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)

The CC chemokine monocyte chemotactic protein-1 (MCP-1) was markedly elevated in the cerebrospinal fluid (CSF) of human immunodeficiency virus (HIV)-infected patients with cytomegalovirus (CMV) encephalitis. The MCP-1 CSF levels in CMV encephalitis were markedly higher than those in the CSF of HIV-infected patients with or without unrelated neurologic diseases, including progressive multifocal leukoencephalopathy, cryptococcal meningitis, toxoplasmic encephalitis, and primary lymphoma. Interleukin-8, RANTES, macrophage inflammatory protein (MIP)-1 alpha, and MIP-1 beta were not substantially increased in the CSF of CMV encephalitis patients. High levels of MCP-1 may underlie monocyte recruitment and tissue damage in CMV encephalitis and may represent a rapid and useful tool in the diagnostic armamentarium for neurologic disorders associated with HIV infection.
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PMID:Selective elevation of monocyte chemotactic protein-1 in the cerebrospinal fluid of AIDS patients with cytomegalovirus encephalitis. 889 15

Two polyomaviruses, JC virus (JCV) and BK virus (BKV), affect humans. JCV is the causative agent of progressive multifocal leukoencephalopathy (PML), and detection of JCV in the central nervous system (CNS) is a prerequisite for confirmation of the disease. BKV is generally not associated with neurological disease, but involvement of BKV in patients with CNS disorders has been reported. In the present study polyomavirus DNA was detected by a nested PCR at a sensitivity corresponding to the detection of 10 copies of JCV DNA in 10 microliters of cerebrospinal fluid (CSF). CSF samples from 212 patients with neurological symptoms and immunodeficiencies were investigated for the presence of polyomavirus DNA. Of 128 human immunodeficiency virus (HIV)-infected patients, 14 (11%) had JCV DNA in their CSF, and all 14 patients had clinical PML. BKV DNA was detected in one HIV-infected patient with neurological symptoms not compatible with PML. Among 84 HIV-negative patients, 6 (7%) had detectable JCV DNA in their CSF, confirming PML in patients with clinical conditions of T-cell lymphoma, chronic lymphatic leukemia, status postliver transplantation, congenital immunodeficiency, sarcoidosis, and immunodeficiency of unknown origin. The specificity of the PCR was confirmed by a clinical follow-up study which showed full agreement between the detection of JCV DNA in CSF and clinically manifest PML. The described PCR is a rapid, reproducible, and easily performed assay.
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PMID:Analysis of PCR as a tool for detection of JC virus DNA in cerebrospinal fluid for diagnosis of progressive multifocal leukoencephalopathy. 894 Apr 24

HIV-induced neurological disease is postulated to be caused by indirect mechanisms. Tumor necrosis factor (TNF)alpha is increased in the brains in human immunodeficiency virus (HIV)-associated dementia and in the spinal cord in vacuolar myelopathy and may play a pathogenetic role in these diseases. Microglia, astrocytes and infiltrating macrophages can be induced to produce TNF alpha and each has been identified as a source of TNF alpha in neurological disease. Reverse transcriptase synthesis of cDNA and polymerase chain reaction amplification of the cDNA was combined with immunocytochemistry to identify the cellular source of TNF alpha in HIV-induced neurological disease. Cells positive for TNF alpha mRNA were more abundant in white matter than gray matter of the brain from demented individuals. TNF alpha mRNA-positive cells in brains and spinal cords were almost exclusively macrophage-lineage cells. Only rare TNF alpha mRNA-positive cells were astrocytes. We conclude that macrophage-lineage cells are the primary source of elevated central nervous system TNF alpha mRNA in providing further evidence that macrophage activation is an important element in the pathogenesis of HIV-associated neurological disease.
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PMID:Cellular localization of tumor necrosis factor mRNA in neurological tissue from HIV-infected patients by combined reverse transcriptase/polymerase chain reaction in situ hybridization and immunohistochemistry. 911 60

