Features of the Antitumor Effect of Vaccinia Virus Lister Strain

Zonov, E. V.; Кочнева, Г. В.; Yunusova, Anastasiya; Гражданцева, А. А.; Richter, Vladimír; Ryabchikova, E. I.

doi:10.3390/v8010020

Cited by 14 publications

(8 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such danger signals could be sensed by cells of innate immune system, so it could be suggested that activation of innate immune system might take part in tumor regression in cooperation with the viral oncolytic process [ 45 ]. Moreover, most recently, Zonov et al demonstrated that direct cell destruction have been implicated in vaccinia infection of human carcinoma A431 cells, but in Ehrlich carcinoma cells which poorly supported vaccinia virus replication the virus induced suppression of mitoses [ 46 ]. However, nowadays the mechanisms mediating death of vaccinia virus infected cells are not clear entirely.…”

Section: Discussionmentioning

confidence: 99%

Oncolytic virus efficiency inhibited growth of tumour cells with multiple drug resistant phenotype in vivo and in vitro

et al. 2016

View full text Add to dashboard Cite

BackgroundTumour resistance to a wide range of drugs (multiple drug resistant, MDR) acquired after intensive chemotherapy is considered to be the main obstacle of the curative treatment of cancer patients. Recent work has shown that oncolytic viruses demonstrated prominent potential for effective treatment of diverse cancers. Here, we evaluated whether genetically modified vaccinia virus (LIVP-GFP) may be effective in treatment of cancers displaying MDR phenotype.MethodsLIVP-GFP replication, transgene expression and cytopathic effects were analysed in human cervical carcinomas KB-3-1 (MDR−), KB-8-5 (MDR+) and in murine melanoma B-16 (MDR−), murine lymphosarcomas RLS and RLS-40 (MDR+). To investigate the efficacy of this therapy in vivo, we treated immunocompetent mice bearing murine lymphosarcoma RLS-40 (MDR+) (6- to 8-week-old female CBA mice; n = 10/group) or melanoma B-16 (MDR−) (6- to 8-week-old female C57Bl mice; n = 6/group) with LIVP-GFP (5 × 107 PFU of virus in 0.1 mL of IMDM immediately and 4 days after tumour implantation).ResultsWe demonstrated that LIVP-GFP replication was effective in human cervical carcinomas KB-3-1 (MDR−) and KB-8-5 (MDR+) and in murine melanoma B-16 (MDR−), whereas active viral production was not detected in murine lymphosarcomas RLS and RLS-40 (MDR+). Additionally, it was found that in tumour models in immunocompetent mice under the optimized regimen intratumoural injections of LIVP-GFP significantly inhibited melanoma B16 (33 % of mice were with complete response after 90 days) and RLS-40 tumour growth (fourfold increase in tumour doubling time) as well as metastasis.ConclusionThe anti-tumour activity of LIVP-GFP is a result of direct oncolysis of tumour cells in case of melanoma B-16 because the virus effectively replicates and destroys these cells, and virus-mediated activation of the host immune system followed by immunologically mediated destruction of of tumour cells in case of lymphosarcoma RLS-40. Thus, the recombinant vaccinia virus LIVP-GFP is able to inhibit the growth of malignant cells with the MDR phenotype and tumour metastasis when administered in the early stages of tumour development.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-1002-x) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionmentioning

confidence: 99%

Oncolytic virus efficiency inhibited growth of tumour cells with multiple drug resistant phenotype in vivo and in vitro

et al. 2016

View full text Add to dashboard Cite

show abstract

“…VV-L replication in the models used in this study was likely restricted to the virus-injected tumors with limited hematogenous spread of the virus. 43 The majority of animals did not have detectable VV-L in the serum, and those that did had peak levels of less than 10 3 TCID 50 /mL, suggesting that VV-L has very limited ability to disseminate beyond the injected tumor. Although toxicities to normal tissues as a consequence of combining VV-L with RNA viruses was not observed in the studies reported here, there are several effective antiviral agents that could be administered to limit VV-L replication if toxicity were ever observed.…”

Section: Discussionmentioning

confidence: 93%

Collateral Lethal Effects of Complementary Oncolytic Viruses

Maroun

Penza

Weiskittel

et al. 2020

Molecular Therapy - Oncolytics

View full text Add to dashboard Cite

Virus-infected cells release type 1 interferons, which induce an antiviral state in neighboring cells. Naturally occurring viruses are therefore equipped with stealth replication strategies to limit virus sensing and/or with combat strategies to prevent or reverse the antiviral state. Here we show that oncolytic viruses with simple RNA genomes whose spread was suppressed in tumor cells pretreated with interferon were able to replicate efficiently when the cells were coinfected with a poxvirus known to encode a diversity of innate immune combat proteins. In vivo the poxvirus was shown to reverse the intratumoral antiviral state, rescuing RNA virus replication in an otherwise restrictive syngeneic mouse tumor model leading to antitumor efficacy. Pairing of complementary oncolytic viruses is a promising strategy to enhance the antitumor activity of this novel class of anticancer drugs.

show abstract

“…The L-IVP strain was used for the production of most of the vaccines donated to the Intensified Smallpox Eradication Programme after 1971 ( 3 ). Both nonrecombinant and recombinant variants of the L-IVP strain demonstrated high levels of tumor cell selectivity and oncolytic activity ( 4 – 6 ).…”

Section: Genome Announcementmentioning

confidence: 99%