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Inhibition of adenovirus oncogenicity in hamsters by adeno-associated virus DNA
Abstract:
Adeno-associated virus (AAV) DNA partially inhibited in Syrian golden hamsters the formation of tumors by the human adenovirus (Ad) type 12. Furthermore, defective interfering AAV particles or their DNA also reduced tumorigenesis. Defective AAV particles contain aberrant genomes with extensive deletions of the internal AAV DNA sequences. Variant AAV DNA, containing 30% of the viral genome, decreased the incidence of Ad-induced tumors from 44 to 18%. Defective AAV particles, which have a buoyant density of 1.32 g/cm3 in CsCl and which are highly enriched for the DNA of the terminal regions (map positions, 0-5 and 95-100), completely suppressed Ad oncogenicity. This observation suggested that the AAV DNA sequences close to the terminal region of the genome mediated the inhibition of the Ad oncogenicity.
Insights
Adeno-associated virus (AAV) DNA suppressed human adenovirus type 12 tumor formation in hamsters. Defective AAV particles, particularly those with terminal DNA sequences, completely inhibited oncogenicity, suggesting a key role for these regions.
Area of Science:
- Virology
- Oncology
- Molecular Biology
Background:
- Human adenovirus (Ad) type 12 is a known oncogenic virus.
- Adeno-associated virus (AAV) has previously shown potential in modulating viral oncogenesis.
Purpose of the Study:
- To investigate the inhibitory effect of Adeno-associated virus (AAV) DNA on tumor formation induced by human adenovirus (Ad) type 12.
- To determine if defective AAV particles or their DNA can reduce Ad-induced tumorigenesis.
Main Methods:
- Experiments were conducted using Syrian golden hamsters as a model system.
- Tumor formation was monitored after co-administration or administration of AAV components with Ad type 12.
- Defective AAV particles and variant AAV DNA were characterized based on genome integrity and density.
Main Results:
- Adeno-associated virus (AAV) DNA partially inhibited Ad type 12-induced tumor formation.
- Defective interfering AAV particles and their DNA significantly reduced tumorigenesis.
- Variant AAV DNA (30% of the genome) decreased tumor incidence from 44% to 18%.
- Defective AAV particles enriched for terminal DNA sequences completely suppressed Ad oncogenicity.
Conclusions:
- Adeno-associated virus (AAV) DNA, especially sequences near the terminal regions, plays a crucial role in inhibiting adenovirus-induced oncogenicity.
- Defective AAV particles represent a promising avenue for therapeutic strategies against adenovirus-driven cancers.