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Retrovirus Life Cycles01:10

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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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RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...
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Inhibitors of Viral Protein Synthesis01:30

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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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Size and Structure of Viral Genomes01:26

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Viral genomes exhibit remarkable diversity in size, structure, and composition, influencing their replication strategies and interactions with host cells. These genomes consist of either DNA or RNA and may be linear or circular. Additionally, they can be single-stranded or double-stranded, with each configuration affecting how the virus propagates within a host. RNA viruses, for instance, generally have smaller genomes than DNA viruses, a factor that contributes to their high mutation rates and...
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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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High-Affinity Nanobody Against the LEDGF PWWP Domain Inhibits Chromatin Binding In Vitro.

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The LEDGIN GS-9822 inhibits HIV-2 infection and enhances HIV-2 latency.

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Related Experiment Video

Updated: Apr 4, 2026

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

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Targeting Virus-host Interactions of HIV Replication.

Caroline Weydert, Jan De Rijck, Frauke Christ

  • 1Laboratory for Molecular Virology and Gene Therapy, Department for Pharmaceutical and Pharmacological Sciences, KU Leuven, Kapucijnenvoer 33 VCTB+5, Leuven, Flanders, Belgium. zeger.debyser@med.kuleuven.be.

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|September 2, 2015
PubMed
Summary

New antiretroviral therapies target HIV

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Area of Science:

  • Virology
  • Drug Discovery
  • Molecular Biology

Background:

  • HIV hijacks cellular proteins (cofactors) for replication.
  • Protein-protein interactions between viral and cellular proteins are key targets.
  • Existing therapies validate cofactor inhibition as a viable strategy.

Purpose of the Study:

  • To review compounds targeting specific cofactor-HIV protein interactions.
  • To highlight the potential of targeting cellular proteins for HIV therapy.
  • To provide an overview of novel compounds in development.

Main Methods:

  • Focus on compounds inhibiting Integrase-LEDGF/p75 interactions.
  • Review of compounds targeting Tat-P-TEFb interactions.
  • Examination of compounds targeting Vif-APOBEC3G interactions.

Main Results:

  • Approved drugs like Maraviroc demonstrate proof of concept.
  • LEDGINs targeting Integrase-LEDGF/p75 are in early clinical trials.
  • Compounds targeting Vif-APOBEC3G interactions have been described.

Conclusions:

  • Targeting cofactor-HIV protein interactions offers promising therapeutic avenues.
  • Ongoing research is developing novel compounds for HIV treatment.
  • Inhibiting viral hijacking of cellular machinery is a key strategy.