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)

Infection with the human immunodeficiency virus (HIV) manifests neurological symptoms in some patients. 3 cases of ascending polyneuritis associated with HIV infection are presented. A 28-year-old female had a 2-day weakness in the lower limbs moving to the upper extremities. On admission she had left facial nerve palsy and lower motor neurone weakness of both legs as well as weakness of the upper limbs. No reflexes were present. Both serum and cerebrospinal fluid (CSF) were positive for HIV antibody with the enzyme-linked immunosorbent assay (ELISA). After 5 weeks ventilation she died from bronchopneumonia. The 2nd case involved a 19-year-old woman admitted with weakness in the lower limbs, left facial nerve palsy, and severe lower motor neurone weakness of the upper and lower limbs. HIV antibodies were found in serum and CSF. She improved somewhat, returned home, and was lost to follow-up. The 3rd case had to do with a 29-year- old female admitted with weakness in the lower limbs radiating to the upper limbs. She had a right facial nerve palsy and a partial left 3rd nerve palsy. Lower motor neurone weakness was present in the limbs. Serum and CSF were both positive for HIV antibody. Her condition improved, and 1 month later she was discharged. It is probable that HIV was directly implicated in the neurological disease. It is possible that Guillain-Bare syndrome is a manifestation of seroconversion, but this hypothesis could only be proven if previous sera samples were available.
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PMID:HIV infection presenting as Guillain-Barre syndrome in Lusaka, Zambia. 263 6

BALB/c mice infected with ts1, a mutant of Moloney murine leukemia virus-TB, develop generalized body wasting, profound neurologic disorders, severe thymic atrophy and lymphopenia due to destruction of T lymphocytes and drastic immunodeficiency. ts1 was found not only able to infect T lymphocytes but also to impair their function. In addition, ts1 also infects and induces syncyntia formation in macrophages. The genetic determinant(s) responsible for ts1's ability to induce immunodeficiency has been localized to the env gene.
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PMID:ts1, a mutant of Moloney murine leukemia virus-TB, causes both immunodeficiency and neurologic disorders in BALB/c mice. 272 46

3'-Azido-2',3'-dideoxythymidine (AZT) has been administered to 7 patients with human immunodeficiency virus-associated neurological disease: 3 with dementia, 2 with peripheral neuropathy, 1 with dementia and peripheral neuropathy, and 1 with T-10 paraplegia. Six of the patients showed improvement in their neurological dysfunction on being administered AZT, as assessed by clinical evaluation, neuropsychological testing, nerve conduction studies, and/or positron emission tomographic scans. Three of these 6 patients showed sustained improvement 5 to 18 months after the initiation of AZT therapy. These results suggest that certain human immunodeficiency virus-associated neurological abnormalities are at least partially reversible following the administration of antiretroviral therapy and provide a rationale for further studies using antiretroviral chemotherapy.
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PMID:Long-term administration of 3'-azido-2',3'-dideoxythymidine to patients with AIDS-related neurological disease. 283 6

A variety of clinical syndromes, including AIDS and neurological disorders, may follow as a consequence of infection with the human immunodeficiency virus type 1 (HIV-1). It is not yet clear, however, to what extent the destruction of lymphocytes and neural cells associated with these conditions is caused by adverse immune responses to HIV-1 or how much is due to cytopathic effects of the virus itself. Here we document the existence of HLA-restricted, HIV-1-specific cytotoxic T lymphocytes in the cerebrospinal fluid of two AIDS patients manifesting neurologic disorders. These cytotoxic T lymphocytes showed dual specificity, recognizing target cells coated with purified HIV-1 envelope glycoprotein (gp 120) or inactivated HIV-1 in the context of HLA antigens. Cytotoxic T-cell clones derived from one of the AIDS patients revealed restriction specificities representing both HLA class I and HLA class II antigens. Considerable phenotypic heterogeneity was observed amongst these clones, some expressing conventional combinations of cytotoxic T-cell surface markers, and others displaying unusual phenotypes. The presence of HIV-specific cytotoxic T lymphocytes in AIDS patients, and in particular in their cerebrospinal fluid, suggests that these cytotoxic effectors may participate in the lymphoid cell and/or neurologic damage observed in such patients.
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PMID:Phenotypic heterogeneity of cerebrospinal fluid-derived HIV-specific and HLA-restricted cytotoxic T-cell clones. 284 92

Subacute encephalitis caused by infection of the central nervous system by the human immunodeficiency virus (HIV) is the most frequent cause of neurologic dysfunction in patients with the acquired immunodeficiency syndrome (AIDS). This disorder results in progressive cognitive, motor, and behavioral abnormalities in at least two thirds of patients with AIDS. Pathologic evidence of subacute encephalitis is found in 90% of these patients at autopsy. Human immunodeficiency virus is also the etiologic agent of aseptic meningitis, a disease that can occur at the time of seroconversion. Other neurologic disorders frequently associated with HIV include peripheral neuropathies and vacuolar myelopathy. Thus, HIV is neurotropic and may enter the central nervous system early in the course of infection. Neurologic disease may be the only clinical manifestation of HIV infection. Although mechanisms of pathogenesis are unclear, cells of monocyte-macrophage lineage may be important in viral spread to and within the central nervous system. Effective antiviral therapy will probably require penetration of drugs across the blood-brain barrier.
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PMID:Neurologic manifestations of infection with human immunodeficiency virus. Clinical features and pathogenesis. 303 90

