Oncolytic enteroviruses

Chumakov, P. M.; Morozova, Vera; Бабкин, И. В.; Байков, И. К.; Нетесов, С. В.; Tikunova, Nina

doi:10.1134/s0026893312050032

Cited by 22 publications

(9 citation statements)

References 82 publications

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“…Further, echoviruses such as Echo 1, Echo 7, and Echo12 possess oncolytic activity (Haley et al, 2009;Israelsson et al, 2011;Shafren et al, 2005;Ylä -Pelto et al, 2016). RIGVIR, the Echo 7-based oncolytic drug, has been approved for clinical use in Latvia for melanoma treatment (Chumakov et al, 2012;Donin ‚ a et al, 2015). However, the lack of receptor information for Echo 7 hampered our understanding and evaluation of this type of oncolytic therapy (Chumakov et al, 2012;Tilgase et al, 2018).…”

Section: Implications For Antiviral Drug Design and Enterovirus-basedmentioning

confidence: 99%

“…RIGVIR, the Echo 7-based oncolytic drug, has been approved for clinical use in Latvia for melanoma treatment (Chumakov et al, 2012;Donin ‚ a et al, 2015). However, the lack of receptor information for Echo 7 hampered our understanding and evaluation of this type of oncolytic therapy (Chumakov et al, 2012;Tilgase et al, 2018). The discovery of FcRn as its receptor will improve the development of echovirus-based oncolytic therapeutics.…”

Section: Implications For Antiviral Drug Design and Enterovirus-basedmentioning

confidence: 99%

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Human Neonatal Fc Receptor Is the Cellular Uncoating Receptor for Enterovirus B

Zhao

Zhang

Liu

et al. 2019

Cell

141

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Graphical Abstract Highlights d CRISPR screening identified FcRn as an essential and universal EV-B receptor d FcRn facilitates EV-B uncoating and CD55 for attachment d High-resolution Cryo-EM structures described the mechanism of virus entry d The molecular mechanism of dual (attachment versus uncoating) receptor-usage was illustrated SUMMARY a structural basis for understanding the mechanisms of enterovirus entry.

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Section: Implications For Antiviral Drug Design and Enterovirus-basedmentioning

confidence: 99%

Section: Implications For Antiviral Drug Design and Enterovirus-basedmentioning

confidence: 99%

Human Neonatal Fc Receptor Is the Cellular Uncoating Receptor for Enterovirus B

Zhao

Zhang

Liu

et al. 2019

Cell

141

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“…The first of these is a nongenetically modified, nonpathogenic enteric cytopathic human orphan 7 virus strain that has been adapted to grow in melanoma cells, known as Rigvir. Rigvir was first approved for use in Latvia for melanoma therapy in 2004 [55] and later approved for use in Georgia in 2015 and Armenia in 2016.…”

Section: Ovs In Clinical Developmentmentioning

confidence: 99%

Oncolytic virus-induced cell death and immunity: a match made in heaven?

Munck

Binks

McNeish

et al. 2017

Journal of Leukocyte Biology

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Our understanding of the mechanisms responsible for cancer development has increased enormously over the last decades. However, for many cancers, this has not been translated into a significant improvement in overall survival, and overall mortality remains high. Treatment for many malignancies remains based on surgery, chemotherapy, and radiotherapy. Significant progress has been made toward the development of more specific, more potent, and less invasive treatment modalities, but such targeted therapies remain the exception for most cancers. Thus, cancer therapies based on a different mechanism of action should be explored. The immune system plays an important role in keeping tumor growth at bay. However, in many cases, these responses are not strong enough to keep tumor growth under control. Thus, immunotherapy aims to boost the immune system to suppress tumor growth efficiently. This has been demonstrated by the recent successes of immune checkpoint therapy in several cancers. Oncolytic viruses (OVs) are another exciting class of immunotherapy agent. As well as replicating selectively within and killing tumor cells, OVs are able to elicit potent anti-tumor immune responses. Therapeutic vaccination with OVs, also referred to as cancer virotherapy, can thus be tailored to elicit vigorous cellular immune responses and even target individual malignancies in a personalized manner. In this review, we will describe the intricate link among oncolytic virotherapy, tumor immunology, and immunogenic cell death (ICD) and discuss ways to harness optimally their potential for future cancer therapy.

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“…In nature, the arginine-specific serine protease “Clara” is most likely responsible for the maturation of the virus [ 15 - 7 ]. The ability to process the F0 protein defines the tissue tropism of paramyxoviruses [ 18 ].…”

Section: Antitumor Activity Of the Sendai Virusmentioning

confidence: 99%

“…in oncolytic adenoviruses [ 5 ] and poxviruses [ 6 ]. The genomic RNA of oncolytic viruses can also have different forms: positive sense single- stranded RNA (enteroviruses [ 7 ]), double stranded RNA (reoviruses [ 8 ]), or negative sense single-stranded RNA (paramyxoviruses and rhabdoviruses in [ 9 ]).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Oncolysis by Paramyxovirus Sendai

Matveeva¹,

Кочнева

Нетесов

et al. 2015

Acta Naturae

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Some viral strains of the Paramyxoviridae family may be used as anti-tumor agents. Oncolytic paramyxoviruses include attenuated strains of the measles virus, Newcastle disease virus, and Sendai virus. These viral strains, and the Sendai virus in particular, can preferentially induce the death of malignant, rather than normal, cells. The death of cancer cells results from both direct killing by the virus and through virus-induced activation of anticancer immunity. Sialic-acid-containing glycoproteins that are overexpressed in cancer cells serve as receptors for some oncolytic paramyxoviruses and ensure preferential interaction of paramyxoviruses with malignant cells. Frequent genetic defects in interferon and apoptotic response systems that are common to cancer cells ensure better susceptibility of malignant cells to viruses. The Sendai virus as a Paramyxovirus is capable of inducing the formation of syncytia, multinuclear cell structures which promote viral infection spread within a tumor without virus exposure to host neutralizing antibodies. As a result, the Sendai virus can cause mass killing of malignant cells and tumor destruction. Oncolytic paramyxoviruses can also promote the immune-mediated elimination of malignant cells. In particular, they are powerful inducers of interferon and other cytokynes promoting antitumor activity of various cell components of the immune response, such as dendritic and natural killer cells, as well as cytotoxic T lymphocytes. Taken together these mechanisms explain the impressive oncolytic activity of paramyxoviruses that hold promise as future, efficient anticancer therapeutics.

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Oncolytic enteroviruses

Cited by 22 publications

References 82 publications

Human Neonatal Fc Receptor Is the Cellular Uncoating Receptor for Enterovirus B

Human Neonatal Fc Receptor Is the Cellular Uncoating Receptor for Enterovirus B

Oncolytic virus-induced cell death and immunity: a match made in heaven?

Mechanisms of Oncolysis by Paramyxovirus Sendai

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