By Joseph G. Sinkovics, Joseph Horvath
Surveys attainable study pathways for the remedy of human cancers. Examines the regression of tumors in virally-infected sufferers, in addition to controversies keen on viral oncolysis. Analyzes gene remedy and lively particular immunotherapy of human tumors by way of viral vectors.
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Additional resources for Viral Therapy of Human Cancers (Basic and Clinical Oncology)
In one case, in a female patient, a hemangiosarcoma of the scalp sloughed off after direct inoculation of the PR8 virus; however it regrew and resisted repeated viral inoculations while the patient developed high titers of antibodies, inhibiting viral hemagglutination and neutralizing the virus. The case of another patient (hospital chart on microfilm), whose biopsy-proven hemangiosarcoma regressed during an influenza-like upper respiratory tract infection, remains an anecdote, inasmuch as laboratory proof for the viral infection has not been provided .
Instead, tumor cells may allow the virus to complete its full replicative cycle, leading to cell death by burst as the new viral progeny exits. Reovirus-induced apoptotic cell death involves either or both the extrinsic (through cell surface death receptors) and intrinsic (through cytochrome C release from mitochondria) pathways . From modest beginnings—that is, immunologically mediated rejection of murine leukemia–lymphoma cells and tumors by reovirus, as reported in 1976 and 1988 (especially in combination with the nitrosourea BCNU) 48 Sinkovics [265–267]—reoviruses have now advanced to occupy a prominent place among the most respected oncolytic viruses ready for Phase I and II clinical trials.
Its genome is transcribed within the nucleus of the host cell under the direction of its nucleoprotein (NP) . This NP is a multifunctional RNA-binding protein of 498 amino acids with kinase activity. It interacts with the viral RNAdependent RNA polymerase, the viral matrix protein, importins/exportins, export receptor CRM-l, F-actin, and the enzyme helicase. Dendritic cells of the infected host produce interferons, phagocytize apoptotic influenza virus-infected 38 Sinkovics cells, and express the viral antigens to CD4 and CD8 T cells, eliciting a Th1 response in which CD8 T cells secrete IFN␥ and inhibit a Th2 response.