Feline immunodeficiency virus, like human immunodeficiency virus type 1, is a retrolentivirus causing neurological disease and immune suppression. Primary neurological complications, including human immunodeficiency virus encephalopathy and peripheral neuropathy, and neuropathological changes, including gliosis, neuronal injury and multinucleated giant cells, have been described for human immunodeficiency virus type 1 infection. Excitatory amino acids have been implicated as a basis for human immunodeficiency virus encephalopathy and the accompanying neuronal injury. Here, we test our hypothesis that feline immunodeficiency virus infection results in glial activation accompanied by enhanced glutamatergic activity, causing neuronal loss. Neurological signs observed in naturally and experimentally infected animals included ataxia, aggressivity and reduced motor activity. Neuropathological changes included gliosis, perivascular cuffing and neuronal dropout in the brains of both experimentally and naturally infected animals, but not in uninfected animals. Feline immunodeficiency virus antigen and genome were detected in the brains of all experimentally and naturally infected animals. Proton nuclear magnetic resonance spectroscopy revealed significantly increased glutamate levels in the feline immunodeficiency virus-infected animals. In contrast, glutamate decarboxylase levels in GABAergic neurons were reduced in feline immunodeficiency virus-infected animals. These findings provide direct in vivo evidence for enhanced glutamate levels in conjunction with neuronal loss, supporting the hypothesis of glutamate-mediated neurotoxicity as a major mechanism in the neuropathogenesis of retrolentiviral infections.
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PMID:Feline immunodeficiency virus causes increased glutamate levels and neuronal loss in brain. 913 Jul 96

We recently reported that a chimeric simian/human immunodeficiency virus (SHIVKU-1) developed in our laboratory caused progressive depletion of CD4+ T lymphocytes and AIDS within 6 months of inoculation into pig-tailed macaques (M. nemestrina). None of the pig-tailed macaques showed productive SHIV infection in the central nervous system (CNS). In this report, we show that by further passage of the pathogenic virus in rhesus macaques [M. mulatta], we have derived a new strain of SHIV (SHIVKU-2) that has caused AIDS and productive CNS infection in 3 of 5 rhesus macaques infected with the virus. Productive replication of SHIV in the CNS was clearly shown by high infectivity titers and p27 protein levels in brain homogenates, and in 2 of the 3 rhesus macaques this was associated with disseminated, nodular, demyelinating lesions, including focal multinucleated giant cell reaction, largely confined to the white matter. These findings were reminiscent of HIV-1 associated neurological disease, and our immunohistochemical and in situ hybridization data indicated that the neuropathological lesions were associated with the presence of SHIV-specific viral antigens and nucleic acid respectively. However, the concomitant reactivation of opportunistic infections in these macaques suggested that such pathogens may have influenced the replication of SHIV in the CNS, or modified the neuropathological sequelae of SHIV infection in the rhesus species, but not in pig-tailed macaques. Our findings in the two species of macaques highlight the complexities of lentiviral neuropathogenesis, the precise mechanisms of which are still elusive.
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PMID:Neuropathogenesis of chimeric simian/human immunodeficiency virus infection in pig-tailed and rhesus macaques. 921 70

To examine the relationship between macrophage tropism and neurovirulence, macaques were inoculated with two recombinant hybrid viruses derived from the parent viruses SIVmac239, a lymphocyte-tropic, non-neurovirulent clone, and SIV/17E-Br, a macrophage-tropic, neurovirulent virus strain. The first recombinant, SIV/17E-Cl, contained the portion of the env gene that encodes the surface glycoprotein and a short segment of the transmembrane glycoprotein of SIV/17E-Br in the backbone of SIVmac239. Unlike SIVmac239, SIV/17E-Cl replicated productively in macrophages, demonstrating that sequences in the surface portion of env determine macrophage tropism. None of five macaques inoculated with SIV/17E-Cl developed simian immunodeficiency virus (SIV) encephalitis. The second recombinant, SIV/17E-Fr, which contained the entire env and nef genes and the 3' long terminal repeat of SIV/17E-Br in the SIVmac239 backbone, was also macrophage tropic. Six of nine macaques inoculated with SIV/17E-Fr developed SIV encephalitis ranging from mild to moderate in severity, indicating a significant (P = 0.031) difference in the neurovirulence of the two recombinants. In both groups of macaques, CD4+ cell counts declined gradually during infection and there was no significant difference in the rate of the decline between the two groups of macaques. This study demonstrated that macrophage tropism alone is not sufficient for the development of neurological disease. In addition, it showed that while sequences in the surface portion of the envelope gene determine macrophage tropism, additional sequences derived from the transmembrane portion of envelope and/or nef confer neurovirulence.
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PMID:Pathogenesis of simian immunodeficiency virus encephalitis: viral determinants of neurovirulence. 922 98

