Showing papers on "Viral evolution published in 1981"
TL;DR: The three virus groups to be considered are the lymphoid leukosis viruses, the acute leukaemia viruses, and the avian sarcoma viruses, ASV, which are divided into these groups on the basis of the spectrum and latency of the neoplasia they induce in vivo.
Abstract: Introduction. The three virus groups to be considered are the lymphoid leukosis viruses (LLV), the acute leukaemia viruses, also called the defective leukaemia viruses (DLV) since they are all defective for replication, and the avian sarcoma viruses, ASV. Avian retroviruses are divided into these groups on the basis of the spectrum and latency of the neoplasia they induce in vivo (Table 1). Although this method of classification is by no means absolute, there being many overlaps, it does provide an easy basis upon which to consider these viruses. When considering the mechanism of transformation the most important feature of this classification is the latency period. Viruses which transform rapidly, DLV and ASV, appear to do so by virtue of cellular sequences which have been incorporated into the genome which encode a protein(s) that is responsible for transformation. The method by which viruses with a long latency transform cells is poorly understood but it appears to involve more indirect mechanisms.
37 citations
TL;DR: Nucleotide sequencing of the cellular DNA sequences flanking the viral integration sites and the use of recombinant plasmid DNAs containing a selectable gene (thymidine kinase) and the tumor virus genome should result in a better understanding of the molecular mechanism of the integration of oncogenic viruses in the cellular genome.
Abstract: Publisher Summary This chapter discusses the integration of oncogenic viruses in mammalian cells. Cells transformed by either RNA- or DNA-containing oncogenic viruses retain the genomes of the transforming viruses and, generally, express antigens, coded by the viral genome. The genomes of oncogenic viruses can integrate in different sites in the same or different chromosomes in different viral-transformed cells. It is not clear, however, whether the viral genomes integrate into specific sites or at random in the mammalian cell genome. Nucleotide sequencing of the cellular DNA sequences flanking the viral integration sites and the use of recombinant plasmid DNAs containing a selectable gene (thymidine kinase) and the tumor virus genome should result in a better understanding of the molecular mechanism of the integration of oncogenic viruses in the cellular genome.
12 citations
1 Jan 1981
TL;DR: The present state of knowledge on the replicative cycle of oncornaviruses, and the molecular events involved in cell transformation by such viruses, suggests several points of attack in blocking the onCornavirus-induced transformation or the expression of integrated viral information in the genome of the host cell.
Abstract: The present state of our knowledge on the replicative cycle of oncornaviruses (RNA Tumor Viruses: Retro-viruses), and the molecular events involved in cell transformation by such viruses, suggests several points of attack in blocking the oncornavirus-induced transformation or the expression of integrated viral information (Oncogene) in the genome of the host cell. The life cycle of the oncornaviruses involves the following sequential events: 1) Adsorption and penetration of the virus into the host cell; 2) Release of viral components followed by the synthesis of proviral DNA; Integration of the proviral DNA segment into the host genome; 4) Transcription and processing of virus-related RNA; 5) Translation of viral proteins; 6) Assembly of proteins and RNA; and 7) The envelopment and release (budding) of the virus particles. Adsorption is mainly dependent on the recognition of the host cell surface receptors by the viral envelope proteins. Our present knowledge about the factors which govern the relationship between the viral envelope proteins and the cell surface receptors is still in its infancy; hence a molecular strategy to block this process is difficult. However, this process is amenable to specific immunological control. The next step in the life cycle, formation of proviral DNA, is unique to this class of viruses and is therefore most amenable to chemical control. One of the major concerns of our laboratory is the development of chemical inhibitors which block the synthesis of proviral DNA. These studies will be described here in detail.
1 Jan 1981