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Related Concept Videos

Viral Mutations00:36

Viral Mutations

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 for adaptive...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Retrovirus Life Cycles01:10

Retrovirus Life Cycles

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 retrovirus to...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

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...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...

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Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency
18:10

Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency

Published on: June 16, 2011

Viral resistance evolution fully escapes a rationally designed lethal inhibitor.

Thomas E Keller1, Ian J Molineux, James J Bull

  • 1Section of Integrative Biology, The University of Texas at Austin, USA. tkeller@mail.utexas.edu

Molecular Biology and Evolution
|June 5, 2009
PubMed
Summary

Viruses can evolve drug resistance. Bacteriophage T7 evolved complete resistance to an inhibitor through mutations in RNA polymerase and other genes, suggesting permanent viral inhibition is possible.

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Area of Science:

  • Virology
  • Molecular Biology
  • Evolutionary Biology

Background:

  • Viruses rapidly evolve resistance to antiviral drugs.
  • Drug resistance can limit treatment efficacy.
  • Understanding viral adaptation mechanisms is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the evolutionary pathways of viral resistance to a specific inhibitor.
  • To assess the feasibility of using drug combinations to overcome viral resistance.
  • To quantitatively analyze viral fitness changes during resistance evolution.

Main Methods:

  • Experimental evolution of bacteriophage T7 under drug pressure.
  • Measurement of viral fitness and population growth rates.
  • Genetic analysis of resistance mutations, including sequencing of RNA polymerase (RNAP) and other genes.

Main Results:

  • Bacteriophage T7 evolved complete resistance to the inhibitor.
  • Resistance was mediated by three mutations in the RNAP gene and two in other genes.
  • Unexpectedly, no mutations were found in phage promoters, despite the inhibitor targeting the phage's own promoter.

Conclusions:

  • Viral resistance evolution can lead to complete escape from inhibition.
  • The genetic basis of resistance may involve complex changes in viral machinery like RNAP.
  • The findings offer hope for strategies to achieve permanent inhibition of viral growth.