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)

In addition to immunodeficiency, human immunodeficiency virus type 1 (HIV-1) can cause cognitive impairment and dementia through direct infection of the brain. To investigate the adaptive process and timing of HIV-1 entry into the central nervous system, we carried out an extensive genetic characterization of variants amplified from different regions of the brain and determined their relatedness to those in lymphoid tissue. HIV-1 genomes infecting different regions of the brain of one study subject with HIV encephalitis (HIVE) had a mosaic structure, being assembled from different combinations of evolutionarily distinct lineages in p17(gag), pol, individual hypervariable regions of gp120 (V1/V2, V3, V4, and V5), and gp41/nef. Similar discordant phylogenetic relationships were observed between p17(gag) and V3 sequences of brain and lymphoid tissue from three other individuals with HIVE. The observation that different parts of the genome of HIV infecting a particular tissue can have different evolutionary histories necessarily limits the conclusions that can be drawn from previous studies of the compartmentalization of distinct HIV populations in different tissues, as these have been generally restricted to sequence comparisons of single subgenomic regions. The complexity of viral populations in the brain produced by recombination could provide a powerful adaptive mechanism for the spread of virus with new phenotypes, such as antiviral resistance or escape from cytotoxic T-cell recognition into existing tissue-adapted virus populations.
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PMID:Mosaic structure of the human immunodeficiency virus type 1 genome infecting lymphoid cells and the brain: evidence for frequent in vivo recombination events in the evolution of regional populations. 1048 26

Despite dramatic improvements in the therapeutic management of clients with human immunodeficiency virus (HIV) disease, cognitive disorders still appear as clinical manifestations of the illness trajectory. The development of neuro-cognitive impairment is associated with high levels of HIV activity and the resultant severe degree of immunosuppression. Although many clinicians almost exclusively associate HIV-related cognitive dysfunction with HIV encephalopathy and dementia, the etiologic conditions are numerous and include not only HIV infection affecting the brain, but also infections and neoplasms, as well as adverse effects of prescribed therapies. Treatment strategies include pharmacologic interventions, alternative and complementary therapies, and milieu management.
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PMID:Neurocognitive disorders seen in HIV disease. 1083 52

The concept of slow virus diseases was developed by Sigurdsson in the 1950s in studies of infections of Icelandic sheep, including Visna, a slow (lenti) viral infection of the central nervous system. Human immunodeficiency virus (HIV) belongs to the same lentivirus subfamily of retroviruses and causes significant dysfunction of all levels of the nervous system. Highly active antiretroviral therapy should allow host control of opportunistic infections, producing a clinical state of chronic-treated HIV. However, viral persistence may occur in the sanctuary of the central nervous system. As a consequence, major disabilities in the chronic-treated phase of the HIV epidemic may include cognitive impairment, gait disorders, and various pain syndromes. Policy planning will need to take into account the long-term residential, social, and health care needs of this population.
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PMID:Chronic-treated HIV: a neurologic disease. 1085 1

To prove that primitive reflexes are independent markers of symptomatic human immunodeficiency virus type-1 (HIV-1) infection, a case-control study was carried out in a tertiary care, university teaching hospital. Thirty HIV-1-positive symptomatic cases, 30 seropositive asymptomatic controls and 30 HIV-1 seronegative controls consented to participate and were selected consecutively. A single examiner blinded to serostatus administered the Mini-Mental State Exam and a structured neurological exam to each participant. Up to 45% of cases had cognitive impairment. The occurrence of neurologic signs between seropositive cases and seropositive controls was similar, but the number of primitive reflexes was significantly higher in cases (P < 0.001). By multivariate discriminant analysis, all primitive reflexes but two correctly classified 83.3% of all participants (P = 0.0013). The model had a positive predictive value of 97% when motor, mood, and cognitive symptoms were added (P = 0.0001). Primitive reflexes were independent predictors of HIV-1 serostatus, especially for those with cognitive dysfunction. Primitive reflexes should be included in future case definitions of HIV-1-related neurocognitive disorders.
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PMID:Multivariate analysis of primitive reflexes in patients with human immunodeficiency virus type-1 infection and neurocognitive dysfunction. 1093 80

