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)

Retroviral propagation crucially depends on reverse transcriptase (RT). We have developed murine models to test the biological effectiveness of the RT inhibitor suramin. The drug was active in our assay system, which includes (i) inhibition of RT activity in the murine T-cell tropic virus SL3-3 and Rauscher murine leukemia virus (MuLV), (ii) inhibition of plaque formation in the XC plaque assay, (iii) inhibition of viral infection of cultured murine T cells, and (iv) inhibition of splenomegaly induced by Rauscher MuLV in BALB/c mice. Suramin decreases viral titers significantly, even if started 36 hr after infection. Viral titers and number of infected cells increased to control levels after removal of the drug. BALB/c mice treated i.v. with 40 mg of suramin per kg twice per week following infection with Rauscher MuLV showed a 35% decrease in splenomegaly. Suramin is an active antiretroviral agent whose effect on retroviral propagation is reversible. We conclude that it acts as a virustatic drug and that long-term administration of suramin will be necessary if it is used for experimental treatment of human retroviral illnesses such as the acquired immune deficiency syndrome.
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PMID:Suppression of retroviral propagation and disease by suramin in murine systems. 241 71

Southern blot analysis of genomic DNA of normal mouse thymocytes with a JH4 probe, a probe for JH4 of Igh genes, consistently showed a second band in addition to a germline band. The same band was also observed in analysis with a 5' DQ probe, a 5'-flanking sequence of DQ52, thus suggesting the use of DQ52. By analyzing EcoRI- and PvuII-digested genomic DNA, the above-observed band was demonstrated to be the result of DQ52-JH2 joining. This was further confirmed utilizing a T cell leukemia line with known DQ52-JH joinings. We then quantitatively estimated the frequencies of JH segment usages in joining with DQ52, through plaque hybridization assays. Three hundred and fifty JH4-positive clones were obtained from 7 x 10(5) plaques by plaque hybridization. Forty-eight randomly selected non-germline clones were purified and the use of JH segments was determined through Southern blot analysis. Nine clones used JH1, 29 used JH2, 9 used JH3, and 1 used JH4, thus indicating an apparent preferential usage of JH2 segment. Southern blot analysis of genomic DNA of progenitor B cells in culture showed a dominant band of DQ52-JH2 joining 1 week after initiation of culture. This may indicate that the dominant DQ52-JH2 joining in thymocytes is representative of early D-J joinings in progenitor B cells.
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PMID:Preferential usage of JH2 in D-J joinings with DQ52 in murine lymphocytes. 248 50

For prevention of HIV infection, which is fatal to man and has no known remedy, sterilization of contaminated materials is particularly important. Before applying any sterilization procedures, they have to be checked by accurately following the kinetics of plaque reduction. Though this is almost self-evident, such studies have been few. Here, a microplaque assay of HIV is established using HPB-ALL human T-cells immobilized on a poly-L-lysine-coated plastic dish. This assay was used to compare the ultraviolet and heat inactivation kinetics of HIV (titrated by this method) with those of Moloney murine leukemia virus (MLV) in a liquid matrix. Though the ultraviolet sensitivities of these viruses were identical (D10 = 2,800 ergs/mm2), HIV was far more resistant to high temperatures (50 degrees C-70 degrees C) than MLV. This implies that these two viruses have different virion structures, though both are members of retroviridae. The higher thermostability of HIV should be taken into account when HIV-contaminated materials are handled.
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PMID:Thermostability of human immunodeficiency virus (HIV-1) in a liquid matrix is far higher than that of an ecotropic murine leukemia virus. 249 54

We have established bovine papilloma virus (BPV)-transformed mouse C127 cell lines that synthesize the peplomer protein of the feline infectious peritonitis virus (FIPV) strain 79-1146. For this purpose, a new cassette expression vector pHSL, which carries the Drosophila HSp70 promotor and the polyadenylation signal of the Moloney murine leukemia virus long terminal repeat, was constructed. Cocultivation of the BPV-transformed cell lines with FIPV-permissive feline fcwf-D cells resulted in polykaryocyte formation. Since it depended on the presence of fcwf-D cells, binding of E2 to the cell receptor may be required for membrane fusion. E2 was synthesized as a core-glycosylated protein of 180K which was only slowly transported from the endoplasmic reticulum to the medial Golgi: of the E2-molecules labeled during a 1-hr pulse about half was still completely sensitive to endoglycosidase H after a 2-hr chase, while the remaining E2 had been chased into multiple, partially endoglycosidase H-resistant forms. Immunofluorescence studies also indicated that most E2 was retained intracellularly. Mice immunized with whole lysates of the transformed cells produced FIPV-neutralizing antibodies as shown by plaque reduction.
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PMID:Stably expressed FIPV peplomer protein induces cell fusion and elicits neutralizing antibodies in mice. 254 29

