic pH.
  • The findings provide insights into the structural basis of HRV stability and potential targets for antiviral strategies.

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