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)

Monoclonal immunoglobulins (Eg) are detected in the serum of 7/29 patients treated for leukemia (6 cases) or lymphoma (1 case). All of them developped cytomegalovirus (CMV) infection. The 7 patients were children or young adults; 6/7 were in complete remission of the hematological disease. They completed chemotherapy before the onset of the viral infection and had received blood components. The monoclonal Ig are IgG (6 cases) and IgM (1 case), In 2 sera there are two M components. The level of the peak was under 1 g/100 ml (5 cases) and reached 1.5 and 1.7 g/100 ml in the 2 other sera. Polyclonal Ig are normal except in one case where there is moderate hypo-Ig; Plasmocytic infiltration was observed in none of the 7 patients. Evidence of CMV infection was confirmed by viremia and/or significant rise of complement fixing antibodies. In four cases, the monoclonal Ig disappeared in less than 6 months. The significance of the monoclonal Ig associated with CMV infection is discussed.
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PMID:[Monoclonal immunoglobulins, cytomegalovirus infection and malignant observations blood diseases]. 19 34

Antibodies against feline leukemia virus (FeLV) and the feline oncornavirus-associated cell membrane antigen (FOCMA) were transferred from pregnant cats to their suckling kittens. All of these kittens were protected against infection and oncogenesis by virulent FeLV when challenged at 2 weeks of age. Suckling kittens acquired 25 to 100% of maternal virus-neutralizing and FOCMA titers by 3 days of age, and titers underwent linear decay to undetectable levels by 2 to 3 months of age. FOCMA antibody in dams and kittens was identified as immunoglobulin G (IgG) by use of goat anti-human IgG serum, which cross-reacts with feline IgG in the indirect membrane immunofluorescence test for FOCMA antibody. In an attempt to induce protective maternal antibody by vaccination, 10 pregnant cats were immunized by three to five weekly intramuscular injections with purified FeLV inactivated by ultraviolet irradiation. After the course of immunization, neither virus-neutralizing nor FOCMA antibody was detectable in the dams or in 19 kittens born to these cats. When these kittens were challenged with FeLV at 2 weeks of age, 18 of 19 developed persistent viremia and FeLV-related disease.
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PMID:Passive immunity to feline leukemia: evaluation of immunity from dams naturally infected and experimentally vaccinated. 19 40

Twelve cats were thymectomized at 5 weeks of age. Six of these cats were inoculated at 8 weeks of age and 6 at 4 months of age with the Rickard (R) strain of feline leukemia virus (FeLV), which produces a high incidence of thymic lymphosarcoma. Two groups of age-matched nonthymectomized cats were inoculated with the same FeLV-R stock. Thymectomy prior to FeLV infection had no influence on the induction of viremia or the incidence of lymphosarcoma. In the FeLV-inoculated nonthymectomized cats, lymphosarcoma developed in the thymus. In the thymectomized cats, lymphosarcoma developed in the intestine, mesenteric lymph nodes, and bone marrow, but the malignant lymphoblasts had surface markers characteristic of feline T lymphocytes. It was concluded that the presence of the thymus per se is not required for infection and oncogenesis by FeLV and that feline T lymphocytes may be transformed after peripheralization to other tissues.
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PMID:Influence of thymectomy on the susceptibility of cats to feline leukemia virus and lymphosarcoma. 20 36

The natural resistance of adult specific-pathogen-free cats to feline leukemia virus (FeLV) was abrogated by treatment with various doses of a synthetic corticosteroid, methylprednisolone acetate (MPA), prior to either oral-nasal or i.p. inoculation of FeLV. Persistent viremia was induced in 82% (18 of 22) of MPA-treated cats versus 11% (1 of 9) of age-matched control cats. MPA-treated FeLV-inoculated cats developed prolonged lymphopenia (2 to 8 weeks postinoculation) and a delayed antibody response to the feline oncornavirus-associated cell membrane antigen. The distribution of FeLV group specific antigen in tissues of MPA-treated, FeLV-inoculated cats suggested that corticosteroids enhanced susceptibility to FeLV by impairing early viral containment in the reticuloendothelial and lymphoid tissues.
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PMID:Influence of adrenal corticosteroids on the susceptibility of cats to feline leukemia virus infection. 22 25

The dominant C57BL/10 allele of a single autosomal, non-H-2 gene (Rfv-3) was found to be required for recovery from viremia and leukemia induced by Friend virus complex in H-2b/b mice. In H-2a/a mice, the Rfv-3 gene apparently influenced recovery from viremia in the presence of persistent leukemia because these mice lacked the appropriate H-2 genotype for recovery from leukemia. The Rfv-3 gene was distinct from the Fv-2 gene because recovery from viremia was seen in recombinant-inbred mice with the Fv-2s/s genotype. Furthermore, backcross studies indicated that Rfv-3 and Fv-2 were not linked. The Rfv-3 gene may act by influencing the specific anti-FV humoral antibody response.
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PMID:Identification of a non-H-2 gene (Rfv-3) influencing recovery from viremia and leukemia induced by Friend virus complex. 28 59

