Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An inactivated and lyophilized preparation of a low virulence strain (Su) of Streptococcus pyogenes (group A) was designated OK-432. When 2- and 5-month-old AKR mice were inoculated im with OK-432 twice weekly throughout their life-spans, spontaneous leukemias occurred later and at a lower incidence than in control groups. By virus neutralization and cytotoxicity tests and by immunoelectron microscopy, antibodies against virus and cell-surface antigens of transplanted AKR leukemia were not detectable in sera of nonleukemic mice of any group. Whereas sera from mice treated with OK-432 were the only positive for interferon, viremia was clearly demonstrated in control groups by reverse transcriptase assays of the plasma.
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PMID:Streptococcus pyogenes preparation OK-432: immunoprophylactic and immunotherapeutic effects on the incidence of spontaneous leukemia in AKR mice. 5 50

Four-week-old specific-pathogen-free cats were immunized with a combined vaccine composed of killed feline leukemia virus and killed feline oncornavirus-associated cell membrane antigen-containing tumor cells. Immunization induced feline oncornavirus-associated cell membrane antigen antibody titers ranging from 1:32 to 1:256 but did not elicit detectable virus-neutralizing antibody titers. Kittens immunized with tumor cells alone developed higher feline oncornavirus-associated cell membrane antigen antibody titers (ranging from 1:512 to 1:2048) than those given the combined vaccine. All kittens were challenged with virulent Dynder-Theilen feline sarcoma virus at 12 weeks of age. Seventy-five % of the kittens vaccinated with combined vaccine and 67% of unvaccinated control kittens developed progressive fibrosarcomas after challenge. By contrast, none of the kittens vaccinated with killed tumor cells alone developed progressive fibrosarcomas after challenge. The combined vaccine did not, however, inhibit the induction of feline leukemia virus viremia.
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PMID:Abrogation of resistance to feline oncornavirus disease by immunization with killed feline leukemia virus. 6 86

Various inbred strains of mice respond immunologically to genetically transmitted ecotropic C-type viruses. Part of this response is T cell blastogenesis with type specificity for the viral envelope glycoprotein gp71. Of those nonviremic, nonleukemic strains, and F1 crosses examined, in which virus expression occurs early in life, gp71-specific blastogenic T cells were detected within the first 2 months of age and temporally preceded the development of a humoral immune response. However, in the viremic, highly leukemic strain of AKR mice, gp71-specific T cell blastogenesis in vitro was readily detectable throughout the preleukemic phase, the first 5 months of age. In appropriate F1 crosses and backcrosses, the persistent in vitro blastogenic response segregated with viremia and leukemia. These data suggest that in vivo T cell stimulation by endogenous viral gp71, caused by viremia, may contribute to virus-induced leukemogenesis in mice.
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PMID:Mechanisms of C-type viral leukemogenesis. I. Correlation of in vitro lymphocyte blastogenesis to viremia and leukemia. 9 Jul 8

The effect of methylnitrosourea (MNU), a potent resorptive carcinogen, was evaluated for its influence on the susceptibility of adult cats to infection and induction of oncornavirus disease by feline leukemia virus (FeLV). Young adult cats at an age previously demonstrated to be highly resistant to FeLV, were injected intravenously with moderately toxic doses (15-20 mg/kg) of MNU alone or with infections FeLV (Rickard strain). Following exposure to virus and chemical, cats were monitored for antibody to the feline oncornavirus-associated cell membrane antigen (FOCMA), viremia by direct infectivity and the presence of gsa in peripheral blood leukocytes, and for toxic effects of MNU by hemogram analyses on peripheral blood. Of 8 cats injected with MNU + FeLV, 6 developed persistent viremia, 5 of which became debilitated from thymic lymphoma. Only 1 of 6 non-MNU-treated and infected cats of the same age became transiently viremic. FOCMA antibody development was markedly depressed in MNU + FeLV inoculated cats compared with cats inoculated with FeLV alone. Results show that MNU was apparently responsible for the obliteration of age-related susceptibility in cats to FeLV infection and induction of FeLV-related disease, and suggest that in nature exposure to toxic chemical carcinogens may act as factors which determine susceptibility to feline oncornaviruses in the cat.
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PMID:Enhancement of feline leukemia virus-induced leukemogenesis in cats exposed to methylnitrosourea. 9 86