The effects of chlorhexidine mouthrinses, used as a supplement to mechanical oral hygiene measures, were studied in patients receiving treatment for acute leukemia. Twenty-eight patients were randomly divided into two groups. During two periods, when the patients were taking medication for the leukemia, one group rinsed with a 0.2% chlorhexidine solution twice daily and the other group did not. Chlorhexidine had no effects of any clinical significance on parameters such as number of days with fever, number of oral lesions, plaque score, gingival bleeding score, or occurrence of candidiasis. There was, however, an increased number of patients who had a burning sensation in the mouth, and a tendency toward increased numbers of salivary enterococci, enterobacteria, and/or Pseudomonas in patients who rinsed with chlorhexidine. The results of the present study do not support the use of chlorhexidine mouthrinses in patients who are able to maintain good oral hygiene by mechanical means during their illness.
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PMID:Effects of chlorhexidine mouthrinse on oral health in patients with acute leukemia. 277 74

The effect of ultraviolet-inactivated feline leukaemia virus (UV-FeLV) on the development of feline immunoglobulin-secreting cells (ISC) was investigated using a reverse haemolytic plaque assay. Low concentrations of UV-FeLV at 2 X 10(-4) to 2.0 micrograms/ml stimulated the production of ISC. By contrast, the same concentration of UV-FeLV suppressed the development of pokeweed mitogen (PWM)-driven ISC. Maximum suppression of ISC occurred at 50 micrograms/ml of UV-FeLV. The generation of an interferon resistant to acid, heat and sodium dodecyl sulphate (SDS) in the media of lymphocyte cultures incubated with PWM was also significantly suppressed in the presence of 0.2 microgram/ml of UV-FeLV. These findings suggest that non-infectious viral particles appear to modify feline immunoglobulin and interferon-secreting systems.
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PMID:Influence of inactivated feline retrovirus on feline alpha interferon and immunoglobulin production. 282 Jun 39

Friend virus complex (FV), which comprises replication-competent Friend murine leukemia virus (FMuLV) plus replication-defective spleen focus-forming virus (SFFV), induces a multistage erythroleukemia. We have examined the role of replication-competent helper virus in the early and late stages of FV disease by replacing FMuLV, the native helper, with Akv, the endogenous ecotropic MuLV of AKR mice. SFFVP/FRE, an established fibroblast line nonproductively infected with the polycythemic strain of SFFV, was superinfected with FMuLV or with Akv. Although supernatants from these cells showed similar titers in the XC plaque assay, supernatants from Akv-infected SFFVP/FRE cells showed 100- to 5,000-fold less activity than did those from FMuLV-infected cells with respect to spleen focus induction in vivo. Since virions isolated from these two supernatants contained similar ratios of SFFV to helper virus genomic RNA, it did not appear that the difference was due to a relative inability of Akv to package SFFV. Although FMuLV- and Akv-rescued SFFV are equally infectious in a mouse fibroblast cell line (NIH 3T3), FMuLV-rescued SFFV was far more efficient in inducing erythroid bursts in cultured primary bone marrow cells. Adding Akv to preparations of FMuLV-rescued SFFV did not significantly interfere with burst induction. Helper-free SFFV induced 50- to 500-fold more spleen foci when coinjected with FMuLV than it did with Akv. Helper virus also affected mortality rates that reflect the late stage of the disease. When FMuLV- or Akv-rescued SFFV was injected into NIH Swiss mice at dosage levels adjusted to give equal numbers of spleen foci, all mice receiving FMuLV-rescued SFFV developed splenomegaly and died, whereas no mice receiving Akv-rescued SFFV died or developed detectable splenomegaly. When FMuLV was coinjected with Akv-rescued SFFV, the mortality rate rose from 0 to 100%. Injection of helper-free SFFV alone did not induce mortality, but coinjection of helper-free SFFV with FMuLV resulted in 100% mortality. Thus, the helper virus used to rescue SFFV plays at least a quantitatively important role in the early stage of FV disease and a crucial role in the late stage of the disease in vivo.
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PMID:Loss of pathogenicity of spleen focus-forming virus after pseudotyping with Akv. 282 12