A single genetic locus, Rfv-3, influenced Friend virus (FV) viremia, loss of FV-induced cell-surface antigens from leukemia cells, and generation of anti-FV antibodies. 30--90 d after FV infection leukemic spleen cells from (B10.A X A)F1 and (B10.A X A.BY)F1 mice (Rfv-3r/s) were found to have low FV-induced cell-surface antigen expression compared to leukemic spleen cells from A and A.BY mice (Rfv-3s/s). In addition, these F1 mice recovered from viremia and generated cytotoxic anti-FV antibodies. A and A.BY mice did not recover from viremia and failed to generate anti-FV antibodies. Anti-FV leukemia cell antibody appeared to mediate FV-antigen loss because decrease of FV cell-surface antigens occurred at the same time as anti-FV antibody appeared in the plasma of F1 mice, and passive transfer of anti-FV antisera induced modulation of FV cell-surface antigens. Rfv-3 did not influence an intrinsic ability of FV antigens to be modulated from Rfv-3s/s leukemia cells because FV antigen loss from Rfv-3s/s spleen cells occurred after transfer of cells to an immune environment.
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PMID:Anti-Friend virus antibody is associated with recovery from viremia and loss of viral leukemia cell-surface antigens in leukemic mice. Identification of Rfv-3 as a gene locus influencing antibody production. 28 44

The level of viremia and the appearance of leukemias were studied after inoculation wtih Moloney leukemia virus (M-MuLV) in different H-2 congenic strains of mice. The viremia was regularly measured on individual mice with a radioimmunoassay of the major internal virion component p30. Three genes within the major histocompatibility complex controlled the level of circulating virus. Two of them, called Rmv.1 and Rmv.2, appear to be located in the I region, respectively, in the IA, and the IC-S or G regions. The third gene, Rmv.3, was mapped to the D end of the complex in the D or T region. Crosses between resistant and sensitive strans demonstrated that the H-2 associated resistance was inherited as a dominant or semi-dominant Mendelian trait. Rmv.1, Rmv.2, and Rmv.3 were shown to complement for resistance in trans when the hybrids between sensitive strains were examined. A good correlation was found between viremia and the appearance of leukemias, the most viremic strains being also the most leukemic. Nevertheless, additional non-H-2 genes must control viremia and/or the appearance of leukemia since, despite high levels of viremia, some sensitive strains do not become leukemic.
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PMID:Genetic control of sensitivity to Moloney leukemia virus in mice. II. Mapping of three resistant genes within the H-2 complex. 47

The features of pathogenesis of infection caused in adult Balb/c mice intraperitoneally infected with Sindbis virus, virulent or attenuated strains of West Nile (WN) virus, individually or in combination with Rauscher leukemia virus (RLV) were studied. The influence of the latter on the course of togavirus infections was characterized by 3 features: (a) different effects on the visceral and neural phases of the pathogenesis (increased period of viremia and virus reproduction in the viscera did not lead to stimulation of virus reproduction in the CNS); (b) changes in the time of togavirus persistence in the infectious form; (c) the dependence of the observed effect on the togavirus properties.
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PMID:[Change in the nature of the persistence of alpha- and flaviviruses in the body of BALB/c strain mice with a mixed infection with leukovirus]. 50 4

Mice genetically transmitting the exogenous Moloney leukemia virus (Balb/Mo) have been previously derived. These animals carried one copy of Moloney virus DNA (M-MuLV) in their germ line and transmitted the virus as a single Mendelian gene to the next generation. Homozygous BALB/Mo mice were used to genetically map the M-MuLV locus. Embryo fibroblasts were fused to established Chinese hamster cells and somatic cell hybrids were selected. Segregation of mouse chromosomal markers in the hybrids was correlated to the loss of M-MuLV-specific sequences as detected by molecular hybridization. Of 15 isozymes located on different mouse chromosomes only triosephosphate isomerase segregated syntenic with the M-MuLV gene, suggesting that the virus was integrated on chromosome No. 6. This was confirmed by sexual genetic experiments analyzing segregation of Moloney viremia and two markers on chromosome 6 and 15, respectively. The results show that M-MuLV expression is linked to wa-1 on chromosome 6 at a distance of about 30 map units. These data define a new genetic locus, Mov-1, representing the structural gene of M-MuLV in BALB/Mo mice.
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PMID:Genetic transmission of Moloney leukemia virus: mapping of the chromosomal integration site. 54 67

The appearance of hematopoietic malignancies and the level of viremia were studied in mice of different inbred strains and their F1 or F2 hybrids inoculated with the Moloney leukemia virus (MLV). The viremia was regularly measured in individual mice by radioimmunoassay of the major internal virion component p30. A complex genetic control was found. (1) The level of circulating virus was controlled by at least two genes. An H-2 linked gene, tentatively called Rmv-1, displayed a dominant sensitivity. Alleles for resistance existed in H2b and H-2r haplotypes and alleles for sensitivity in H-2a, H-2d and H-2f. Another gene with dominant resistance mapped outside the H-2 complex and probably interacted with Rmv-1. (2) A good correlation existed between viremia and the appearance of leukemias, the most viremic strains being also the most leukemic. (3) Nevertheless, additional genes which were not involved in the viremia control could be determinant in the induction of malignancies. One of them with a resistant allele in DBA/2 mice seemed to inhibit the appearance of leukemia despite a high level of viremia. Another gene controlled the spleen involvement resulting in generalized leukemias in sensitive lines contrasting with mainly thymus-localized tumors in resistant animals.
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PMID:Genetic control of sensitivity to Moloney-virus-induced leukemias in mice. I. Demonstration of multigenic control. 65 28


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