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Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the...
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Dengue Virus Evolution under a Host-Targeted Antiviral.

Emily Plummer1, Michael D Buck1, Marisa Sanchez1

  • 1La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.

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|March 13, 2015
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The antiviral UV-4B effectively controls dengue virus (DENV) in mice by targeting host proteins. Viral evolution under UV-4B pressure showed mutations in key viral proteins, confirming the drug

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Area of Science:

  • Virology and Drug Discovery
  • Host-Targeted Antiviral Mechanisms
  • Viral Evolution and Genomics

Background:

  • Dengue virus (DENV) poses a significant global health challenge with no approved vaccines or therapies.
  • The host-targeted antiviral UV-4B, an iminosugar, demonstrates efficacy against DENV by inhibiting host glycosylation pathways.
  • Understanding DENV's evolutionary response to host-targeted antivirals is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the in vivo evolution of DENV under selective pressure from the host-targeted antiviral UV-4B.
  • To validate the proposed mechanism of action of iminosugars on viral protein folding.
  • To assess the genetic barrier to resistance mutations against UV-4B in DENV.

Main Methods:

  • Utilized next-generation sequencing to analyze viral populations from DENV-infected mice treated with UV-4B or vehicle control.
  • Quantified single-nucleotide polymorphisms (SNPs) and the ratio of nonsynonymous to synonymous SNPs.
  • Identified specific mutations under positive selection, particularly in glycosylated viral proteins.

Main Results:

  • Viral populations from UV-4B-treated mice exhibited a significant increase in SNPs and nonsynonymous mutations compared to controls.
  • The glycosylated membrane protein showed the strongest evidence of positive selection, validating the iminosugar's mechanism.
  • Mutations in glycosylated proteins emerged rapidly, while other mutations appeared in both treated and untreated groups, suggesting nonspecific pressure.

Conclusions:

  • UV-4B effectively controls DENV replication in vivo, with observed viral evolution validating its mechanism of action.
  • The findings suggest a high genetic barrier to escape mutations for host-targeted antivirals like UV-4B.
  • This study provides a framework for evaluating viral evolution under other host-targeted antiflaviviral therapies.