HIV infection at late stages is associated with neurological complications including impaired motor and cognitive functions. We used simian immunodeficiency (SIV)-infected rhesus monkeys, an animal model of HIV infection, to investigate changes in choline acetyltransferase (ChAT) activity, a biochemical marker of cognitive function, in post-mortem brains during early, asymptomatic SIV infection and AIDS. ChAT activity was dramatically reduced in putamen and hippocampus already during asymptomatic infection. In animals with AIDS, ChAT activity was further decreased. The reduction of ChAT was not related to brain viral load or CNS pathological lesions. Our results demonstrate deficits in ChAT activity already during the first months of SIV infection and imply that cognitive dysfunction may occur early in immunodeficiency viral infections.
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PMID:Brain choline acetyltransferase reduction in SIV infection. An index of early dementia? 1094 91

Human immunodeficiency virus-cognitive motor complex (HIV-CMC), a common complication of the acquired immunodeficiency syndrome (AIDS), is characterized by progressive cognitive impairment and motor dysfunction. Functional imaging methods, such as single-photon emission computed tomography (SPECT) and proton magnetic resonance spectroscopy ((1)H-MRS), have been applied to assess the severity of brain injury. However, it is unclear which of these two methods is more sensitive in detecting brain abnormalities in patients with early HIV-CMC. Twenty-four HIV-CMC patients were compared with 34 healthy subjects; each had quantitative SPECT ((133)Xenon-calibrated (99m)Tc-HMPAO) and quantitative (1)H-MRS. Both modalities were co-registered in order to assess regional cerebral blood flow (rCBF) and metabolite concentrations within the same voxel of interest in four brain regions (midfrontal and midparietal gray matter, temporoparietal white matter, and basal ganglia). On SPECT, only the temporoparietal white matter showed a trend for decreased rCBF in HIV-CMC patients (-13%, P = 0.06). On MRS, HIV-CMC patients showed significantly reduced creatine concentration in the basal ganglia (-8%, P = 0.008), as well as increased myoinositol concentrations in the basal ganglia (+25%, P = 0.01) and the temporoparietal white matter (+18%, P = 0.08). There was no significant correlation between SPECT and MRS variables in the patients in any region. (1)H MRS showed abnormal neurochemistry in the basal ganglia, whereas rCBF on SPECT was normal in the same region. This finding suggests that metabolite concentrations on (1)H MRS are better surrogate markers than rCBF measurements with SPECT for the evaluation of brain injury in early HIV-CMC. J. Magn. Reson. Imaging 2000;12:859-865.
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PMID:Changes in cerebral metabolism are detected prior to perfusion changes in early HIV-CMC: A coregistered (1)H MRS and SPECT study. 1110 23

Approximately two thirds of patients with human immunodeficiency virus encephalitis (HIVE) show cognitive impairment and neurodegeneration, while one third are cognitively unimpaired and their neuronal populations are preserved. Thus, it is possible that these individuals might have the capacity to produce neurotrophic factors capable of protecting neurons against the deleterious effects of HIV. In this context, the main objective of this study was to determine whether fibroblast growth factor 1 (FGF1) is protective against HIV. For this purpose levels of FGF1 immunoreactivity were determined in the frontal cortex of 35 AIDS cases subdivided into 4 groups according to the presence or absence of HIVE and neurodegeneration. In cases without both HIVE and neurodegeneration, mild to moderate levels of FGFI immunoreactivity were observed in pyramidal neurons, while in cases with HIVE but without neurodegeneration, levels were significiantly elevated. In contrast, individuals with both HIVE and neurodegeneration showed low levels of neuronal FGF1 immunoreactivity. Furthermore, studies in primary human neuronal cultures treated with the HIV envelope protein-gp120 in the presence or absence of FGF1 showed that FGF1 was protective against gpl20 neurotoxicity in a dose-dependent manner. Taken together, these results support the notion that upregulation of certain neurotrophic factors, such as FGF1, might protect the central nervous system from the neurotoxic effects of HIV.
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PMID:Amelioration of neurotoxic effects of HIV envelope protein gp120 by fibroblast growth factor: a strategy for neuroprotection. 1124 13