Moloney murine leukemia virus (M-MuLV) is a replication-competent retrovirus which induces T-cell lymphoma in mice. The enhancer sequences present within the M-MuLV long terminal repeat (LTR) region of the proviral genome have been shown to influence the disease specificity of the virus strongly. We examined the contribution of the M-MuLV enhancers to the transcriptional activity and pathogenesis of M-MuLV by constructing LTRs containing heterologous enhancer elements. The simian virus 40 enhancer region (72- and 21-base-pair repeats) was inserted into the U3 region (at -150 base pairs) of the M-MuLV LTR (Mo + SV) and also into a deleted form of the LTR which lacks the M-MuLV enhancer sequences (delta Mo + SV). These chimeric LTRs were used to generate infectious M-MuLVs by transfection of corresponding proviral plasmids into mouse fibroblasts. The relative infectivities of Mo + SV and delta Mo + SV recombinant viruses as determined by rat XC cell plaque assay and reverse transcriptase assay were 60 to 70% of wild-type M-MuLV levels. To study the pathogenicity of these two recombinant viruses, we inoculated newborn NIH Swiss mice with either Mo + SV or delta Mo + SV M-MuLV. Both viruses induced disease more slowly than M-MuLV, which induces disease 2 to 4 months postinoculation. Mo + SV M-MuLV-inoculated animals became moribund at 3 to 13 months postinoculation, whereas delta Mo + SV M-MuLV-inoculated animals became moribund at 6 to 24 months postinoculation. The tumors induced by the two viruses were characterized histologically and molecularly. Mo + SV M-MuLV-induced tumors were primarily T-cell-derived lymphoblastic lymphomas containing extensive rearrangements of the T-cell receptor beta gene. In contrast, delta Mo + SV M-MuLV induced pre-B- and B-cell lymphoblastic lymphomas, B-cell-derived follicular-center cell lymphomas, and acute myeloid leukemia. The delta Mo + SV tumor DNAs from B-lineage tumors were typically rearranged at the immunoglobulin gene loci and contained germ line configurations of the T-cell receptor beta gene. Southern blot hybridization confirmed that the tumor DNAs contained the predicted Mo + SV M-MuLV or delta Mo + SV M-MuLV provirus.
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PMID:Addition of substitution of simian virus 40 enhancer sequences into the Moloney murine leukemia virus (M-MuLV) long terminal repeat yields infectious M-MuLV with altered biological properties. 283 23

A fluorometric enzyme immunoassay using an alkaline phosphatase-conjugated monoclonal antibody was developed to quantitate feline leukemia virus (FeLV) infection. Monoclonal antibodies, directed against the FeLV structural protein p27, were conjugated with alkaline phosphatase using a modified maleimide method. The enzyme immunoassay requires only 4 days to reproducibly measure FeLV production instead of the 12 days required for the commonly used transformation assay using C81 cells. A linear correlation was found between the virion associated reverse transcriptase activity and the amount of intracellular p27 as determined by the fluorometric enzyme immunoassay. An immunocytochemical assay using the same conjugated monoclonal with a different substrate gave visible plaques in infected cell monolayers and was therefore used to titrate FeLV in plaque-forming units. The results obtained by all the procedures followed single hit kinetics for FeLV infection. The fluorometric enzyme immunoassay was adapted to measure FeLV neutralizing antibodies, allowing a sensitive and accurate determination of neutralizing titers.
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PMID:Fluorometric enzyme immunoassay for measurement of infectious feline leukemia virus and its neutralization. 284

The phenotypic and morphological profiles of atypical cells in a case of adult T cell leukaemia/lymphoma were studied using a panel of monoclonal antibodies and electron microscopy. Retroviral sequence restriction analysis showed the presence of human T cell leukaemia/lymphoma virus type I (HTLV-I) in the skin lesion. Our case showed several unique features in the clinical, haematological, histopathological and immunohistochemical findings. An erythematous plaque and tumour nodules in the skin were found without any abnormal lymphocytes such as flower cells in the peripheral blood and bone marrow HTLV-I proviral DNA was detected in the skin tumour cells but not in the peripheral blood lymphocytes, and in the tumour nodule, atypical cells showed a distinct difference in morphology between cerebriform cells in the upper dermis and large lymphoid cells in the lower dermis. The cerebriform cells had, immunohistochemically, a T helper/inducer (Th/i) phenotype whereas the large lymphoblastoid cells possessed both the Th/i and T suppressor/cytotoxic (Ts/c) phenotypes. Ki-I antigen was detected in the large lymphoblastoid cells, but not in the cerebriform cells.
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PMID:Dual surface makers and HTLV-I proviral DNA in a cutaneous tumour nodule in a case of adult T cell leukaemia/lymphoma. 289 71


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