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 human immunodeficiency virus (HIV) Rev protein is essential for viral structural protein expression (Gag, Pol, and Env) and, hence, for viral replication. In transient transfection assays, mutant forms of Rev have been identified that inhibit wild-type Rev activity and therefore suppress viral replication. To determine whether such transdominant Rev proteins could provide long-term protection against HIV infection without affecting T cell function, T leukemia cell lines were stably transduced with a retroviral vector encoding a transdominant mutant of the Rev protein, M10. While all the M10-expressing cell lines remained infectable by HIV-1, these same cells failed to support a productive replication cycle when infected with a cloned isolate of HIV-1. In addition, two out of three M10-expressing CEM clones were also resistant to highly productive infection by a heterogeneous HIV-1 pool. Expression of M10 did not affect induction of HIV transcription mediated by the kappa B regulatory element or Tat. Importantly, constitutive expression of Rev M10 did not alter the secretion of interleukin 2 in response to mitogen stimulation of EL-4 and Jurkat cells. The inhibition of HIV infection in cells stably expressing a transdominant Rev protein, in the absence of any deleterious effect on T cell function, suggests that such a strategy could provide a therapeutic effect in the T lymphocytes of acquired immunodeficiency syndrome patients.
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PMID:Stable expression of transdominant Rev protein in human T cells inhibits human immunodeficiency virus replication. 140 61

This study was intended to examine and identify the nature of CRNAs' attitudes concerning acquired immune deficiency syndrome (AIDS) and patients with homosexual lifestyles. This research question has been previously addressed using sample populations of registered nurses, physicians, and medical students. This inquiry was conducted using a sample population of nurse anesthetists. The target population was 500 CRNAs who reside in areas of high AIDS incidence--New York City, San Francisco, and Houston. The participants were equally divided among the three cities using a randomized list provided by the AANA. The design for this study was an experimental 2 x 2 factorial with two independent variables: disease of the individual, either leukemia or AIDS, and the sexual preference of the individual, either heterosexual or homosexual. The randomly distributed questionnaire consisted of three scales: the interpersonal attraction inventory, the prejudicial evaluation scale, and the social interaction scale. Multivariate analyses of variance (MANOVA) were conducted not only on the main effects, disease and sexual preference, but also on the interaction effects of disease and sexual preference. The significant findings of the MANOVAs were subjected to factorial analysis for each scale, and then the MANOVAs were conducted again. The statistical analysis indicated that CRNAs possess a negative attitude toward AIDS patients but not toward leukemia patients. Their attitudes are based on their perception that AIDS patients are responsible for their illness. Potential behavioral consequences were also reported by CRNAs, based on these attitudes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Attitudes of certified registered nurse anesthetists toward AIDS and AIDS patients. 141 71

Chronic ethanol consumption impairs cellular immune functions. This may explain the increased occurrence of various opportunistic infections in heavy ethanol users. Immunological alterations associated with Acquired Immune Deficiency Syndrome (AIDS) also permit more opportunistic infections. In this study, we used a murine model of retrovirus infection induced by LP-BM5 murine leukemia virus. The combined effects of ethanol use and early retroviral infection (prior to the development of AIDS) on resistance to Streptococcus pneumoniae were investigated. Consumption of ethanol by non-retrovirus-infected mice resulted in decreased resistance to S. pneumoniae. However, retrovirus-infected mice fed a diet containing high concentrations of ethanol (6 and 7% v/v) exhibited a greater resistance to S. pneumoniae infection than retrovirus-infected mice fed diets with lower concentrations (5%) or no ethanol. The total number of white blood cells also decreased as serum ethanol levels increased. There were also fewer lymphocytes and more neutrophils and monocytes in retrovirus-infected mice fed ethanol. Diet consumption decreased as the concentration of ethanol increased in the diet. Consumption was dependent upon the dark-light cycle. The highest diet consumption was observed during the first 4 hr of the dark period. The level of ethanol in serum was influenced by the amount of the diet consumed and its ethanol concentration. Both retrovirus infection and ethanol consumption effected survival after S. pneumoniae infection.
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PMID:Influence of the level of dietary ethanol in mice with murine AIDS on resistance to Streptococcus pneumoniae. 141 8