Leukocyte and urine cultures were done at monthly intervals in 36 children with acute lymphocytic leukemia known to be excreting cytomegalovirus in their or saliva in order to determine the relationship of viremia to clinical cytomegalic inclusion disease. Eleven of 36 (30.5%) patients had viremia. Viremia was related to clinical disease in only three patients; two with chorioretinitis and one with a CMV monomucleosis syndrom. However, the presence of viremia did not serve as a useful means to determine active CID. Viremic patients with CID all had elevated serum levels of IgM and multiple episodes of viremia. Viremia was not related to the duration, type or number of drugs used in immunosuppression, nor to the hematologic status of leukemia. Viremic patients received more blood transfusions than noviremic patients, but the administration of blood products could not be related to the acquisition of infection. Leukopenia, neutropenia, total lymphocyte count, fourfold rise or fall in complement-fixing titer, and viruria had no consistent relationship to viremia or clinical CID.
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PMID:Cytomegaloviremia in children with acute lymphocytic leukemia. 16 38

Radioimmunoprecipitation was used to test cat sera for ability to bind to the purified major internal protein p30 of feline leukemia viurs (FeLV), to the endogenous cat virus (RD-114), and to murine leukemia virus (MuLV). The data were compared with results of tests for antibody to the feline oncornavirus-associated cell membrane antigen FOCMA and for the presence of viremia. In contrast to the general lack of free antibody to FeLV p30 in a random sample of healthy cats, high levels of antibody to FeLV p30 and FOCMA were found in normal animals from high-leukemia-cluster households. Titers of greater than or equal to 200 for p30 and greater than or equal to 32 for FOCMA were found in nonviremic animals; a percentage of animals with high FOCMA titers and lower or no p30 binding activity were viremic. Animals with neoplasms were low or negative for FOCMA antibody and did not have high titers of free p30 antibody. The p30 binding activity could be divided into three main categories: high binding with FeLV p30 and much lower activity with RD-114 and MuLV p30's, as seen with hyperimmune sera; high binding with FeLV and RD-114 p30's and low activity with MuLV p30, possibly indicative of specific antibody to both of the aforementioned proteins; and low level binding to all three p30's.
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PMID:Humoral immune responses of cats to feline leukemia virus: comparison of responses to the major structural protein p30 and to a virus-specific cell membrane antigen (FOCMA). 17 14

Humoral immune response to ectropic leukemia viruses in AKR and C57BL/6 mice was controlled by a gene that mapped in linkage group IX. Mice of the AKR strain had an immune nonresponsive allele of this gene, whereas mice of the C57BL/6 strain had an immune responsive allele. Antibody against murine leukemia virus (MuLV) reacted primarily with p15 protein of the viral envelope. It was concluded that the failure to find antibody production in AKR mice was the result of a genetic immunological defect, rather than the result of immunological tolerance that was induced by the persistent viremia of endogenous MuLV.
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PMID:Genetic control of natural immunity to ecotropic mouse leukemia viruses: immune response genes. 17 49

