Abstract: In June of 1977, a new influenza A pandemic was started by strains of the H1N1 serotype. Oligonucleotide fingerprint analysis of the RNA from viruses isolated during the early stage of this pandemic demonstrated that genetic variation among these 1977 strains could be attributed to sequential mutation [Young, J.F., Desselberger, U. & Palese, P. (1979) Cell, 18, 73-83]. Examination of more recent strains revealed that the H1N1 variants that were isolated in the winter of 1978-1979 differed considerably from the H1N1 viruses isolated the previous year. Oligonucleotide and peptide map analysis of the new prototype strain (A/Cal/10/78) suggested that it arose by recombination. It appears that only the HA, NA, M, and NS genes of this virus are derived from the earlier H1N1 viruses and that the P1, P2, P3, and NP genes most likely originate from an H3N2 parent. These data suggest that genetic variation in influenza virus strains of the same serotype is not restricted to mutation alone, but can also involve recombination (reassortment).

Abstract: Reticuloendotheliosis viruses have been shown to be causative of tumors in a variety of avian species. The major structural protein of these non-genetically transmitted viruses is demonstrated to possess antigenic determinants common to those of all known mammalian type C viruses. These findings establish a mammalian origin for this oncogenic avian retrovirus group. None of the known mammalian type C virus groups demonstrated a closer immunological relationship to avian reticuloendotheliosis viruses. These results suggest that reticuloendotheliosis viruses have been non-genetically transmitted for a long period of evolution or that these viruses may have arisen by relatively recent infection of birds with an as yet undiscovered mammalian type C retrovirus.

Abstract: Publisher Summary This chapter discusses the current knowledge about tumor viruses, belonging to retroviridae and herpetoviridae , isolated from normal and malignant tissues of nonhuman primates. In addition, certain retroviruses of nonprimate origin are considered to a limited extent since they can induce experimental tumors in simian species. The utilization of nonhuman primates in virus-induced tumorigenesis studies increased subsequently to the demonstration that Rous sarcoma virus (RSV) can induce tumors in rhesus monkeys. Despite the availability of many virus-induced tumor models in common laboratory animals and the fact that many simian species may be either endangered or threatened of becoming extinct, the following considerations warrant the continued–judicious use of nonhuman primates in tumor-virus research related to human malignancies. That nonhuman primates are not in any way specifically resistant to tumor development is suggested by the reported outbreaks of malignant neoplastic diseases in several primate colonies. Retroviridae is a recent name assigned to a family of enveloped RNA viruses that contain an antigenically specific RNA-directed DNA polymerase (reverse transcriptase). Since retroviruses are (endogenous retroviruses) or can become (infectious retroviruses) an integral part of the cellular genome; it has been possible to use retroviruses as molecular tools to study the cellular as well as viral evolution. Several vaccines are currently in use against diseases caused by viruses that have a horizontal mode of transmission. Since herpesviruses, including those with proven oncogenicity, are transmitted horizontally, it may be feasible to develop an appropriate vaccine for the prevention of the diseases they cause, such as EBV-induced infectious mononucleosis and perhaps Burkitt's lymphoma and nasopharyngeal carcinomas.

Abstract: Publisher Summary This chapter explores the recent developments in the biochemistry of viruses. The goal of molecular viroligists is to understand the structure, expression, and control of viral genes. Probably, the most complete genome map has been determined for the small transforming papovavirus SV40. The goal of mapping a mutant is to determine what function is affected by the mutation, and where that function is located on the physical map. Consequently, the protein or protein region responsible for the function can be determined. The variations found in the genomes of the different strains of all the viruses examined, suggests that one might expect the structures of their gene products to vary considerably, also this could account for variations in disease severity, and suggests that antiviral chemicals may vary considerably in effectiveness. Viruses that contain RNA genome can be classed as positive and negative-stranded viruses depending on whether their genome RNA serves directly as mRNA (positive) or requires RNA transcription to synthesize mRNA molecules (negative). The positive-stranded RNA viruses are best represented by the picornaviruses, of which poliovirus is a model virus. The negative-stranded RNA viruses are larger and more complex than the positive-stranded viruses. They contain an RNA polymerase that transcribes their genome RNAs into functional mRNAs. Probably without exception among the animal viruses, enzymatic cleavage of viral proteins occurs in or on the surface of infected cells. The evidence collected for some of the representative viruses indicates that the cleavages are essential for the successful production of viral progeny. The growth of the virus in a high yielding cell gave infectious virions with virtually all the glycoprotein in a cleaved form. Cleavage allows the virus to proceed successfully through the early stages of infection to the point where the viral nucleic acid is released into the host cell.