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

Primate and non-primate species have been used to study the pathobiology of the simian immunodeficiency virus (SIV) and of the human immunodeficiency virus type 1 (HIV-1), respectively, and to develop new therapeutic regimes. Transgenic mice which express either the entire HIV-1 provirus or subgenomic fragments have been used to analyze viral gene products in vivo and may serve as models for the development of agents targeted to select viral functions. Chimeric mice which were created by transplanting human hematolymphoid cells into mice suffering from congenital severe combined immunodeficiency (scid/scid or so called SCID mice), can be infected with HIV-1 and allow one to study the entire HIV-1 replicative cycle. Type C murine leukemia virus models have been used to develop new prophylactic and therapeutic strategies but their use is restricted to the evaluation of select antiviral drug inhibition, targeted to retroviral genes common to both Lentivirinae and Oncovirinae. The role of various animal model systems in the development of anti-HIV-1 and anti-AIDS therapies is summarized.
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PMID:Animal models for anti-AIDS therapy. 144 26

We have developed an experimental mouse model to study the effect of daily cocaine administration on the immune system during an acquired immune deficiency syndrome (AIDS). Mice were infected with LP-BM5 murine leukemia virus, a retrovirus which causes immunosuppression with the development of functional murine AIDS. Increasing doses of cocaine given by daily intraperitoneal injection for 11 weeks reduced body weight. A daily cocaine injection in some mice as well as a saline injection in others showed a decrease in the percentage of Thy 1.2+, CD4+ and CD8+ cells, while both treatments increased the percentage and absolute numbers of B-cells per spleen. Saline and cocaine treatment induced an increase in gamma-IFN and TNF-alpha production by splenocytes. Cocaine treatment favored a decrease in sIL-2R secretion. Saline and cocaine treatment had slightly different effects on the splenocytes of protein-malnourished mice. Cocaine treatment induced an increase in the percentage of CD8+ cells. Saline and cocaine treatments decreased the number of Mac 1+ cells in the spleen. Moreover, saline- and cocaine-treated protein-malnourished mice splenocytes did not present the increase in gamma-IFN production as well-nourished mice splenocytes showed. Retrovirus-infected mice showed a decrease in the percentage of Thy 1.2+ and CD8+ cells and an increase in the percentage and absolute numbers of CD4+, IL-2R+, Mac 1+ and B-cells. Cocaine partially prevented the enlargement of lymphoid organs due to lymphoid cell proliferation induced by murine retrovirus infection, but had little effect on the elevated percentage of CD4+ cells or B-cells or the depressed numbers of CD8+ cells associated with virus infection. However, cocaine did reduce the number of activated IL-2R+ cells and macrophages (Mac 1+) in addition to reducing the total number of cells per spleen in all subsets in retrovirus-infected mice, but not in uninfected controls. Cocaine treatment and retrovirus infection alone or in combination suppressed the release of sIL-2R into supernatant fluid during in vitro culture of splenocytes. These data illustrate that cocaine treatment modulates cell proliferation in retrovirus-infected mice and thus modifies the absolute number of cells in those subsets already altered by retrovirus infection. Retrovirus-infected and retrovirus-infected cocaine-treated protein-malnourished mice showed similar results.
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PMID:Modification of spleen cell subsets by chronic cocaine administration and murine retrovirus infection in normal and protein-malnourished mice. 145

Dendritic cells (DC), important antigen-presenting cells for recruiting T cells into immune responses, are susceptible to infection with HIV-1 and this can cause either stimulatory or suppressive effects on T cells. We examined another human retrovirus, HTLV-1, to determine whether DC were infected and caused any changes in T-cell function. Patients infected with HTLV-1 who have tropical spastic paraparesis (TSP) show high 'spontaneous' lymphocyte proliferation. We studied the basis for this by analyzing the interactions in vitro between lymphocytes and antigen-presenting cells and compared cells taken from HTLV-1-positive TSP patients with those taken from HTLV-1-positive healthy carriers and HTLV-1-negative family members. In HTLV-1-positive individuals, 0.4-5.1% of the DC were infected with HTLV-1 as determined by in situ hybridisation. In TSP patients, depletion of DC and purification of T cells abolished 'spontaneous' lymphocyte proliferation. Reinstating the DC, but not B cells or macrophages, restored proliferation, an effect that was blocked by antibodies either to class II major histocompatibility antigens or to HTLV-1 itself. Thus, presentation of HTLV-1 antigens by infected DC to autologous T cells could result in the abnormal T-cell proliferation and cause the inflammatory reaction leading to tissue damage in TSP. We also speculate that persistent infection of DC with HTLV-1 and consequent continuous stimulation of T cells might be instrumental in the development of HTLV-1-mediated T-cell leukemia.
AIDS Res Hum Retroviruses 1992 Sep
PMID:Dendritic cells from patients with tropical spastic paraparesis are infected with HTLV-1 and stimulate autologous lymphocyte proliferation. 145 15

