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Genetic strategy to decrease complement activation with adenoviral therapies.

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Modifying adenovirus (Ad5) vectors with a complement-inhibiting peptide reduced liver uptake in mice. This strategy may decrease liver tropism for gene therapy vectors.

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Area of Science:

  • Gene Therapy
  • Immunology
  • Virology

Background:

  • Recombinant adenoviral vectors face challenges in gene therapy due to their activation of complement pathways.
  • This activation leads to increased liver uptake and enhanced immune responses after systemic delivery.

Purpose of the Study:

  • To engineer adenovirus type 5 (Ad5) vectors to reduce complement activation and liver tropism.
  • To evaluate the efficacy of a complement-inhibiting peptide displayed on the Ad5 capsid.

Main Methods:

  • Genetically modified replication-defective Ad5 vectors by incorporating a complement-inhibiting peptide (rH17d') into the hexon protein's hypervariable regions (HVR2 or HVR5).
  • Constructed control vectors with a 6-histidine tag in HVR2 or HVR5.
  • Assessed vector infectivity in mouse liver cells and liver sequestration in immunocompetent mice.

Main Results:

  • One modified vector (Ad5.HVR5-rH17d') showed no serum-mediated enhancement of liver cell infectivity.
  • Mice injected with rH17d'-modified vectors exhibited significantly lower luciferase expression in the liver compared to control vectors.
  • Intratumoral injection showed similar tumor transduction efficiency for both modified and control vectors.

Conclusions:

  • Displaying a complement-inhibiting peptide on the Ad5 capsid via hexon modification is a viable strategy to reduce liver tropism.
  • This approach may be applicable to other gene therapy vectors prone to liver sequestration.