A young female patient with a long history of intravenous drug abuse died after a fulminant course of aplastic anemia. At postmortem examination, she was found to have multinucleate giant cells and immunocytochemical evidence of human immunodeficiency virus (HIV) infection of the central nervous system. This case raises the possibility that HIV infection contributed to the patient's aplastic anemia, and suggests that HIV-associated giant cells might be found retrospectively or prospectively within the brains of patients who die of conditions other than those narrowly defined as acquired immune deficiency syndrome (AIDS) or AIDS-related complex (ARC). It furthermore emphasizes that HIV infection of the nervous system is not necessarily accompanied by clinically apparent neurological disease.
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PMID:Evidence for human immunodeficiency virus (HIV) infection of the brain in a patient with aplastic anemia. 321 36

Human immunodeficiency virus (HIV) is the causative agent of the acquired immune deficiency syndrome (AIDS). A large number of AIDS patients show evidence of neurologic involvement, known as AIDS-related subacute encephalopathy, which has been correlated with the presence of HIV in the brain. In this study, two genetically distinct but related viruses were isolated from one patient from two different sources in the central nervous system: brain tissue and cerebrospinal fluid. Both viruses were found to replicate in peripheral blood lymphocytes, but only virus from brain tissue will efficiently infect macrophage/monocytes. The viruses also differ in their ability to infect a brain glioma explant culture. This infection of the brain-derived cells in vitro is generally nonproductive, and appears to be some form of persistent or latent infection. These results indicate that genetic variation of HIV in vivo may result in altered cell tropisms and possibly implicate strains of HIV with glial cell tropism in the pathogenesis of some neurologic disorders of AIDS.
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PMID:Dual infection of the central nervous system by AIDS viruses with distinct cellular tropisms. 364 51

Human immunodeficiency virus (HIV), the etiologic agent of acquired immune deficiency syndrome (AIDS) and AIDS-related complex, has recently been implicated as a factor in the development of AIDS-related neurologic dysfunction and may be responsible for an increasing number of neonatal immunologic and neurologic disorders. However, as yet there is no model system available to investigate the interaction of HIV with the developing human nervous system in vitro. To approximate the intracellular events associated with HIV infection of the human fetus nervous system we infected cells obtained by enzymatic dissociation of aborted human fetus dorsal root ganglia and their attached spinal roots and nerves. The expression of the HIV gag gene protein products (p17 and p24) was detected in a subpopulation of cells with a nonneuronal morphology, reaching a maximum within 3 days. Although 70% of the nonneuronal cells were p17- and p24-positive 3 days after infection, a majority of the cell population survived acute HIV infection, with the expression of p17 and p24 decreasing below the limit of detection by 12 days postinfection. This system may prove useful for examining the neuropathology and neurobiology of acute, persistent, or latent HIV infection of the developing human nervous system.
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PMID:Human immunodeficiency virus infection of the developing human nervous system. 365 7

We found a significant increase in fibronectin receptor (FNR) levels in the sera of adult human immunodeficiency virus type 1 (HIV-1)-infected patients, especially in those with AIDS (1,026.9 +/- 583.9 ng/ml; P < 0.0001). In contrast, AIDS patients with neurologic disorders and HIV-1-seropositive patients showed normal levels of FNR in serum. In addition, HIV-1-infected children showed increased levels of FNR in serum (824.4 +/- 333.5 ng/ml; P = 0.03). We suggest that an increase of FNR levels in AIDS patients is related to enhanced expression of FNR on HIV-1-infected cells.
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PMID:Levels of circulating fibronectin receptor in adult and pediatric patients with human immunodeficiency virus type 1 infection. 749 74

Glia are the predominant brain cells infected by the lentiviruses human immunodeficiency virus (HIV) and feline immunodeficiency virus (FIV). The importance of astrocytes in maintenance of central nervous system homeostasis suggests that astrocytes are likely to play a strategic role in the progression of neurological disease in lentiviral-infected patients. In consideration of this postulate, the ability of FIV to cause injury by infection of cultured feline astroglia was examined via vital fluorescence assays. Intracellular Ca2+ homeostasis, plasma membrane permeability and fluidity, and cytosolic glutathione (GSH) levels were evaluated. Although basal intracellular Ca2+ was not significantly different between groups, FIV-infected astroglia displayed both a significant delay in development of peak Ca2+ levels following ionophore application and a decrease in the amount of Ca2+ released from intracellular stores. Plasma membrane lipid mobility was increased in FIV-infected cells within 24 h of infection. Glutathione levels were affected in a dose dependent fashion. With a standard viral inoculum there was a decrease in GSH which became significant after 8 days postinfection. With a high inoculum dose there was rapid loss of cell viability with an increase in GSH in surviving cells. We have identified several cellular processes altered in FIV-infected astroglia and our findings suggest that FIV-infection of feline astroglia affects cellular membranes, both structurally and functionally.
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PMID:Laser cytometric analysis of FIV-induced injury in astroglia. 764 18


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