It would require a detailed knowledge of virology, molecular biology, epidemiology, clinical medicine and politics, to appropriately compare and contrast the hypotheses on the causes of AIDS. The purpose of this review was not to do that, but to inform colleagues that alternative etiologies for AIDS have been considered. No doubt, this healthy questioning will continue until it has been demonstrated--via controlled studies of high-risk groups (both HIV positive and negative), matched for all other characteristics--that only those individuals with HIV positivity actually develop AIDS. It cannot be denied that a common theme to the hypotheses is the presence of high-risk activities. This has been used against the risk-AIDS hypothesis. How, for example, could it explain babies born with immunodeficiencies, K. Bergalis contacting AIDS from her dentist, the British nurse who died of AIDS after contracting HIV from her husband, or AIDS in the wives of hemophiliacs? It may be that these people died of specific diseases (leukemia, pneumonia, infections), which 20 years ago would have been diagnosed as such. Now, because these individuals are found to be HIV positive, they are viewed as AIDS patients. Alternatively, they may not have been asked about their nutritional status, use of psychoactive drugs, and immunosuppressive sexual practices. Additionally, it is possible that by the time AIDS was diagnosed they may have already received numerous antibiotic (immunosuppressive) drug treatments. In North America, for whatever reason, AIDS is associated with high-risk groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does HIV cause AIDS? A review. 832 31

Pulmonary cavitation and pneumothorax may complicate severe cases of Pneumocystis carinii pneumonia. Both complications likely result from tissue necrosis, although how such injury occurs is unknown. To investigate mechanisms of tissue destruction in P carinii pneumonia, histochemical, immunocytochemical, and electron microscopic studies were conducted in pulmonary wedge resections or autopsy specimens from patients with the acquired immunodeficiency syndrome (n = 7) or leukemia (n = 2). Tissue invasion, defined as Pneumocystis organisms in the interstitial compartment, was present in eight of nine cases. Organisms were found in alveolar septa (eight cases), pleura (six cases), and vessel walls (two cases). All cases with tissue invasion exhibited regional necrosis as well as extensive invasion of apparently viable parenchyma. Pulmonary cavitation occurred in seven of eight cases with tissue invasion, and six of these patients developed pneumothoraces. Despite extensive tissue invasion and necrosis there was little host inflammatory or stromal response. Ultrastructurally, both the tissue-invasive and intra-alveolar organisms were predominantly of the trophozoite form; they were present in much greater numbers than suggested by routine silver stains (which detect only cysts). Immunocytochemical techniques, which detect both trophozoite and cyst forms, were much more sensitive than silver stains. These results indicate that extensive tissue invasion by P carinii can occur in severe P carinii pneumonia. We hypothesize that such invasion is an important step in the development of pulmonary necrosis, cavitation, and pneumothorax.
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PMID:Tissue invasion by Pneumocystis carinii: a possible cause of cavitary pneumonia and pneumothorax. 146 75

Cavitating necrosis is rare in Pneumocystis carinii pneumonia. In this report, we describe an autopsy patient with adult T-cell leukemia associated with cavitating Pneumocystis carinii pneumonia. The patient, a 61-year-old woman, died of an acute crisis of adult T-cell leukemia associated with diffuse pulmonary infection of Pneumocystis carinii. Postmortem examination revealed necrotic foci in both lungs, one of which, in the left lower lobe, had a central cavitation. Microscopically, leukemic cell infiltration was abundant in the lung parenchyma but not in the necrotic lesions. Pneumocystis carinii organisms were distributed diffusely in the alveoli and also in the cavity wall. Intranuclear and intracytoplasmic inclusion bodies were scattered in the lung indicating cytomegalovirus infection. However, no bacterial or fungal infection was detected in the lungs, even in the necrotic lesions. Cavitating Pneumocystis carinii pneumonia occurs in other immunodeficiency diseases apart from AIDS. To our knowledge, this report is the first case of cavitating Pneumocystis carinii pneumonia in adult T-cell leukemia.
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PMID:Cavitating Pneumocystis pneumonia in an autopsied case of adult T-cell leukemia. 147 36


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