Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-nine sequential cerebrospinal fluid (CSF) samples from 28 human immunodeficiency virus-1 (HIV-1)-infected patients were analyzed during the follow-up of 9 months to 4 years. Intrathecal synthesis of HIV-antibodies and IgG (p < 0.01), and the levels of beta-2-microglobulin (beta 2m) in the CSF (p < 0.05) and serum (p < 0.01) increased with duration of HIV-1 infection. No effect of duration of HIV-1 infection was observed on the individual CSF white cell counts and the levels of blood-brain-barrier (BBB) permeability. In 13 patients with HIV-1-associated central nervous system (CNS) disease, the effect of duration was seen as an increase of the individual beta 2m levels in serum (p < 0.01). Moreover, 7 of 9 patients who developed neurological disease or showed its progression during the study increased the level of beta 2m in the CSF. All of them increased the level of beta 2m in serum. In 15 neurologically healthy subjects, the effect of duration was expressed as an increase of the level of individual beta 2m in CSF (p < 0.05) and intrathecal IgG synthesis (p < 0.01). In the AIDS group, the level of beta 2m in the CSF increased, but in less severe stages the dependency of the individual CSF parameters on disease duration was not found. Our results indicate that elevated levels of beta 2m in CSF and serum appear to predict progression of neurological and systemic diseases, respectively. Elevated beta 2m in the CSF of clinically intact individuals may indicate subclinical neurological disease caused by HIV-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:CSF follow-up in HIV-1 infection: intrathecal production of HIV-specific and unspecific IGG, and beta-2-microglobulin increase with duration of HIV-1 infection. 833 44

Infection by human immunodeficiency virus type 1 (HIV-1), the etiologic agent of the acquired immunodeficiency syndrome (AIDS), is often complicated with a high incidence of neurologic disorders. It is believed that HIV-1, in addition to infecting both macroglial and microglial cells, may influence the expression of several strategic genes of uninfected neighboring or latently infected brain cells. It is suspected that the viral-encoded transregulatory protein, Tat, facilitates cross-communications between these cells. In support of this concept, earlier studies demonstrated that Tat is released from the infected cells, and has the capacity to be taken up by the uninfected cells and exert its biological activity on the responsive gene. Recent studies in several laboratories suggest the involvement of Tat in altering the expression of a limited number of cellular regulatory factors which, in turn, may mediate the altered physiology of the cells. In this communication, we demonstrate the ability of the HIV-1 Tat protein to increase expression of transforming growth factor beta 1 (TGF-beta 1), a cytokine with potent immunosuppressive activity, in human astrocytic glial cells. Implications of the Tat-mediated induction of TGF-beta 1 expression and cytokine involvement in the regulation of immune response and central nervous system (CNS) pathology are discussed.
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PMID:Evidence for stimulation of the transforming growth factor beta 1 promoter by HIV-1 Tat in cells derived from CNS. 833 45

Individuals with HIV-1 infection show two major immunological effects--the early persistent stimulation of immune responses (e.g. of CD8 cells and antibody production) and later catastrophic immunodeficiency. Peripheral blood dendritic cells (DC) become infected with HIV-1 and infected cells can stimulate responses to virus. By contrast infected DC show a reduced capacity to stimulate either primary or secondary responses to other antigens. We have proposed that the block, particularly in primary responses, may be instrumental in the development of immunodeficiency. In HTLV-1 infected patients with tropical spastic paraparesis (TSP) a major feature of disease is 'spontaneous' T cell proliferation thought to underlie development of inflammatory neurological disease. We have now shown that some DC in addition to T cells are infected in TSP and that DC stimulate the persistent T cell activity. Here we demonstrate this using cells from an informative family where the daughter was normal, the father an HTLV-1 seronegative carrier and the mother had TSP. DC from all individuals stimulated normal allogeneic T cells in a mixed leukocyte reaction (MLR) and T cells responded well to normal allogeneic DC. T cells from the daughter showed little stimulation with autologous DC, those from the father showed significant but low stimulation, and T cells from the TSP patient gave a response to autologous DC which exceeded that to allogeneic DC. Taken together, the studies of DC and both HIV-1 and HTLV-1 indicate that infection of DC may play a central role in development of T cell abnormalities in human retrovirus-induced diseases.
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PMID:Dendritic cells in HIV-1 and HTLV-1 infection. 837 24

HIV can invade the CNS, where it replicates principally in macrophages. Yet, neurological disease is more often correlated with levels of neurotoxins or tumor necrosis factor alpha than with viral replication or specific viral determinants in brain. In experimental systems, HIV glycoprotein affects functions of uninfected microglia and astrocytes to eventually cause neuronal death. While the cellular basis of cognitive and neurological dysfunction are unravelled in the simian immunodeficiency virus model, the molecular mechanisms of HIV neurotoxicity are being studied in newly developed mouse models.
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PMID:HIV interactions with cells of the nervous system. 858 Jul 17

