Construction and characterization of an adenovirus type 5/adenovirus type 12 recombinant virus

Bernards, René; Vaessen, M.J.; Eb, A. J. Van Der; Sussenbach, J.S.

doi:10.1016/0042-6822(83)90530-5

Cited by 17 publications

(3 citation statements)

References 22 publications

(4 reference statements)

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“…Isolation of recombinant viruses. The isolation of the Ad5 d1309 Xba A fragment-terminal protein complex has been described previously (4). To obtain Ad5/Adl2 recombinants, human 293 cells in 6 cm dishes were cotransfected with 1 ,ug of the Xba A fragment and 5 ,ug of EcoRI-linearized plasmid p5125E1 by the calcium phosphate coprecipitation technique (39).…”

Section: Ad5 Dl309mentioning

confidence: 99%

Oncogenicity by adenovirus is not determined by the transforming region only

Bernards¹,

Leeuw²,

Vaessen³

et al. 1984

J Virol

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We have constructed a nondefective recombinant virus between the nononcogenic adenovirus S (AdS) and the highly oncogenic AdM2. The recombinant genome consists essentially of Ad5 sequences, with the exception of the transforming early region 1 (El) which is derived from Adl2. HeLa cells infected with the recombinant virus were shown to contain the Adl2-specific El proteins of 41 kilodaltons (Ela) and 19 and 54 kilodaltons (both encoded by Elb). The recombinant virus replicated efficiently in human embryonic kidney cells and HeLa cells, showing that the transforming regions of Ad5 and Adi2 had similar functions in productive infection. After the recombinant virus was injected into newborn hamsters, no tumors were produced during an observation period of 200 days. Thus, despite the fact that all products required for oncogenic transformation in vitro were derived from the highly oncogenic Adl2, the recombinant virus did not produce tumors in vivo. These data show that tumnor induction by adenovirus virions is not determined only by the gene products of the transforming region.

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Section: Ad5 Dl309mentioning

confidence: 99%

Oncogenicity by adenovirus is not determined by the transforming region only

Bernards¹,

Leeuw²,

Vaessen³

et al. 1984

J Virol

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“…Our data confirm and extend the earlier observation that Bam HI-digested wt Ad12 (subgroup A) and Ad7 (subgroup B) could efficiently complement an E1 deletion of Ad2 (subgroup C) (Brusca & Chinnadurai, 1981 ). Also, hybrid Ad5 and Ad12 viruses in which the E1 region had been replaced (in part) by the corresponding region of Ad12 and Ad5, respectively, were demonstrated to be viable (Bernards et al ., 1983 ). However, another study showed that a defect in the E1 region of Ad2 could only be complemented poorly by Ad9 (subgroup D) (Jannun & Chinnadurai, 1987 ).…”

Section: Full Textmentioning

confidence: 99%

Efficient mobilization of E1-deleted adenovirus type 5 vectors by wild-type adenoviruses of other serotypes

Rademaker

Hassan

Versteeg

et al. 2002

Journal of General Virology

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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 (wt) adenoviruses of subgroup A (Ad12), B (Ad7, 11 and 16), C (Ad1, 2 and 5) and E (Ad4) can efficiently mobilize Ad5CMVluc, a ∆E1∆E3-Ad5 vector carrying the firefly luciferase gene as reporter. In addition, we show that Ad5CMVluc can be propagated on Ad12E1-transformed human embryonic retinoblasts. This provides evidence that expression of the E1 region of Ad12 is sufficient for mobilizing ∆E1-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 wt Ads, new vectors should be developed in which essential functions such as the initiation of DNA replication and genome packaging are restricted.Adenoviruses (Ad) are a diverse family of viruses. In humans at least 51 different serotypes have been described, which have been divided into six subgroups (formerly species) based on haemagglutination properties with red blood cells, oncogenic potential and GjC content of their DNA (Horwitz, 1995). Replication-defective derivatives of serotypes 5 (Ad5) and 2 (Ad2), generated by deletion of sequences of the viral E1, E2 and E4 regions, have been widely used as gene-transfer vehicles in experimental gene therapy (Benihoud et al., 1999). Therapeutic application of recombinant Ad vectors is complicated by the presence of replication-competent adenoviruses (RCA). The presence of RCA in the vector batches may lead to inflammation and tissue damage in the recipient (Fallaux et al., 1999 ;Hermens & Verhaagen, 1997). In addition, RCA can mobilize the Ad vector (Imler et al., 1995), and this could lead Author for correspondence : Rob Hoeben.Fax j31 71 527 6284. e-mail R.C.Hoeben!lumc.nl increased vector shedding. The development and implementation of improved helper cells (Fallaux et al., 1998) and vectors (Hehir et al., 1996), as well as stringent quality-control measures (Roitsch et al., 2001 ;Fallaux et al., 1999), can virtually eliminate the problem of RCA in the vector batches.However, this does not solve the mobilization problem completely. It is conceivable that after receiving gene therapy, patients develop a viraemia with a wild-type (wt) Ad. Indeed, administration of wt Ad5 into lungs of cotton rats previously exposed to replication-defective Ad5 vectors led to mobilization of the vector (Imler et al., 1995). The risk of a mobilization by wt Ad of the same serotype is limited, as most patients will develop immunity against the vector serotype ( Harvey et al., 1999). It is not known, however, whether the vectors can be mobilized by other serotypes, viz. serotypes different from the one from which the vector had been derived. To study this possibility, we determined whether wt Ads of subgroups A, B, C and E could mobilize the vector Ad5CMVluc, a ∆E1∆E3-Ad5 vector carrying the firefly luciferase gene as a reporter.Fi...

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“…la) (7,13). Reconstitution of infectious virus from subgenomic fragments has also been reported for smaller viruses like spleen necrosis virus (12) and adenovirus (5,6). Regeneration of these viruses was performed by cotransfection of overlapping cloned fragments.…”

mentioning

confidence: 97%

Regeneration of herpesviruses from molecularly cloned subgenomic fragments

Zijl

Quint

Briaire

et al. 1988

J Virol

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The ability to manipulate the genomes of herpesviruses is of eminent importance for obtaining insight into gene function and regulation of gene expression of these complex viruses. Here we report the use of in vivo overlap recombination to generate pseudorabies virus mutants. Cotransfection of up to five overlapping cloned subgenomic fragments, which together constitute the entire genomic information of pseudorabies virus, results in the efficient reconstitution of virus. This allows the efficient introduction of multiple well-defined mutations in herpesvirus genomes in a single step, without any selection or screening for a particular phenotype.

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Construction and characterization of an adenovirus type 5/adenovirus type 12 recombinant virus

Cited by 17 publications

References 22 publications

Oncogenicity by adenovirus is not determined by the transforming region only

Oncogenicity by adenovirus is not determined by the transforming region only

Efficient mobilization of E1-deleted adenovirus type 5 vectors by wild-type adenoviruses of other serotypes

Regeneration of herpesviruses from molecularly cloned subgenomic fragments

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