Adenovirus vectors for gene delivery

Benihoud, Karim; Yeh, Patrice; Perricaudet, Michel

doi:10.1016/s0958-1669(99)00007-5

Cited by 317 publications

(187 citation statements)

References 60 publications

Supporting

Mentioning

178

Contrasting

Unclassified

Order By: Relevance

“…37 Thus, the efficacy of a second administration of vector, if required, may be compromised depending on the route of injection. [31][32][33] A second issue concerning this new vector is safety, particularly when all viral genes are present in recombinant viruses. This is the subject of continuing studies, but so far it has been shown that OAdV does not replicate in a variety of cell human lines, 39 nor does it transform rodent cells that are transformed by human AdV5.…”

Section: Discussionmentioning

confidence: 99%

“…However, pre-existing immunity against human adenoviruses that are endemic in man may compromise their use, depending on the route of inoculation. [31][32][33] In addition, CAR, the primary Ad5 receptor 34,35 which is required for effective virus uptake, 36 is absent from certain human cell types. We are therefore assessing ovine adenovirus (OAdV) as a vector.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Gene therapy for prostate cancer delivered by ovine adenovirus and mediated by purine nucleoside phosphorylase and fludarabine in mouse models

et al. 2002

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Gene therapy for prostate cancer delivered by ovine adenovirus and mediated by purine nucleoside phosphorylase and fludarabine in mouse models

et al. 2002

View full text Add to dashboard Cite

show abstract

“…Our results show that it is possible to transduce and express adequate amounts of these molecules in primary lymphoma cells using adenoviral vectors, provided the NHL cells have been cultured with fibroblasts to up -regulate expression of the V 3 integrin, which serves as an adenovector co-receptor. 40,41,42 We are currently testing the approach in a phase I study in patients with CD40 -positive B -NHL.…”

Section: Discussionmentioning

confidence: 99%

Transgenic expression of CD40L and interleukin-2 induces an autologous antitumor immune response in patients with non-Hodgkin's lymphoma

et al. 2001

View full text Add to dashboard Cite

The malignant B cells of non -Hodgkin's lymphoma ( B -NHL cells ) express peptides derived from tumor -specific antigens such as immunoglobulin idiotypes, and also express major histocompatibility complex antigens. However, they do not express costimulatory molecules, which likely contributes to their protection from host antitumor immunity. To stimulate NHL -specific immune responses, we attempted to transfer the human CD40 ligand ( hCD40L ) gene to B -NHL cells and enhance their costimulatory potential. We found that an adenoviral vector encoding human CD40L ( AdhCD40L ) was ineffective at transducing B -NHL cells because these cells lack the coxsackievirus B -adenovirus receptor and v integrins. However, preculture of the B -NHL cells with the human embryonic lung fibroblast line, MRC -5, significantly up -regulated expression of integrin v 3 and markedly increased their susceptibility to adenoviral vector transduction. After prestimulation, transduction with AdhCD40L increased CD40L expression on B -NHL cells from 1.3 0.2% to 40.8 11.9%. Transduction of control adenoviral vector had no effect. Expression of transgenic human CD40L on these CD40 -positive cells was in turn associated with up -regulation of other co -stimulatory molecules including B7 -1 / -2. Transduced B -NHL cells were now able to stimulate DNA synthesis of autologous T cells. However, the stimulated T cells were unable to recognize unmodified lymphoma cells, a requirement for an effective tumor vaccine. Based on previous results in an animal model, we determined the effects of combined use of B -NHL cells transduced with AdhCD40L and AdhIL2 vectors. The combination enhanced initial T -cell activation and generated autologous T cells capable of specifically recognizing and killing parental ( unmodified ) B -NHL cells via major histocompatibility complex ± restricted cytotoxic T lymphocytes. These findings suggest that the combination of CD40L and IL2 gene -modified B -NHL cells will induce a cytotoxic immune response in vivo directed against unmodified tumor cells.

show abstract

“…While AAV2 is not considered pathogenic and has not been implicated in known human diseases, [17][18][19] rAd-mediated gene transfer is associated with inflammation and cellular immune responses. 20,21 We, therefore, sought an improved strategy to avoid these complications.…”

Section: Introductionmentioning

confidence: 99%

Long-term correction of murine glycogen storage disease type Ia by recombinant adeno-associated virus-1-mediated gene transfer

Ghosh

et al. 2005

Gene Ther

View full text Add to dashboard Cite

Glycogen storage disease type Ia (GSD-Ia) is caused by a deficiency in glucose-6-phosphatase-a (G6Pase-a), a ninetransmembrane domain, endoplasmic reticulum-associated protein expressed primarily in the liver and kidney. Previously, we showed that infusion of an adeno-associated virus (AAV) serotype 2 vector carrying murine G6Pase-a (AAV2-G6Pase-a) into neonatal GSD-Ia mice failed to sustain their life beyond weaning. We now show that neonatal infusion of GSD-Ia mice with an AAV serotype 1-G6Pase-a (AAV1-G6Pase-a) or AAV serotype 8-G6Pase-a (AAV8-G6Pase-a) results in hepatic expression of the G6Pase-a transgene and markedly improves the survival of the mice. However, only AAV1-G6Pase-a can achieve significant renal transgene expression. A more effective strategy, in which a neonatal AAV1-G6Pase-a infusion is followed by a second infusion at age 1 week, provides sustained expression of a complete, functional, G6Pase-a system in both the liver and kidney and corrects the metabolic abnormalities in GSD-Ia mice for the 57 week length of the study. This effective use of gene therapy to correct metabolic imbalances and disease progression in GSD-Ia mice holds promise for the future of gene therapy in humans. Gene Therapy (2005) 13, 321-329.

show abstract

Adenovirus vectors for gene delivery

Cited by 317 publications

References 60 publications

Gene therapy for prostate cancer delivered by ovine adenovirus and mediated by purine nucleoside phosphorylase and fludarabine in mouse models

Gene therapy for prostate cancer delivered by ovine adenovirus and mediated by purine nucleoside phosphorylase and fludarabine in mouse models

Transgenic expression of CD40L and interleukin-2 induces an autologous antitumor immune response in patients with non-Hodgkin's lymphoma

Long-term correction of murine glycogen storage disease type Ia by recombinant adeno-associated virus-1-mediated gene transfer

Contact Info

Product

Resources

About