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PubMed1979

Changes in hemopoiesis of mice of the C3H strain following transplantation of Gardner lymphosarcoma and infection with LDH-virus. I. Circulating blood.

The values of red and white blood count, of spleen and liver weight were determined in mice of the C3H strain after transplantation of Gardner solid lymphosarcoma contaminated with LDH-virus and after infection of LDH-virus, and compared with those found in normal intact mice. Special attention was devoted to early post-transplantation period and the final stage of tumor growth. The second day after infection of mice with LDH-virus, leukopenia with marked lymphopenia was observed, together with a reduced number of reticulocytes and spleen enlargement. The same changes became more pronounced in tumorous mice on the second posttransplantation day. The changes--with the exception of spleen enlargement--following LDH-virus infection became normalized within the period of the final stage of tumor growth. Contrarily, in mice with tumors in the final stage of the disease besides spleen enlargement also the reduced erythrocyte counts, leukopenia with pronounced lymphopenia and thrombocytopenia were found.

Animals↗
PubMed1978

Protracted circulating lifetimes of mannose-terminated glycoproteins and aggregated albumin in mice infected with LDH-elevating virus.

Several macromolecular homeostasis-regulating mechanisms were tested for functional integrities in mice during acute and early chronic phases of infection with lactic dehydrogenase-elevating virus (LDV). Fractional catabolic rates of carbodiimide-aggregated albumin and immunoglobulin G were studied to evaluate glomerular filtration and hepatic Kupffer cell phagocytic activities. Several glycoproteins (fetuin, IgG antibodies, and ovalbumin) were also compared with their deglycosylated counterparts for fractional catabolic rates and organ distributions as a basis for evaluating virus-induced modifications of saccharide-binding "receptor functions" in vivo. Findings were that normal hepatic clearance of aggregated albumin and of ovalbumin is slowed from the onset of viremia. Fractional catabolic rates of amannosyl-ovalbumin and amannosyl-IgG are similar in uninfected animals to those seen with native ovalbumin or with mannose-terminated IgG in LDV-infected animals. Ovalbumin and aggregated albumin were also found to be mutually competitive for hepatic uptake in uninfected animals. It is proposed that LDV, which replicates in cells of the mononuclear phagocyte system (reticuloendothelial system), alters the clearance functional state of fixed tissue macrophage, thereby explaining in part the protracted circulatory longevity of several enzymes, aggregated albumin and mannose-terminated ovalbumin, and IgG in LDV-infected mice.

Animals↗
PubMed1975

Purification and electron microscopy of lactic dehydrogenase virus of mice.

Lactic dehydrogenase virus (LDV) was purified from infectious ascites fluid of mice bearing Ehrlich tumours using Sepharose gel filtration and rate zonal and isopycnic sedimentation. In glycerol gradients, a sedimentation coefficient of about 200S and a buoyant density of 1-14 g/ml was determined for the virus particle. Spherical particles with diam. between 62 and 80 nm, depending on the method of fixation and staining, have been identified electron microscopically. The virus particle consists of a spherical nucleocapsid wrapped into a double-layered envelope. The nucleocapsids, isolated by treatment with NP40 and purified by centrifuging on sucrose gradients had a sedimentation coefficient of 176S. Electron micrographs show spherical particles with a diam of 35 plus or minus nm. Classification of LDV as a member of the togaviridae family is discussed.

Animals↗
PubMed1975

Effect of a potent interferon inducer on acute and chronic lactic dehydrogenase virus viremia.

The effect of a single and multiple doses of polyinosinic-polycytidylic acid (poly (I). poly(C) on lactic dehydrogenase virus viremia has been studied. A single injection of 200 mug of poly (I)-poly(C) given 6 h before infection with lactic dehydrogenase virus caused a temporary decrease in viremia of about 2.5 log10. Repeated injections of 100 mug of poly(I)-poly(C) every 24 h beginning at -24 h caused a temporary decrease in viremia of about 4.0 log 10. Therapeutic treatment with optimal dosage schedules (100 mug every 24 h) caused a reduction in viremia of 1.0 to 2.0 log10. This decrease lasted for at least 24 h after the treatment was stopped. Some possible reasons for the limited effectiveness of poly (I)-poly(C) in this system are discussed.