The neurological features of 13 patients with primary hypogammaglobulinaemia are described. Seven patients had X-linked agammaglobulinaemia (XLA) and six had common variable immunodeficiency (CVID). Three clinical pictures emerged: (i) a progressive myelopathy (one case); (ii) a myelopathy progressing to an encephalopathy (four cases); (iii) a pure encephalopathy (eight cases). In four patients the encephalopathy was temporarily reversible; the relationship of this to immunoglobulin therapy is unclear. Additional features occurred in some patients. Three had retinopathy interpreted as retinitis pigmentosa, in one of whom the retinopathy resolved. Two patients had a sensori-neural hearing loss and three had features of dermatomyositis; a variable pleocytosis was found in the CSF of nine patients. Imaging revealed atrophic changes in the cerebral hemispheres in eight cases. Ten patients have died, 1-11 years after the onset of the CNS manifestations, and in four autopsies were obtained. Two patients had encephalopathy, one with XLA had evidence of end-stage encephalitis and the other with CVID had a multi-focal leucoencephalopathy. The other two with XLA had leptomeningitis without evidence of encephalitis. Enteroviral infection is probably an important cause of neurological disease in these patients as CSF from seven patients was either positive by polymerase chain reaction (PCR) or by culture for enteroviruses. Other possible mechanisms are discussed.
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PMID:Encephalomyelitis in primary hypogammaglobulinaemia. 862 73

The high incidence of neurological disorders in patients afflicted with acquired immunodeficiency syndrome (AIDS) may result from human immunodeficiency virus type 1 (HIV-1) induction of chemotactic signals and cytokines within the brain by virus-encoded gene products. Transforming growth factor beta1 (TGF-beta1) is an immunomodulator and potent chemotactic molecule present at elevated levels in HIV-1-infected patients, and its expression may thus be induced by viral trans-activating proteins such as Tat. In this report, a replication-defective herpes simplex virus (HSV)-1 tat gene transfer vector, dSTat, was used to transiently express HIV-1 Tat in glial cells in culture and following intracerebral inoculation in mouse brain in order to directly determine whether Tat can increase TGF-beta1 mRNA expression. dSTat infection of Vero cells transiently transfected by a panel of HIV-1 long terminal repeat deletion mutants linked to the bacterial chloramphenicol acetyltransferase reporter gene demonstrated that vector-expressed Tat activated the long terminal repeat in a trans-activation response element-dependent fashion independent of the HSV-mediated induction of the HIV-1 enhancer, or NF-kappaB domain. Northern blot analysis of human astrocytic glial U87-MG cells transfected by dSTat vector DNA resulted in a substantial increase in steady-state levels of TGF-beta1 mRNA. Furthermore, intracerebral inoculation of dSTat followed by Northern blot analysis of whole mouse brain RNA revealed an increase in levels of TGF-beta1 mRNA similar to that observed in cultured glial cells transfected by dSTat DNA. These results provided direct in vivo evidence for the involvement of HIV-1 Tat in activation of TGF-beta1 gene expression in brain. Tat-mediated stimulation of TGF-beta1 expression suggests a novel pathway by which HIV-1 may alter the expression of cytokines in the central nervous system, potentially contributing to the development of AIDS-associated neurological disease.
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PMID:Human immunodeficiency virus tat gene transfer to the murine central nervous system using a replication-defective herpes simplex virus vector stimulates transforming growth factor beta 1 gene expression. 865 Feb 21

Human T-lymphotropic virus type I (HTLV-1) is associated with tropical spastic paraparesis (TSP) and adult T-cell leukemia/lymphoma. HTLV-I infection is endemic in certain parts of the Natal/KwaZulu region of South Africa. No studies on the seroprevalence of HTLV-I infection in the Free State (FS) have been published. This study was designed to determine the prevalence of HTLV-I antibodies among different patient groups in the FS. Sera from 863 patients were analyzed. There were: 178 asymptomatic rural Blacks, 200 asymptomatic urban Blacks, 50 asymptomatic Whites, 60 patients with spastic myelopathy, 70 patients with other neurologic disorders, 12 patients with T-cell haematologic malignancies and 293 human immunodeficiency virus (HIV) seropositive patients. Sera were tested for the presence of HTLV-I/II antibodies using an enzyme linked immunosorbent assay (ELISA). Positive results were confirmed using a modified Western blot assay. None of the asymptomatic Whites were HTLV-I antibody positive (95 pc confidence interval (CI): 0 to 7 pc), while 2 pc (95 CI: 0.5 to 5 pc) of asymptomatic urban Blacks and 1.1 pc (95 pc CI: 0.14 to 4 pc) of asymptomatic rural Blacks had HTLV-I antibodies. Of the group of patients with spastic myelopathy 33.3 pc (95 pc CI: 21.7 to 46.7 pc had HTLV-I antibodies, while none of the patients with T-cell haematologic malignancies (95 pc CI: 0 to 26.5 pc) or other neurologic disorders (95 pc CI: 0 to 5 pc) had HTLV-I antibodies. Of the HIV seropositive patients 6.1 (95 pc CI: 4 to 9.5) were co-infected with HTLV-I. HTLV-I infection is present in the Free State. It is strongly associated with spastic myelopathy in this region. HIV seropositive patients have a high rate of HTLV-I co-infection.
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PMID:HTLV-I infection in the Free State region of South Africa: a sero-epidemiologic study. 865 70

