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 simian immunodeficiency virus (SIV) is closely related to the human immunodeficiency virus (HIV) in genomic organization and morphology. More important, SIV and HIV are both primate lentiviruses that cause transmissible immunodeficiency and encephalitis, with an apparently increased virulence in the immature host. The neuropathological features in common between SIV encephalitis in juvenile macaque monkeys and HIV encephalitis in children include the invasion of brain with virus-laden macrophages, the formation of multinucleated (syncytial) giant cells, and white matter lesions and subtle white matter astrocytosis. Important differences include giant cell leptomeningitis and evidence of necrosis and karyorrhexis in brain macrophage infiltrates in SIV-infected monkeys. These changes probably represent a more acute inflammatory process. The importance of future studies to define pathogenetic features of SIV encephalitis, using molecularly characterized isolates with varying neurovirulence and host range, are emphasized.
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PMID:Comparison of simian immunodeficiency virus and human immunodeficiency virus encephalitides in the immature host. 283 97

Brain tissue was examined for evidence of human immunodeficiency virus (HIV) infection in 23 intravenous drug users who died suddenly some years after seroconversion but while still in presymptomatic stages of infection. None showed giant cell encephalitis, but 14 showed T cell lymphocytic leptomeningitis and 3 showed other significant neuropathologic features. Quantitative polymerase chain reaction for HIV was applied to 13 of the 23 with negative results in 6 and very low positive results in the other 7, a finding consistent with contamination by residual infected blood in the brain tissue. This contrasted with findings in AIDS-infected tissue, in which substantial amounts of provirus were found. It is concluded that significant infection in brain tissue does not occur in presymptomatic stages of HIV infection and that invasion of the central nervous system may be delayed until the transition to symptomatic AIDS.
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PMID:Human immunodeficiency virus and the brain: investigation of virus load and neuropathologic changes in pre-AIDS subjects. 837 29

Early HIV infection of the CNS, as demonstrated by cerebrospinal fluid studies, seems relatively common. However most HIV carriers remain neurologically unimpaired during the incubation period. A few psychometric, radiological, and electrophysiological studies suggest that neurological abnormalities are present at early stages of HIV infection; the findings of these studies are controversial and until recently, they have not been supported by neuropathological data. Early brain changes, including leptomeningitis and vasculitis with myelin pallor and gliosis of the deep white matter are probably secondary to vascular inflammation and opening of the blood-brain barrier. Such conclusions are drawn from the examination of brains of asymptomatic HIV-positive individuals who died from unnatural causes, and of rare cases with acute fatal encephalopathy revealing HIV infection. In addition, early experimental simian immunodeficiency virus infection and feline immunodeficiency virus encephalopathy have demonstrated similar changes to those in man. Although small amounts of viral genome were detected by PCR in a few cases, the early changes in the human brain do not seem to result from a productive HIV infection of the CNS, as seen in HIV encephalitis. The occurrence of a usually asymptomatic and transient immunopathological reaction coinciding with early HIV infection of the nervous system appears to be more likely.
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PMID:Early central nervous system changes in human immunodeficiency virus (HIV)-infection. 847 97

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

Early HIV-1 invasion of the central nervous system has been demonstrated by many cerebrospinal fluid studies; however, most HIV-1 carriers remain neurologically unimpaired during the so called "asymptomatic" period lasting from seroconversion to symptomatic AIDS. Therefore, neuropathological studies in the early pre-AIDS stages are very few, and the natural history of central nervous system changes in HIV-1 infection remains poorly understood. Examination of brains of asymptomatic HIV-1 positive individuals who died accidentally and of rare cases with acute fatal encephalopathy revealing HIV infection, and comparison with experimental simian immunodeficiency virus and feline immunodeficiency virus infections suggest that, invasion of the CNS by HIV-1 occurs at the time of primary infection and induces an immunological process in the central nervous system. This includes an inflammatory T-cell reaction with vasculitis and leptomeningitis, and immune activation of brain parenchyma with increased number of microglial cells, upregulation of major histocompatibility complex class II antigens and local production of cytokines. Myelin pallor and gliosis of the white matter are usually found and are likely to be the consequence of opening of the blood brain barrier due to vasculitis; direct damage to oligodendrocytes by cytokines may also interfere. These white matter changes may explain, at least partly, the early cerebral atrophy observed, by magnetic resonance imaging, in asymptomatic HIV-1 carriers. In contrast, cortical damage seems to be a late event in the course of HIV-1 infection. There is no significant neuronal loss at the early stages of the disease, no accompanying increase in glial fibrillary acid protein staining in the cortex, and only exceptional neuronal apoptosis. Although HIV-1 proviral DNA may be demonstrated in a number of brains, viral replication remains very low during the asymptomatic stage of HIV-1 infection. This makes it likely that, although opening of the blood brain barrier may facilitate viral entry into the brain, specific immune responses including both neutralising antibodies and cytotoxic T-lymphocytes, continuously inhibits viral replication at that stage.
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PMID:Neuropathology of early HIV-1 infection. 886 43