To identify varicella-zoster virus (VZV) infections of the nervous system in patients infected with human immunodeficiency virus (HIV), polymerase chain reaction (PCR) analysis of cerebrospinal fluid (CSF) samples from 514 consecutive HIV-infected patients with neurological disease was performed to detect VZV DNA. VZV DNA was detected in CSF of 13 (2.5%) of 514 patients. Four of 13 patients had VZV encephalitis or meningoencephalomyelitis. These four patients received intravenous acyclovir therapy; CSF became negative for VZV DNA and clinical conditions improved for two, whereas CSF remained positive for VZV DNA and clinical conditions worsened until death for two. In nine of 13 patients, the neurological symptoms were likely caused by other simultaneous HIV-related complications in the central nervous system. After intravenous therapy with high doses of acyclovir or foscarnet, VZV was cleared from CSF in eight of nine patients. VZV DNA can be detected in CSF of HIV-infected patients in association with either manifestations of neurological VZV disease or subclinical reactivation of VZV infection. Antiviral treatment may be effective in suppressing VZV replication in the nervous system.
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PMID:Varicella-zoster virus (VZV) DNA in cerebrospinal fluid of patients infected with human immunodeficiency virus: VZV disease of the central nervous system or subclinical reactivation of VZV infection? 931 52

The high incidence of neurologic dysfunction from human immunodeficiency virus (HIV) infection has heightened interest in neuropathogenesis of other lentiviruses, including that associated with feline immunodeficiency virus (FIV). Both HIV and FIV efficiently enter the central nervous system and cause primary neurological disease that is not attributable to opportunistic infections or systemic disease. Cells in the brain infected by FIV are similar to those observed in HIV infection, both viruses infect macrophages, microglia, and astrocytes. Although substantial neuronal loss can occur in the cortex of HIV- or FIV-infected patients, most studies agree that neurons are not infected and indirect mechanisms of neurotoxicity are postulated. This review describes recent information on the neuropathogenesis of FIV and how this information correlates with what is known about the neuropathogenesis of HIV. Although the pathogenesis of neurological dysfunction in HIV- and FIV-infected patients is far from clear, it is becoming increasingly evident that the relationship between lentivirus presence in the brain and neurological signs is not straightforward and cannot be explained by simple cytolytic infection. The observed neurologic dysfunction is likely multifactorial and complex involving an intricate web of subcellular pathways and neurotoxic factors interacting with multiple cell types.
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PMID:Cellular mechanisms of feline immunodeficiency virus (FIV)-induced neuropathogenesis. 934 Dec 40

The AIDS-dementia complex remains one of the more common neurologic disorders associated with human immunodeficiency virus (HIV) infection. Despite several advances that have been made in elucidating some of its clinical and biological features, pathogenesis is not well understood, and effective treatments are scarce. This article reveals the results of these studies and discusses how these different approaches have already enabled clinicians to study further the effects of HIV infection on brain function and to explore the functional anatomy of this important clinical syndrome.
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PMID:Functional imaging of the AIDS dementia complex and the metabolic pathology of the HIV-1-infected brain. 937 62

Cerebrospinal fluid (CSF) human immunodeficiency virus (HIV) RNA levels were measured with the Nucleic Acid Sequence-Based Amplification (NASBA) assay to determine the relationship with neurological status; 37 subjects with HIV dementia (HIV-D) were compared with 77 with HIV with minor neurological signs (HIV-MCMD) and 93 neurologically normal HIV-seropositive individuals (HIV-NML). The NASBA assay had a lower limit of detection of 100 copies per milliliter. Mean CSF log HIV RNA levels were significantly higher in those with dementia after adjusting for CD4 count and were correlated with dementia severity. Plasma levels did not distinguish comparably immunosuppressed subjects with or without dementia. CSF and plasma RNA levels were significantly intercorrelated for subjects with CD4 counts <200/mm3 and also correlated inversely with CSF beta2-microglobulin. CSF RNA levels were independent of CSF pleocytosis or antiretroviral exposure. Brain RNA levels were consistently higher than CSF but correlated with CSF values for dementia subjects. The NASBA assay can be used reliably to determine HIV RNA levels in CSF, brain, and plasma samples. CSF HIV RNA may be a surrogate marker for brain infection, based on the observed correlation with brain levels. The association between plasma HIV RNA and CSF levels of HIV and beta2-microglobulin suggests that both viral load and CNS immune activation are important determinants of neurological disease.
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PMID:Relationship between human immunodeficiency virus-associated dementia and viral load in cerebrospinal fluid and brain. 939 65


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