Animals↗
PubMed1979

Immune responses in mice infected with lactic dehydrogenase virus. IV. Functional status of the macrophage during acute LDV infection.

Macrophages from uninfected and lactic dehydrogenase virus (LDV)-infected mice were compared with respect to the affinity and number of their Fc receptors for IgG2a; no differences were found regarding these parameters. When the uptake of DNP-BGG by macrophages from uninfected and acutely LDV-infected mice was compared, again no differences were observed. However, when the per cent membrane-bound DNP-BGG was determined as a function of time after antigen uptake in these two groups, more DNP-BGG was found membrane-bound on the macrophages from the LDV-infected mice, than on uninfected macrophages. In view of the fact that humoral immunity is enhanced during acute LDV infection, these data provide a positive correlation between increased retention of membrane-bound antigen and enhanced humoral immune responses.

Acute Disease↗
PubMed1977

Immune responses in mice infected with lactic dehydrogenase virus. I. Antibody response to DNP-BGG and hyperglobulinaemia in BALB/c mice.

The humoral immune response to DNP-BGG of BALB/c mice acutely infected with lactic dehydrogenase virus (LDV) has been investigated. Virus-infected mice injected with antigen in saline exhibit a greater anti-DNP response than uninfected controls. When this antigen is presented in Freund's complete adjuvant (FCA) the anti-DNP response is greater than obtained with antigen in saline, but significant differences between infected and uninfected controls are not observed. These data are consistent with the view that acute LDV infection can have an adjuvant-like effect when this T-dependent antigen is introduced in saline. In addition, the effect of viral infection on plasma Ig class and subclass levels has been investigated. LDV infection leads to a gradual increase in plasma Ig concentration. This effect is restricted to the IgG2a subclass in most animals, but occasionally is restricted to IgG1. The mechanisms responsible for these changes have not been delineated.

Adjuvants, Immunologic↗
PubMed1978

Lactic dehydrogenase virus alteration of lymphocyte circulation.

Acute infection with lactic dehydrogenase virus (LDV) causes a systemic alteration in lymphocyte circulatory patterns. Peripheral lymph nodes (LN) and spleens in acutely, but not chronically, infected mice retain a significantly greater proportion of injected 51Cr-labeled lymphocytes than the respective tissues in noninfected controls. This increase in lymphocyte localization in LN and spleen is dependent upon the dose of LDV injected and the timing of the infection. A relatively large dose of LDV (10(8) infectious units) causes an early but very transient increase in splenic lymphocyte localization accompanied by an early but prolonged increase in lymphocyte recovery in LN. Smaller doses of LDV cause more prolonged effects on splenic lymphocyte recovery and retarded effects on lymphocyte localization in LN. Increases in splenic recovery were always accompanied by decreases in hepatic recovery of lymphocytes. LDV-induced alteration in lymphocyte circulation may be responsible for many previously observed modifications of immune responses in LDV-infected mice.

Animals↗
PubMed1975

Distribution along the axon and into various subcellular fractions of molecules labeled with (3H)leucine and rapidly transported in the garfish olfactory nerve.

The distribution of molecules labeled with [3H]leucine by fast axoplasmic transport in vivo has been studied in the garfish olfactory nerve after incorporation of the amino acid by the olfactory mucosa. Owing to the size of the nerve, it has been possible to follow the fate of the labeled molecules in 10 different subcellular fractions of 6 consecutive nerve segments. Each segment represents a different part of the profile developed by the transported radioactive molecules. In order to determine the influence of the perikaryon (rate of protein synthesis and rate of protein release into the axon) transport was studied under 3 different conditions: (1) intact nerves (simply labeled with [3H]leucine); (2) nerves cut from the cell bodies 6 h after application of [3H]leucine; and (3) nerves pulse-chase labeled for 1 h. Several conclusions can be drawn. (1) The bulk of the rapidly transported molecules are membranous axonal proteins, as determined by enzyme markers. Most are found in subcellular fractions representing 17% of the total axonal protein. They are synthesized very rapidly in the cell bodies (less than 1 h after isotope deposition) and exhibit the highest specific activities measured. These high specific activities were found in the same axonal membrane fractions in both plateau and crest, suggesting that the membrane precursors are transported as particles rather than as subunits. (2) The majority of these proteins are released into the axon immediately after synthesis; however, at least 30% of the labeled axonal membranous proteins are not released with the fast wave itself but progressively over a long period of time. (3) The majority of the moving material, particularly in membranous fractions, is left behind the fast wave and is deposited in the axon. When the front base of the fast wve has covered 70% of the total nerve length, only 19% of the labeled material of the main axonal membranous fraction appears still to be moving. (4) Proteins with high specific activities are found near the cell bodies and may be the result of early axonal transport of amino acids, diffusing later into the surrounding cells and being incorporated into proteins. Some free amino acids are also transported along the axon.