Early HIV-1 invasion of the central nervous system has been demonstrated by many cerebrospinal fluid studies; however, most HIV-1 carriers remain neurologically unimpaired during the so-called "asymptomatic" period lasting from seroconversion to symptomatic AIDS. Therefore, very few neuropathological studies have been conducted in the early pre-AIDS stages, and the natural history of central nervous system changes in HIV-1 infection remains poorly understood. Examination of brains of asymptomatic HIV-1 positive individuals who died accidentally and of rare cases with acute fatal encephalopathy revealing HIV infection, and comparison with experimental simian immunodeficiency virus and feline immunodeficiency virus infections suggest that, invasion of the CNS by HIV-1 occurs at the time of primary infection and induces an immunological process in the central nervous system. This includes an inflammatory T-cell reaction with vasculitis and leptomeningitis, and immune activation of brain parenchyma with increased number of microglial cells, upregulation of major histocompatibility complex class II antigens and local production of cytokines. Myelin pallor and gliosis of the white matter are usually found and are likely to be the consequence of opening of the blood-brain barrier due to vasculitis; direct damage to oligodendrocytes by cytokines may also be involved. These white matter changes may explain, at least partly, the early cerebral atrophy observed, by magnetic resonance imaging, in asymptomatic HIV-1 carriers. In contrast, cortical damage seems to be a late event in the course of HIV-1 infection. There is no significant neuronal loss at the early stages of the disease, no accompanying increase in glial fibrillary acid protein staining in the cortex, and only exceptional neuronal apoptosis. Although HIV-1 proviral DNA may be demonstrated in a number of brains, viral replication remains very low during the asymptomatic stage of HIV-1 infection. This makes it likely that, although opening of the blood brain barrier may facilitate viral entry into the brain, specific immune responses including both neutralising antibodies and cytotoxic T-lymphocytes, continuously inhibit viral replication at this stage.
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PMID:[Central nervous system lesions in the early stages of HIV infection]. 938 1

Early HIV-1 invasion of the central nervous system has been demonstrated by many cerebrospinal fluid studies; however, most HIV-1 carriers remains neurologically unimpaired during the so called "asymptomatic" period lasting from seroconversion to symptomatic AIDS. Therefore, there are very few neuropathological studies in the early pre-AIDS stages and the natural history of central nervous system changes in HIV-1 infection remains poorly understood. Examination of brains of asymptomatic HIV-1 positive individuals who died accidentally and of rare cases with acute fatal encephalopathy revealing HIV infection, and comparison with experimental simian immunodeficiency virus and feline immunodeficiency virus infections suggest that invasion of the CNS by HIV-1 occurs at the time of primary infection and induces an immunological process in the central nervous system. This includes an inflammatory T-cell reaction with vasculitis and leptomeningitis, and immune activation of brain parenchyma with increased number of microglial cells, upregulation of major histocompatibility complex class II antigens and local production of cytokines. Myelin pallor and gliosis of the white matter are usually found are likely to be the consequence of opening of the blood brain barrier due to vasculitis; direct damage to oligodendrocytes by cytokines may also interfere. These white matter changes may explain, at least partly, the early cerebral atrophy observed, by magnetic resonance imaging, in asymptomatic HIV-1 carriers. In contrast, cortical damage seems to be a late event in the course of HIV-1 infection. There is no significant neuronal loss at the early stages of the disease, no accompanying increase in glial fibrillary acid protein staining in the cortex, and only exceptional neuronal apoptosis. Although HIV-1 proviral DNA may be demonstrated in a number of brains, viral replication remains very low during the asymptomatic stage of HIV-1 infection. This makes it likely that, although opening of the blood brain barrier may facilitate viral entry into the brain, specific immune responses including both neutralising antibodies and cytotoxic T-lymphocytes, continuously inhibits viral replication at that stage.
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PMID:[Lesions of the central nervous system in the early stages of human immunodeficiency virus infection]. 968 50

The clinical course and the postmortal pathological findings in a female newborn showing parental consanguinity are presented. One week afterbirth, the infant developed fever, hepatosplenomegaly and polyserositis. Rapidly progressing immunodeficiency due to pancytopenia led to pneumonia and untreatable respiratory distress with fatal outcome after 2 weeks. Autopsy findings revealed multisystem lymphohistiocytic infiltration with marked erythrophagocytosis. Neuropathological findings included lymphohistiocytic leptomeningitis, perivascular cuffing by lymphohistiocytic infiltrations in the cerebral white matter, predominantly in subependymal location, and multifocal lymphohistiocytic infiltrations of the cerebral grey matter and the cervical spinal cord. Erythrophagocytosis was the histopathological hallmark at all sites. Regarding the fatal clinical course, the medical history of parental consanguinity and the histopathological features, postmortem diagnosis was familial erythrophagocytic lymphohistiocytosis (FEL, Farquhar's disease). The present case is discussed with focus on CNS involvement in FEL by reviewing the relevant literature.
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PMID:Familial erythrophagocytic lymphohistiocytosis (Farquhar's disease): involvement of the central nervous system. 1214 24