Antibody-Mediated Immunity to Transplantable Tumors Following Reovirus Oncolysis

Klein, P.

doi:10.1159/000161662

Cited by 3 publications

(4 citation statements)

References 17 publications

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“…It would no longer be necessary to use mice genetically resistant to certain oncolytic viruses, such as PRI (25) or A2G (9), or to use viruses of intrinsically low virulence, such as NDV (28) or reo 3 (29). Neither would the choice of viruses have to be limited to those having dramatic oncolytic effects.…”

Section: Discussionmentioning

confidence: 99%

“…Tumor cells infected in vitro with influenza virus induced immunity to the tumor (27). A tumor-adapted strain of Newcastle disease virus led to oncolysis and postoncolytic tumor immunity (28), as did a strain of reovirus type 3 (29).…”

Section: Discussionmentioning

confidence: 99%

“…The possibility of vaccinating animals with the viral agent prior to injecting them with virus-infected cells opens new perspectives for the study of virusenhanced immunogenicity of tumors and other tissues. It would no longer be necessary to use mice genetically resistant to certain oncolytic viruses, such as PRI (25) or A2G (9), or to use viruses of intrinsically low virulence, such as NDV (28) or reo 3 (29). Neither would the choice of viruses have to be limited to those having dramatic oncolytic effects.…”

Section: Discussionmentioning

confidence: 99%

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Viral Oncolysis: Increased Immunogenicity of Host Cell Antigen Associated With Influenza Virus

Lindenmann

Klein

1967

The Journal of Experimental Medicine

215

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A2G mice could be solidly immunized against the Ehrlich ascites tumor by single intraperitoneal injections of homogenized and lyophilized tumor cells which had been infected with oncolytic strains of influenza A virus. Similar homogenates from noninfected tumor cells were not immunogenic, even when mixed with egg-grown virus. The immunizing principle in viral oncolysates could not be separated from the oncolytic virus by differential centrifugation or adsorption to and elution from red cells. It could be inhibited by antibody raised in rabbits against the egg-grown oncolytic virus. This reaction showed serologic specificity. Thus, the immunogenicity of an oncolysate produced with the WSA strain of neurotropic influenza virus could be inhibited by rabbit anti-WSA, but not by rabbit antibody to the TUR strain of fowl plague virus. Conversely, the immunogenicity of an oncolysate prepared with the TUR strain could be inhibited by rabbit anti-TUR, but not by anti-WSA. When mice were preimmunized (primed) with egg-grown WSA virus, their antitumor response to a later injection of WSA oncolysate was of the anamnestic type. Priming with egg-grown influenza B virus had no such effect. It was concluded that the immunogenicity of certain host cell components was greatly increased by incorporation into the makeup of the oncolytic virus.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Viral Oncolysis: Increased Immunogenicity of Host Cell Antigen Associated With Influenza Virus

Lindenmann

Klein

1967

The Journal of Experimental Medicine

215

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“…The oncolytic properties of reovirus were first observed by Klein et al (Table 1), who noticed that mice infected with this virus developed humoral immunity to transplanted tumors (5). Even more interestingly, it was shown that mouse NIH 3T3 cells, which generally are impervious to reovirus replication, lost this resistance upon transfection with activated Ras.…”

Section: Wild-type Replication Competent Viruses That Display Tumor S...mentioning

confidence: 91%

Oncolytic viruses for the therapy of brain tumors and other solid malignancies a review

Fulci

Chiocca²

2003

Front Biosci

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In spite of significant advances in the understanding of molecular processes in tumor biology that have led to the development of oncologic therapeutic strategies, the prognosis for several types of tumors (such as brain, pancreas, or hepatic malignancies) remains dismal. Without question, a strong need exists for continued investigations in new agents and new therapeutic regimens. The realization that several genes used by viruses in their lytic life cycle interact and/or complement the function of genes employed by cells in cellular events linked to cell cycle progression, apoptosis, and/or metabolism immediately suggests the development of treatment strategies wherein viral mutants could be employed as selective anticancer agents. Such viruses (designated as oncolytic viruses) can selectively grow in tumor cells, produce viral progeny in those cells, lyse them and release this progeny that can then infect additional cells in the tumor mass. A theoretical advantage of oncolytic viruses (OV) is that their numbers should augment within the tumor mass, a property that is lacking with drugs or radiation treatments. Additionally, Ovs' mode of tumor killing differs from standard anticancer agents, providing the possibility for synergistic interactions in multimodal tumor therapies. In this review, we will describe the development of OVs and briefly review the life cycle of their wild-type (wt) counterparts. We will also summarize published results from OV clinical trials and attempt to provide a perspective on research in this area.

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Reoviruses

Rosen¹

1968

ECHOViruses Reoviruses

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Antibody-Mediated Immunity to Transplantable Tumors Following Reovirus Oncolysis

Cited by 3 publications

References 17 publications

Viral Oncolysis: Increased Immunogenicity of Host Cell Antigen Associated With Influenza Virus

Viral Oncolysis: Increased Immunogenicity of Host Cell Antigen Associated With Influenza Virus

Oncolytic viruses for the therapy of brain tumors and other solid malignancies a review

Reoviruses

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