Acetylcholinesterase↗
PubMed1979

Matching of chemotherapy to mouse strain and lymphoid tumor type to prevent tumor-induced suppression of specific T- and B-cell functions.

Specific immunological and hematopoietic functions were studied during treatment with antineoplastic agents in mice bearing syngeneic lymphoid tumors: 70Z/2, a B-cell lymphoma of C57BL X DBA/2 F1 (hereafter called (BD2F1) mice; EL4, a T-cell lymphoma of C57BL/6 mice; or J774, a macrophage tumor of BALB/c mice. Both B- and T-lymphocyte function (antibody-forming cells and cell-mediated lymphocyte lympholysis toward alloantigens) were suppressed in spleen cells of mice bearing these tumors. Other hematopoietic functions (granulocyte, macrophage, and megakaryocyte progenitor cells) were variably influenced by growth of these lymphoid tumors. J774 enhanced, but 70Z/2 suppressed, megakaryocyte progenitor cells. J774 and 70Z/2 increased levels of granulocyte-macrophage progenitor cells. EL4, the T-cell lymphoma, did not influence either cell type. Significant variation in strain sensitivity to drug toxicity and drug effectiveness in different tumor-host systems was observed. Increased median survival time with reversal of tumor-induced immune dysfunction, without toxicity to hematopoietic progenitor cells, was realized in two tumor-host-drug combinations. Polyinosinic-polycytidylic acid was effective against J774, while actinomycin D was active against 70Z/2. Mitomycin C effectively reduced tumor load, as evidenced by loss of splenic tumor colony-forming cells for all three tumors. This agent prolonged survival and concomitantly restored immunological responsiveness in hosts immunosuppressed by growth of 70Z/2 or J774. Paralleling tumor reduction with mitomycin C therapy, the splenic hematopoietic progenitor and colony-forming B-cells were reduced in tumor-bearing and tumor-free mice, thus compromising its therapeutic effectiveness. 1-beta-D-Arabinofuranosylcytosine reduced tumor load with marginal toxicity toward hematopoietic progenitor and colony-forming B-cells. However, immune responsiveness was only partially restored, and median survival was not increased. The results presented show the diversity of therapeutic drug effectiveness in increasing mean survival time and influencing other life-sustaining parameters (immunological and hematopoietic functions).

Animals↗
PubMed1979

Correlation of extracts obtained by high efficiency gel chromatography of lactic dehydrogenase virus infected mouse serum and cytosol from human tumors using leukocyte adherence inhibition assay.

Immunochemically active fractions were obtained using Separon Hema-300-glc(R) from serum of lactic dehydrogenase virus (LDV) infected mice and from homogenates of human tumors. The mixture of proteins of tumorous origin from the cytosol giving a positive reaction in the leukocyte adherence inhibition (LAI) test was found in the same fractions showing maximum of absorbance at 340 nm in the spectrophotometer and a corresponding peak in the refractometer. Analogous peaks were not proved in material obtained from healthy controls, but they were found in some human placentas and fetal organs. The LDV fraction obtained from mouse serum served as a "control" antigen in LAI test for human tumor testing, and results corresponded with those obtained using cytosol specific for the tumor under study.

Animals↗
PubMed1977

Immunodepression, ascites tumour and lactate dehydrogenase virus.

The delayed hypersensitivity (DH) response to picryl chloride was studied in Ehrlich ascites tumour-bearing and normal control mice. A significant depression of the DH response was found in the tumour-bearing mice, which was associated with a marked elevation of serum lactate dehydrogenase (LDH). Depression of DH was also observed in mice receiving cell-free ascitic fluid. These mice also showed an elevated serum LDH which is assumed to be associated with the lactate dehydrogenase virus. A method for assaying DH in vivo is described.

Animals↗