Abstract: I. INTRODUCTION Although the bulk of this text is concerned with the biology and molecular biology of the RNA tumor viruses, we consider here and, to some extent, in Chapters 6 and 8 the entire Retroviridae virus family. The family encompasses all viruses containing an RNA genome and an RNA-dependent DNA polymerase (reverse transcriptase) enzymic activity (Fenner 1975). The family is divided into three subfamilies: (1) Oncovirinae, including all the oncogenic members and many closely related nononcogenic viruses; (2) Lentivirinae, the “slow” viruses, such as visna virus; and (3) Spumavirinae, the “foamy” viruses that induce persistent infections without any clinical disease. The latter two subfamilies are generally given summary treatment in discussions on retroviruses and, therefore, we propose to present at least some of their salient features. The spumaviruses provide an excellent model system for chronic viral disease, whereas the lentiviruses are in the mystical realm of slow neurological diseases. To some extent, a taxonomical description is, of necessity, a tedious job and relatively unimaginative, since the essence of the matter is covered in the chapters to follow. What we propose to do here is to cover the viruses isolated (or particles seen but without infectious transmission) in the different invertebrate and vertebrate genera. Obviously, much of the focus in later chapters is devoted to the viruses from the best-characterized systems: chickens, mice, cats, cattle, and monkeys. Therefore, the coverage here of the more familiar isolates may seem disproportionately small with respect to the plethora of available data; needless to...

Abstract: Thus the connection between tumor viruses and abnormal differentiation was noted at the very beginning of tumor virology. In this paper I shall remind you of some history of the connection between RNA tumor viruses and differentiation and of RNA tumor viruses and movable genetic elements; summarize very briefly the relevant present knowledge of RNA tumor viruses; discuss the present status of the hypothesis of the existence of protoviruses in vertebrate genomes; and finally, discuss the possible role of movable genetic elements in differentiation and evolution. I shall start with Barbara McClintock and maize. In the 1940s, McClintock started studying the mutable loci that arose after breakage-fusion-bridge cycles in maize. These cycles are occasioned by the presence of an inverted repeat in one of a pair of chromosomes followed during meiosis by crossing over and formation of a dicentric chromosome. In later mitoses, a break occurs in anaphase, followed by fusion of sister chromatids in later prophase. This fusion then results in a dicentric chromosome which again is broken and then fuses, etc. McClintock realized that after these cycles some factor was present that controlled the time or frequency of

Abstract: I. INTRODUCTION As with other animal viruses, the molecular biology of retroviruses has depended on the use of experimental laboratory procedures for the isolation, propagation, assay, and cloning of biologically active virions. The development of monolayer and suspension cell-culture systems has played a crucial role in experimental biology of retroviruses. The replication of retroviruses need not kill the host cell. The maturation of viral particles by budding from the plasma membrane does not usually cause cytopathic effects; therefore, an infected cell can become transformed and proliferate while producing virus progeny. However, as Temin (1963) first reported, virus replication is not necessary for cell transformation; neither is cell transformation necessary for virus replication (see Fig. 3.1). These phenomena are discussed in detail in later sections. Originally, the retroviruses were classified according to the disease that they caused and were named after their discoverers. C-type RNA tumor viruses may be broadly divided into sarcoma and leukemia (leukosis) viruses. The division is not a clear one because some leukemia viruses can also produce a wide spectrum of solid tumors (see Chapter 8). Also, leukemia viruses are commonly present in stocks of sarcoma viruses, and src deletion mutants (transformation-defective [ td ] viruses) of nondefective avian Rous sarcoma viruses (RSVs) are leukemogenic. Sarcoma viruses transform fibroblasts in culture, and cell transformation is the criterion by which these viruses are usually assayed. Avian leukemia viruses (ALVs) do not usually transform fibroblasts, although they readily infect and replicate in them. Some acute, defective leukemia viruses transform fibroblasts (e.g...

Abstract: Influenza is caused by highly variable RNA viruses belonging to the orthomyxovirus group. These viruses are capable of constantly changing the genes coding for their surface proteins as well as for their nonsurface proteins. The mechanisms responsible for these changes in type A influenza viruses include recombination (reassortment) of genes among strains, deletions and insertions in genes, and, frequently, point mutations. In addition, old strains may reappear in the population. Influenza viruses of types B and C appear to vary to a lesser degree. The mechanisms responsible for changes in these viruses are not well characterized.