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Related Concept Videos

Retroviruses02:33

Retroviruses

Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
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Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
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Related Experiment Video

Updated: May 7, 2026

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
05:46

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Published on: April 9, 2014

[Telaprevir resistance].

Eva Poveda1, Federico García

  • 1División de Virología Clínica, INIBIC-Complejo Hospitalario Universitario de A Coruña, A Coruña, España.

Enfermedades Infecciosas Y Microbiologia Clinica
|September 26, 2013
PubMed
Summary

Telaprevir, a potent hepatitis C virus (HCV) drug, faces resistance due to mutations. Understanding these mutations and their rapid reversion aids in developing effective "recycling" treatment strategies.

Keywords:
Hepatitis C virusResistanceResistenciaTelaprevirVirus de la hepatitis C (VHC)

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Area of Science:

  • Hepatology
  • Virology
  • Pharmacology

Background:

  • Hepatitis C virus (HCV) direct-acting antiviral agents, like telaprevir, are potent but susceptible to resistance mutations.
  • HCV's high replication rate, lack of polymerase error correction, low genetic barrier to resistance, and poor adherence facilitate mutation emergence.

Purpose of the Study:

  • To characterize genotypic and phenotypic resistance to telaprevir in combination therapy.
  • To identify specific mutation positions and their impact on telaprevir resistance across different HCV subtypes.

Main Methods:

  • Analysis of Phase II/III clinical trials (ADVANCE, ILLUMINATE, REALIZE).
  • Genotypic and phenotypic characterization of telaprevir resistance mutations.
  • Assessment of mutation prevalence and cross-resistance patterns.

Main Results:

  • Key resistance mutations are selected at positions 36, 54, 55, 155, and 156, varying by HCV subtype (1a vs. 1b).
  • High-level resistance (>25-fold) is conferred by V36M+R155K and A156F/T/V variants.
  • Prevalence of high-impact resistance mutations is low (<1%), and resistance mutations rapidly revert post-treatment.

Conclusions:

  • Telaprevir resistance is influenced by specific mutations and HCV subtypes.
  • Rapid reversion of resistance mutations suggests potential for protease inhibitor "recycling" strategies.
  • Understanding resistance profiles is crucial for optimizing HCV treatment regimens.