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)

The CD4+ CD8- inducer helper cell and the CD4- CD8+ cytotoxic/suppressor cell absolute numbers were measured in the peripheral blood of patients with various pathological conditions: with leukemia-lymphomas or solid tumors, patients with bone marrow grafts suffering from GvH, HIV-1 asymptomatic carriers, ARC and AIDS patients. The study was carried out during observation periods when they were not suffering from opportunistic infections and were untreated. In all the groups a decrease of the CD4+ CD8- cell absolute number was observed. In the leukemia-lymphoma and solid tumor bearing patients the CD4- CD8+ absolute value was lower than normal, while in the GvH- and HIV-infected patients, it was significantly higher. The clinical follow-up of each group indicates that GvH, ARC and AIDS patients developed infection in 40-68% of the cases, ie the only groups at risk of infection are those in which the CD4- CD8+ absolute values are high: we suggest that the balance CD4+ versus CD8+ should be considered rather the absolute CD4+ when discussing appropriate use of immuno-regulators.
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PMID:Retrospective study correlating clinical infectious history and peripheral blood T-cell subpopulations in cancer, GvH and HIV+ patients. 142 Oct 30

Sera from 634 homosexual men with Western blot-confirmed human immunodeficiency virus (HIV) infection were subjected to radioimmunoprecipation assay (RIPA) using an HTLV-I-infected human T-cell line (SLB-I). Sera obtained from Japanese adult T-cell leukemia patients, noninfected healthy individuals served as positive and negative controls. HIV-infected groups were comprised of asymptomatic homosexuals (n = 131), AIDS-related complex (n = 115), Kaposi's sarcoma (n = 300), AIDS-defining opportunistic infections (n = 76), and high-grade lymphomas (n = 12). Only two patients were known to be intravenous drug users. No instances of dual retroviral infection were detected. As a corollary, no cross reactivity between HTLV and HIV gene products was noted by RIPA. We conclude that HTLV infection is uncommon among select groups of HIV seropositive homosexuals who do not engage in intravenous drug abuse. Additional studies examining the seroprevalence and consequence of HTLV infection in broader based populations at risk for retroviral infection are required.
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PMID:Human T-cell leukemia virus infection in non-intravenous drug using HIV seropositive men in Los Angeles. 167 93

It has been reported that in vitro uridine (Urd) can reverse azidothymidine (AZT) cytotoxicity without decreasing anti-human immunodeficiency virus (HIV) activity. Our studies in mice have shown that daily oral doses of benzylacyclouridine (BAU), an inhibitor of Urd breakdown, also reduces AZT hematologic toxicity, presumably by elevating the plasma concentration of Urd. We now extend these murine studies and report the effect of various doses of exogenous Urd, various doses of BAU, or the combination of BAU and Urd, administered daily, on AZT-induced toxicity. In mice receiving concomitant AZT, daily doses of Urd of 1,000 to 2,000 mg/kg increase peripheral reticulocytes and slightly reduce AZT-induced hematologic toxicity. However, the range of effective doses is narrow, and higher doses of Urd (greater than 3,000 mg/kg/d) significantly enhance hematologic toxicity. At its most effective dose, (2,000 mg/kg/d), Urd produces 28% mortality. In contrast, BAU doses up to 300 mg/kg/d reduced AZT-related hematologic toxicity in a dose-dependent manner without mortality. Higher daily doses of BAU and the combination of BAU with low doses of Urd were not more effective. Studies conducted in mice infected with the Rauscher murine leukemia virus (RLV) indicate that BAU does not impair the antiretroviral effect of AZT when administered at doses that reduce AZT-induced anemia and leukopenia. These findings may be significant for the treatment of patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex.
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PMID:Different effect of benzylacyclouridine on the toxic and therapeutic effects of azidothymidine in mice. 225 95

