Oncolytic viruses: From bench to bedside with a focus on safety

Buijs, Pascal; Verhagen, Judith H E; Eijck, Casper H.J. van; Hoogen, Bernadette G. van den

doi:10.1080/21645515.2015.1037058

Cited by 114 publications

(106 citation statements)

References 137 publications

(142 reference statements)

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“…The development of novel oncolytic viruses underlined several advantages of their clinical applications such as enhanced selectivity for tumor cells and effective control of tumor growth with limited side effects (31,32). There are several common mechanisms by which oncolytic viruses can destroy malignant cells (31)(32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

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Development of novel AAV serotype 6 based vectors with selective tropism for human cancer cells

et al. 2015

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Viral vectors-based gene therapy is an attractive alternative to common anti-cancer treatments. In the present studies, AAV serotype 6 vectors were identified to be particularly effective in the transduction of human prostate (PC3), breast (T47D) and liver (Huh7) cancer cells. Next, we developed chimeric AAV vectors with Arg-Gly-Asp (RGD) peptide incorporated into the viral capsid to enable specific targeting of integrin-overexpressing malignant cells. These AAV6-RGD vectors improved transduction efficiency approximately 3-fold compared with wild-type AAV6 vectors by enhancing the viral entry into the cells. We also observed that transduction efficiency significantly improved, up to approximately 5-fold, by the mutagenesis of surface-exposed tyrosine and threonine residues involved in the intracellular trafficking of AAV vectors. Therefore, in our study, the AAV6-Y705-731F+T492V vector was identified as the most efficient. The combination of RGD peptide, tyrosine and threonine mutations on the same AAV6 capsid further increased the transduction efficiency, approximately 8-fold in vitro. In addition, we mutated lysine (K531E) to impair the affinity of AAV6 vectors to heparan sulfate proteoglycan. Finally, we showed a significant increase in both specificity and efficiency of AAV6-RGD-Y705-731F+T492V+K531E vectors in a xenograft animal model in vivo. In summary, the approach described here can lead to the development of AAV vectors with selective tropism to human cancer cells.

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Section: Discussionmentioning

confidence: 99%

“…There are several common mechanisms by which oncolytic viruses can destroy malignant cells (31)(32)(33)(34). First the viruses, such as the adenovirus or herpes virus, destroy tumor cell by replicating, this cycle will repeat by infection of adjacent cells by the same mechanism.…”

Section: Discussionmentioning

confidence: 99%

Development of novel AAV serotype 6 based vectors with selective tropism for human cancer cells

et al. 2015

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“…Thereafter, other DNA viruses were modified to improve the safety of viruses and tumor selectivity. Some RNA viruses were also considered as candidates for oncolytic virotherapy because they showed tumor-specific cytotoxicity with low pathogenesis in humans [10][11][12][13][14][15][16]. A reverse genetic technique subsequently allowed for the genomes of RNA viruses to be modified to improve tumor selectivity and safety [17,18].…”

Section: Introductionmentioning

confidence: 99%

Development of oncolytic virotherapy for the treatment of oral cancer – At the waiting stage for clinical use

Yura

Hamada

2016

Oral Science International

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Oncolytic virotherapy originated from the finding that virus‐infected tumor cells are destroyed by the cytopathic effects of viruses. Cell death induced by viral infections in tumor tissues also promotes inherent tumor immunity in cancer patients. Several DNA and RNA viruses have been proposed as candidates for this treatment through in vitro and in vivo studies as well as clinical trials. Oral cancer is often accompanied by lymph node metastasis, resulting in worse patient prognoses. Some oncolytic viruses have been investigated for their therapeutic effects on patients with advanced head and neck cancer, including oral cancer. Oncolytic virotherapy is expected to become a treatment modality that will be essential for controlling chemoradio‐resistant oral cancer.

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“…Newcastle disease virus (NDV), an avian paramyxovirus type 1 in the family Paramyxoviridae, is being developed as an oncolytic virus for cancer therapy due to its selective oncolysis of tumour cells and anti-tumour immunity elicited by viral replication (Buijs et al, 2015;Chiocca & Rabkin, 2014;Cassel & Murray, 1992;Zamarin & Palese, 2012;Cassel & Garrett, 1965;Moore et al, 1952;Prince & Ginsberg, 1957a, b). We recently developed a potent recombinant NDV (73T-R-198v, referred to as rNDV in this study) from the mesogenic 73T strain that is attenuated in chickens without affecting its oncolytic activity (Cheng et al, 2016).…”

mentioning

confidence: 99%

CD55 is a key complement regulatory protein that counteracts complement-mediated inactivation of Newcastle Disease Virus

Rangaswamy

Cotter

Cheng

et al. 2016

Journal of General Virology

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MedImmune LLC, Mountain View, California, USA Newcastle disease virus (NDV) is being developed as an oncolytic virus for virotherapy. In this study we analysed the regulation of complement-mediated inactivation of a recombinant NDV in different host cells. NDV grown in human cells was less sensitive to complement-mediated virus inactivation than NDV grown in embryonated chicken eggs. Additionally, NDV produced from HeLa-S3 cells is more resistant to complement than NDV from 293F cells, which correlated with higher expression and incorporation of complement regulatory proteins (CD46, CD55 and CD59) into virions from HeLa-S3 cells. Further analysis of the recombinant NDVs individually expressing the three CD molecules showed that CD55 is the most potent in counteracting complement-mediated virus inactivation. The results provide important information on selecting NDV manufacture substrate to mitigate complement-mediated virus inactivation.

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Oncolytic viruses: From bench to bedside with a focus on safety

Cited by 114 publications

References 137 publications

Development of novel AAV serotype 6 based vectors with selective tropism for human cancer cells

Development of novel AAV serotype 6 based vectors with selective tropism for human cancer cells

Development of oncolytic virotherapy for the treatment of oral cancer – At the waiting stage for clinical use

CD55 is a key complement regulatory protein that counteracts complement-mediated inactivation of Newcastle Disease Virus

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