Virus Specific RNA in Cells transformed by RNA Tumour Viruses

Virus specific RNA comprises 5% of the nuclear RNA and 0.5–1.0% of the cytoplasmic RNA of cells transformed by murine sarcoma viruses. Even cryptically transformed cells which possess no detectable virus or viral proteins synthesize detectable amounts of viral RNA.     

Cell-free Studies on the Regulation of the Arabinose Operon

A DNA directed, cell-free system which synthesized L-ribulokinase coded by the L-arabinose operon ara OIBAD, has been developed. L-arabinose but not the araC gene product is required for the expression of this operon and, in addition, cyclic AMP and guanosine tetraphosphate are needed for optimal synthesis.     

Inhibitors of the RNA and DNA Dependent Polymerase Activities of RNA Tumour Viruses

RNA viruses of several animal leukaemias and sarcomas possess what seems so far to be a unique enzyme—an RNA dependent DNA polymerase^1–6. Specific inhibitors of the viral enzyme will not only be useful in the analysis of its possible role in neoplasia, but might provide drugs for leukaemia and cancer therapy.     

Interactions between Marek's Disease Herpesvirus and Avian Leucosis Virus in Tissue Culture

A GROUP B herpesvirus is important in the aetiology of Marek's disease, a highly contagious lymphoproliferative disease of chickens^1,2. Chicks inoculated with enveloped Marek's disease herpesvirus (MDHV), extracted from feather follicle epithelium of chickens with the disease, developed tumour-like aggregates of lymphoid cells in the viscera and frequently in the peripheral nerves^3,4. Cultures of chicken embryo fibroblast (CEF) cells infected with MDHV develop discrete foci of altered cells⁵. Our data show that MDHV infection of cultures of CEF cells, previously infected with an avian leucosis virus (RAV-2), results in both a reduction in the number of MDHV foci and an increase in the complement fixing avian leucosis antigen (COFAL)⁶ titre.     

Effect of Interferon on Some Aspects of Transformation by Polyoma Virus

WHEN BHK 21 hamster cells are infected with polyoma virus¹, there is no vegetative growth of virus, but stably transformed cells appear. These transformed cells are more easily transplanted than BHK 21 cells; they initiate their growth cycle in otherwise restrictive cultural conditions such as the absence of serum, high density and suspension; they grow with random orientation and have exposed on their surfaces receptor sites for certain glycoprotein agglutinins^2–5. The proportion of stably transformed cells is low, even after high doses of virus. But a much higher proportion (sometimes all cells) shows abortive transformation—changes characteristic of transformation, but which last only a few days. In suspension cultures, for example, most of the infected cells grow into small colonies of four to thirty-two cells⁶. In surface cultures deprived of serum DNA synthesis is initiated and the cells may then divide at least once⁷: they also temporarily lose the normal parallel orientation and develop the typical random appearance of transformed cells. Moreover, the polyoma nuclear T-antigen and also a surface antigen detected by immunofluorescence, appear temporarily in most polyoma infected BHK 21 cells⁸, while 3T3 cells exposed to SV40 virus show transient exposure of cell surface sites reacting with conconavalin A (ref. 9).     

Action of Angiotensins and Synthetic Renin Substrate on Isolated Rat Colon

AIKEN and Vane have reported¹ the independent actions of angiotensin I (AI) and angiotensin II (AII) on various isolated smooth muscle preparations, including rat colon. Tney showed that the apparent contractile action of AI on these preparations depended primarily on its in situ conversion to All by “converting enzyme” and that when the activity of the enzyme was inhibited by a pentapeptide extracted from Bothrops jararaca venom, the residual contractile action, probably due to unchanged AI, was very small. I have investigated the action of synthetic tetradecapeptide renin substrates (TPRS) on rat colon, in the light of the known actions of AI and All.     

Cooperation between Carrier-reactive and Hapten-sensitive Cells <Emphasis Type="Italic">in vitro</Emphasis>

THE mechanism, known as the carrier effect, whereby immunity to one or more determinant groups enhances the response to other determinants on the same multivalent antigen, was first recognized in delayed hypersensitivity to haptens, in which, for an appreciable response, the hapten must be coupled to the same protein carrier for priming and challenge^{1, 2}. Carrier specificity has also been demonstrated in the secondary antibody responses to hapten protein conjugates³. Two alternative hypotheses have been advanced to explain this specificity. The “local environment” hypothesis supposes that the hapten-sensitive cell recognizes both the hapten and the carrier determinants. However, the antihapten antibodies produced do not distinguish details of the carrier molecule and so do not reflect the specificity of the cellular receptor. Furthermore, inert spacer molecules inserted between hapten and carrier do not interfere with carrier specificity in the antibody response³. Reflecting current views on the cooperation between thymus-derived (T) and bone marrow derived (B) lymphocytes in the antibody response to various antigens⁴, the second hypothesis invokes two or more cells, one with receptors directed towards the hapten (hapten-sensitive cell), the others specific for the carrier molecule proper (carrier-reactive cells). Supporting this is the observation that pre-immunization to a particular protein carrier alone could potentiate the primary or secondary antihapten response to a hapten conjugated to that protein⁵. In an adoptive transfer system, moreover, the efficiency of antihapten antibody production by cells primed to a particular hapten-protein conjugate and stimulated with the hapten conjugated on a heterologous protein, is significantly enhanced by the introduction of cells primed to the heterologous carrier alone. Anti-carrier serum antibody does not cause such enhancement⁶. The carrier-reactive cells must therefore cooperate in increasing the efficiency of the hapten-sensitive cells in some way other than by providing humoral anti-carrier antibody. Recent work strongly suggests that carrier reactive cells are thymus-derived^{6, 7}.