Sixty-seven specific-pathogen-free cats of various ages (newborn, 2 wk, 1 mo, 2 mo, 4 mo, and 1 yr) were inoculated ip with either the Rickard (R) or the Kawakami-Theilen (KT) strain of feline leukemia virus (FeLV). Susceptibility to FeLV was judged by induction of a) FeLV group-specific antigens (gsa) in leukocytes, b) FeLV-related disease, c) antibody to feline oncornavirus-associated cell membrane antigen (FOCMA), and d) virus-neutralizing (VN) antibody. Susceptibility to FeLV-decreased with age. Persistent viremia and FeLV-related disease developed in 100% of cats inoculated as newborns, in 85% of cats inoculated at 2 weeks to 2 months of age, and in 15% of cats inoculated at 4 months or 1 year of age. Cats susceptible to FeLV leukemogenesis became persistently FeLV gsa-positive (viremic) at 4 weeks post inoculation and thereafter and produced little or no FOCMA or VN antibody. Cats that resisted leukemogenesis by FeLV all developed persistent FOCMA and VN titers and never became FeLV gsa-positive. The disease in inoculated cats was influenced by virus strain; FeLV-R induced predominantly thymic lymphosarcoma, whereas FeLV-KT caused fatal nonregenerative anemia without concurrent neoplasia.
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PMID:Feline leukemia virus infection: age-related variation in response of cats to experimental infection. 18 71

Ten post-weanling 4-month-old cats, designated "tracers", were placed in a feline leukemia cluster household to determine the efficiency of horizontal transmission of feline leukemia virus (FeLV). The tracer cats were confirmed as negative for prior exposure to FeLV. Following the placement in the leukemia cluster environment, the tracer cats were serologically monitored at intervals of 3-6 weeks for a total period of 1 year. The tests employed included the detection of FeLV using fixed-cell immunofluorescence and the detection and titration of antibody to : (1) the feline oncornavirus-associated cell membrane antigen (FOCMA), as detected by membrane immunofluorescence; (2) viable FeLV, using serum neutralization; (3) virion core protein p30, using radioimmunoprecipitation; and (4) virion glycoprotein gp70, using radioimmunoprecipitation. All of the tracers had evidence of horizontal infection by FeLV, by several criteria. Seven of the 10 had virus that could be isolated from plasma. All of these 7 developed a terminal illness within 18 months; 3 developed aplastic anemia, 3 infectious peritonitis, and 1 lymphoma. The remaining 3 were negative for FeLV by both virus isolation and fixed-cell immunofluorescence. These 3 did, however, develop high antibody titers by all four criteria and they remained healthy throughout the examination period. These results clearly indicate that unprotected pros-weanling cats brought into a leukemia exposure household environment have a high risk of becoming infected with FeLV. Furthermore, a large proportion of the cats are at risk for development of persistent viremia and FeLV-related diseases.
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PMID:Horizontal transmission of feline leukemia virus under natural conditions in a feline leukemia cluster household. 18 73

334C murine leukemia virus, which induces a high incidence of lymphatic leukemias (80-90%) in susceptible mice following a long latency period, was found to cause a severe in vivo suppression of direct plaque-forming cells from the spleen, following antigenic stimulation with sheep red blood cells. Neonatally infected inbred BALB/c and outbred Ha/ICR Swiss mice, which develop a sustained viremia, were highly susceptible to the immunosuppressive effect of this virus as early as 1 week after virus infection, long before any detectable histologic evidence of leukemia development. Ha/ICR Swiss mice, which are highly resistant to the leukemogenic potential of this virus following infection in adult life, were highly resistant to its immunosuppressive action; only a moderate and transient suppression, without viremia, occurred 2 weeks after virus infection. In marked contrast, BALB/c mice were highly susceptible to the immunosuppressive action of 334C murine leukemia virus following infection in adult life; a severe and sustained suppression was observed as early as 1 week after virus infection and was followed by a sustained viremia, beginning at 2 weeks, with a 55-60% incidence of leukemia observed over a period of 1 year. Infectious virus was essential to produce theimmunosuppressive effect; heat-inactivated (56 degrees C/30 min) and attenuated (4 degrees C/4 1/2 mo) virus preparations were ineffective. The plaque-forming response of spleen cells from lethally irradiated syngeneic adult BALB/c mice was markedly suppressed following reconstitution with thymus-dependent (T) or thymus-independent (B) cells from the thymus and bone marrow, respectively, of virus-infected mice, in combination with each other, or with the appropriate cell populations from normal mice.
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PMID:Immunosuppression in mice after inoculation with 334C, a murine lymphatic leukemia-inducing virus. 19 Apr 12


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