Information Transfer in Cells Infected by RNA Tumor Viruses and Extension to Human Neoplasia

Abstract

Publisher Summary This chapter focuses on the molecular studies and attempts particularly to interpret and correlate recent findings that bring us to a working model for their origin, evolution, function, and especially their relationship to neoplasia. RNA tumor viruses have been identified in many species, including birds, snakes, mice, rats, hamsters, pigs, cats, dogs, monkeys and possibly man. Many of these will induce leukemias, lymphomas, and sarcomas in their natural hosts. None are regularly derived from or cause carcinomas with the exception of the “type-B virus, the mouse mammary tumor virus (MMTV). Some of the viruses of the leukemialymphoma-sarcoma complex (type-C) have been isolated from spontaneous cancers. This is notable in birds, mice, cats, and monkeys. There are 4 types of primate RNA tumor viruses of special interest to us because of their relatedness to man and because they recently have been useful in showing the presence of RNA tumor virus information in human leukemic cells. The chapter also provides an overview on a new concept to virogenesis as described by the established oncogene-virogene and provirus-protovirus theories. Several observations suggest that RNA processing is a key event in the origination and replication of RNA tumor viruses. The RNA genomes of RNA tumor viruses resemble unprocessed nuclear RNA of normal cells. This raises the possibility, supported by several lines of evidence that an alteration in the normal processing of nuclear RNA in differentiated cells can result in the cytoplasmic appearance of RNA with the physical properties of type-C virus RNA. The coding potential of the unprocessed cytoplasmic RNA determines whether virus particles will form and determines the physiological effect of the RNA on cells.