Human immunodeficiency virus (HIV) infection is commonly associated with neurological disease that occurs in the apparent absence of extensive infection of brain cells by HIV, suggesting that indirect mechanisms account for neuropathogenesis in the CNS, perhaps including changes in the normal neuroprotective functions of astrocytes. To test this hypothesis, we examined the effect of the pro-inflammatory cytokine, tumor necrosis factor alpha (TNFalpha), produced by HIV-1-infected macrophages and microglia, on glutamate transport by primary human fetal astrocytes (PHFAs). A dose-dependent inhibition of high affinity glutamate uptake sites was observed 12-24 h after addition of exogenous recombinant human TNFalpha to PHFAs. This effect was specific since it was blocked by a neutralizing monoclonal antibody directed against TNFalpha. Furthermore, the inhibitory effect was reproduced by a monoclonal antibody that is an agonist at the 55-kDa TNF receptor. These results suggest that the neurotoxic effects of TNFalpha may be due in part to its ability to inhibit glutamate uptake by astrocytes, which in turn may result in excitotoxic concentrations of glutamate in synapses.
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PMID:Tumor necrosis factor alpha inhibits glutamate uptake by primary human astrocytes. Implications for pathogenesis of HIV-1 dementia. 866 35

The new onset of headache in a person infected with human immunodeficiency virus (HIV) may be an ominous sign of a significant underlying neurological disorder. This case control study compares the prevalence of headache in HIV-seropositive persons without identifiable neurological disease on study entry to that in an HIV-seronegative control population with similar risk factors for HIV infection. Features of headache that were evaluated included frequency, duration, location, severity, and recent change in characteristics. In the HIV-seropositive population, the presence of headache and its specific features were correlated with the degree of immunosuppression as determined by absolute CD4 counts and Centers for Disease Control stages, the presence of other neurological symptoms and neurological signs, cranial magnetic resonance imaging (MRI) findings, and cerebrospinal fluid (CSF) values. Headaches were common; approximately 50% of all subjects reported headache at study entry and 2 years later. Headache frequency and characteristics were not different between HIV-seropositive and HIV-seronegative subjects. Headache was neither more frequent nor different in HIV-seropositive individuals with advanced immunosuppression. There was no correlation between headache and abnormal CSF parameters, cranial MRI abnormalities, including the presence of sinusitis, or the use of zidovudine.
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PMID:Headache and human immunodeficiency virus infection: a case control study. 881 27

Neurological dysfunction has been shown to be associated with human immunodeficiency virus (HIV) infection. The incidence of these abnormalities is greater in HIV-infected children when compared with adults, and the patterns of neurological disease are also known to differ from those observed in the adult population. The reasons for these differences are unclear but are most likely related to the immaturity of the host's immune and central nervous systems at the time of infection. This is thought to be particularly true for infants infected with HIV prenatally. To examine these questions, the brains of fetal rhesus macaques that were infected with SIVmac251 at various time points in utero were examined. Direct fetal inoculations were performed on gestational day (GD) 65 (n = 8; early second trimester), GD 110 (n = 4; early third trimester) and GD 130 (n = 2; mid third trimester), with harvest of fetal tissues on GD 80, 100, 130, or 145. Eleven sham controls were included with harvest at correlative time points. Specimens were examined by routine histology, immunohistochemistry, and in situ hybridization to localize viral antigens and SIV nucleic acid. Histologically, scattered glial nodules, spongiosis, and mineralization were found in the basal ganglia and deep white matter in 4 of the 14 fetuses (3 inoculated on GD 65 and one on GD 110). These fetuses and those without histological lesions had viral nucleic acid and SIV antigen in the stroma of the choroid plexus, meninges, and external granular layer of the cerebellum and in columns of cells in the cortical plate. In contrast to juvenile and adult macaques, very few SIV-positive perivascular mononuclear cells were present. These findings suggest that SIV has a different distribution in the brain of fetal macaques after direct infection when compared with adult or juvenile animals. Furthermore, the results of these studies suggest that differences in neurological disease between pediatric and adult patients with acquired immune deficiency syndrome are most likely related to the time of infection.
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PMID:Localization of simian immunodeficiency virus nucleic acid and antigen in brains of fetal macaques inoculated in utero. 886 58


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