1887

Abstract

Mobilization of replication-deficient adenovirus vectors can lead to spread and shedding of the vector. Here we show that in cultured HepG2 cells wild-type () adenoviruses of subgroup A (Ad12), B (Ad7, 11 and 16), C (Ad1, 2 and 5) and E (Ad4) can efficiently mobilize Ad5CMV, a ΔΔ-Ad5 vector carrying the firefly luciferase gene as reporter. In addition, we show that Ad5CMV can be propagated on Ad12E1-transformed human embryonic retinoblasts. This provides evidence that expression of the E1 region of Ad12 is sufficient for mobilizing Δ-Ad5-derived vectors. Thus, in therapeutic applications of replication-defective Ad vectors any active Ad infection is of potential concern, independent of the serotype involved. To prevent vector mobilization by Ads, new vectors should be developed in which essential functions such as the initiation of DNA replication and genome packaging are restricted.

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2002-06-01
2024-04-27
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