Studies were done on 53 cats with community-acquired infection with the feline immunodeficiency virus (FIV) to determine if hematologic abnormalities were comparable with those observed in patients seropositive for the human immunodeficiency virus (HIV). Nine cats were asymptomatic, 24 had clinical symptoms equivalent to AIDS-related complex (ARC), and 20 had AIDS-like disease. Hematologic abnormalities were detected in 75% (40 of 53) of FIV-seropositive cats, and multiple concurrent cytopenias were common. Anemia, lymphopenia, neutropenia, and thrombocytopenia occurred in 36%, 53%, 34%, and 8% of FIV-seropositive cats, respectively. Cytopenias were seen only in symptomatic (ARC or AIDS) cats. The occurrence of cytopenias and the distribution of clinical stages were similar in cats with concurrent feline leukemia virus (FeLV) infection and those with FIV alone, suggesting that these abnormalities were a direct consequence of FIV infection. In addition, abnormalities were noted in 72% of marrows from symptomatic cats and included hyperplasia of individual cell lineages and dysmorphic features. Our results demonstrate that the hematologic manifestations of FIV infection are strikingly similar to those reported in HIV-seropositive patients. Thus, FIV infection in cats is an excellent animal model to study the pathogenesis of blood and marrow abnormalities in AIDS, as well as to evaluate the hematologic toxicities of drug therapies.
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PMID:Hematologic manifestations of feline immunodeficiency virus infection. 240 Aug 6

Avarol and avarone are two antimitotic and antimutagenic agents that preferentially inhibit proliferation of T-cell leukemia lines in vitro. This report shows that these compounds have a dose-dependent inhibitory effect on the replication of the etiologic agent of acquired immune deficiency syndrome (AIDS), human T-lymphotropic retrovirus (HTLV-III)/lymphadenopathy-associated virus, in human H9 cells in vitro. Both compounds show a significant cytoprotective effect on HTLV-IIIB-infected H9 cells at concentrations as low as 0.1 microgram/ml (0.3 microM). Both avarone and avarol block in a dose-dependent manner the expression of the p24 and p17 gag proteins of HTLV-III in H9 cells after virus infection and block viral replication, as judged by approximately 80% inhibition of reverse transcriptase activity. These results strongly suggest that these compounds may prove to be useful in the treatment of patients with AIDS and AIDS-related complex.
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PMID:Inhibition of replication of the etiologic agent of acquired immune deficiency syndrome (human T-lymphotropic retrovirus/lymphadenopathy-associated virus) by avarol and avarone. 243 42

Seven cases of acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) associated with human T-cell leukemia (lymphotropic) virus (HTLV)-III infection were documented in married males whose family members consented to medical evaluation. Five spouses also had evidence of HTLV-III infection documented by isolation of virus and by detection of serum antibody directed against viral structural proteins. Three of the five HTLV-positive spouses also had clinical evidence of ARC. The remaining four spouses were clinically healthy. Eleven children (between 14 months and 13 years of age) were also evaluated for evidence of disease and exposure to HTLV-III. Only one 14-month-old child was seropositive for antibody to HTLV-III. These data support the opinion that close household contact to patients with ARC or AIDS is not an efficient mechanism for virus transmission, while demonstrating that HTLV-III can be transmitted by repeated heterosexual contact.
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PMID:Frequent transmission of HTLV-III among spouses of patients with AIDS-related complex and AIDS. 298 27

The isolation of the human T-cell leukaemia (lymphotropic) virus type III (HTLV-III or lymphadenopathy-associated virus) from cells of many patients with acquired immune deficiency syndrome (AIDS) presented the first evidence that the virus was the aetiological agent of the disease. Subsequent seroepidemiological studies have shown the presence of HTLV-III-specific antibodies in the serum of most patients with AIDS and AIDS-related complex (ARC), and in the serum of many individuals at risk for AIDS. Despite these extensive studies, there are no reports of protective effects of HTLV-III antibodies. In contrast, neutralizing antibodies specific for HTLV-I and -II have been identified previously. Therefore, we investigated whether HTLV-III-exposed individuals possess antibody activities capable of inhibiting viral infection. Here, we report that natural antibodies capable of neutralizing HTLV-III infection of H9 cells were detected in most adults AIDS and ARC patients but in no normal healthy heterosexual controls. Geometric mean antibody titres in ARC patients were double those in AIDS patients, and were even higher in two antibody-positive healthy homosexuals. This suggests that virus neutralizing antibodies may exert an in vivo protective effect. The presence of these antibodies indicates an immunological response to HTLV-III which potentially may be manipulated for therapeutic advantage. The methodology used here will be useful in monitoring future vaccine approaches.
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PMID:HTLV-III-neutralizing antibodies in patients with AIDS and AIDS-related complex. 298 7

Acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) are thought to be caused by human T-cell leukemia/lymphotropic virus type III (HTLV-III). Since the fall of 1982, independent isolates of HTLV-III have been obtained in this laboratory, in collaboration with several clinical groups, from 101 AIDS and ARC patients and healthy donors at risk for AIDS. Most isolates were from peripheral blood T lymphocytes established in cell culture, but some were obtained from bone marrow, lymph node, brain tissue, and cell-free plasma and from cells associated with saliva, cerebrospinal fluid, and semen. Virus was isolated from approximately 50% of AIDS patients, 85% of ARC patients, and 30% of healthy individuals at risk for AIDS. The risk groups included homosexuals, promiscuous heterosexuals, i.v. drug users, recipients of blood or blood products, and spouses and offspring of AIDS patients and others at risk for AIDS. A high correlation was seen between persistent levels of serum antibody and the ability to isolate virus from patient or donor leukocytes. Immunologic and nucleic acid analysis demonstrated that the virus isolates were highly related, although substantial diversity was observed in the restriction enzyme cleavage patterns of those studied in detail. Biological analysis of cells from infected patients and donors as well as from normal peripheral blood mononuclear cells exposed to virus in vitro demonstrated that OKT4/Leu3a+ (helper/inducer) lymphocytes were preferentially infected and were subjected to a characteristic cytopathic effect. The availability of multiple isolates of virus from a number of different patients and donors will greatly facilitate the characterization of HTLV-III and the study of possible biological and/or biochemical variants of the virus responsible for the development of AIDS, ARC, and related diseases.
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PMID:Isolation of infectious human T-cell leukemia/lymphotropic virus type III (HTLV-III) from patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) and from healthy carriers: a study of risk groups and tissue sources. 299 31

The newly identified human HTLV-III virus, the etiologic agent for AIDS, shares many of the biological and physicochemical properties common to a family of retroviruses named human T-cell leukemia (lymphotropic) viruses, or HTLV. Because of the similarities, and because of the uniform nomenclature for human T-cell leukemia (lymphotropic) viruses adopted at the first Cold Spring Harbor Meeting on HTLV (19, 79), this newly discovered virus associated with AIDS as HTLV-III was named HTLV-III. Other investigators making independent isolations of virus have suggested naming the virus lymphadenopathy virus or LAV (3, 16), immunodeficiency associated virus or IADV (48), AIDS-related virus (41). Immunological and nucleic acid comparison has now demonstrated that these viruses are, not surprisingly, very similar to HTLV-III (55, 63, 78). In view of the wide range of disease manifestations caused by the virus, and previous discussions concerning a uniform nomenclature for human T-lymphotropic retroviruses, it would seem ill-advised to restrict the name of this virus to one clinical manifestation of one disease. The frequent isolation of HTLV-III from patients with AIDS and ARC, the detection of antibodies specific for HTLV-III in nearly all patients with these diseases and in a high proportion of individuals at risk, and finally its effect on cells in vitro, leaves little doubt that HTLV-III is causatively involved in the development of these diseases. This etiologic association is further strengthened by the detection of HTLV-III infection in many instances where a direct cause-and-effect association can be made, e.g., hemophiliacs and children with AIDS, and blood from HTLV-III infected donors and the otherwise normal recipients of this blood who subsequently develop AIDS.
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PMID:Etiology of AIDS: biological and biochemical characteristics of HTLV-III. 299 17

Antibodies against the human T-leukemia virus III (HTLV III) were detected by immunofluorescence in the sera of 17 out of 48 hemophiliacs (35.4%) without AIDS or ARC, frozen in 1983-84. Immunological data collected at that time were re-evaluated by separating HTLV III-positive and negative subjects. HTLV III positive patients had significantly reduced OKT4 cells (both in %: 26.1 +/- 10.9 vs 41.2 +/- 15.2; P less than 0.01; and in absolute numbers: 469 +/- 291 vs 1,038 +/- 541; P less than 0.005) and OKT3 lymphocytes (in absolute numbers: 1,234 +/- 550 vs 2,050 +/- 1,067; P less than 0.01). Subpopulations identified by other monoclonal reagents (OKT8, Leu 7, OKM1, anti-Tac) showed no significant differences between the two groups. Patients subsequently found to be seropositive had significantly more frequent anergy to skin tests to recall antigens and often an impairment of in vitro response to phytohemagglutinin A. Despite these relevant defects of some tests of cell-mediated immunity, in HTLV III-positive cases no clinical progression toward AIDS-related complex was observed in a mean period of follow-up of more than 1.5 years.
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PMID:Impairment of cellular immunity and OKT4 lymphocytes in symptom-free hemophiliacs with antibodies to human T leukemia virus III (HTLV III). 299 21


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