Human immunodeficiency virus infection (HIV) at late stages of the disease is accompanied by neurological complications, including motor, behavioral and cognitive impairment. Using simian immunodeficiency virus (SIV)-infected rhesus monkeys, an animal model of HIV infection, we found that during the asymptomatic SIV infection dopamine (DA) deficits are early components of central nervous system (CNS) dysfunction. To investigate the role of the DA system in SIV infection and to restore the DA deficiency, we administered selegiline, an agent with DAergic and neuroprotective properties, to SIV-infected monkeys. Selegiline increased DA availability but induced CNS vacuolization, SIV encephalitic lesions, and enhanced CNS viral replication during early SIV infection. The pathological changes seem to be mediated by DA, as treatment with L-DOPA, the precursor of DA, had similar effects. We propose that any natural or induced DAergic dysregulation which results in increased DA availability may potentiate HIV-associated neurological disease (ND). Our findings raise new questions regarding the pathogenesis of HIV-ND and generate concerns about the safety of dopaminergic drugs in the clinical management of HIV-infected patients.
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PMID:Enhancement of central nervous system pathology in early simian immunodeficiency virus infection by dopaminergic drugs. 1127 77

The Mental Alternation Test (MAT) is a bedside test of cognition that was used for the detection of human immunodeficiency virus (HIV)-related cognitive impairment. It has been shown to have good reproducibility and inter-rater reliability, and takes only 60 seconds to administer. To assess the utility of the MAT in the geriatric primary care and geriatric psychiatric settings, we used the Mini-Mental State Examination (MMSE) as a further validation of the test. This cohort study included 20 geriatric psychiatric inpatients, 15 normal geriatric controls, and four normal adult controls. The study was conducted within the inpatient psychiatric unit of a referral hospital. Scores on the MAT and the MMSE were compared using correlation calculations. Test score means and standard deviations were computed for each study population. Test score cutoffs derived from a previous study were used to determine the sensitivity and specificity of the MAT as compared with the MMSE. The MAT score was found to correlate significantly with the MMSE score (r =.84, P <.0001). Scores on the MAT were predictive of scores on the MMSE, with a sensitivity of 91% and a specificity of 100%. We conclude that MAT is a good test of cognition in both geriatric primary care and geriatric psychiatric populations. It has both good specificity and sensitivity, and its ease of administration and inter-rater reliability make it a useful diagnostic tool for identifying those patients who may need further cognitive evaluations.
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PMID:Validation of the Mental Alternation Test with the Mini-Mental State Examination in geriatric psychiatric inpatients and normal controls. 1134 38

The relationship between monocyte immune responses and cognitive impairment during progressive human immunodeficiency virus type 1 (HIV-1) infection was investigated in 28 subjects receiving highly active antiretroviral therapy. The mean+/-SEM CD4(+) T lymphocyte count and virus load for all patients were 237+/-41 cells/mm(3) and 77,091+/-195,372 HIV-1 RNA copies/mL, respectively. Levels of soluble tumor necrosis factor-alpha type II receptor (sTNF-RII) and soluble CD14 (sCD14) were measured in plasma by ELISA and were correlated with results from neuropsychological, magnetic resonance imaging, and magnetic resonance spectroscopy tests. Plasma sCD14 and sTNF-RII levels were elevated in subjects with cognitive impairment and in those with brain atrophy. Furthermore, both factors were correlated with spectroscopic choline:creatine ratios. These findings support the idea that peripheral immune responses are linked to cognitive dysfunction during advanced HIV-1 disease.
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PMID:Plasma levels of soluble CD14 and tumor necrosis factor-alpha type II receptor correlate with cognitive dysfunction during human immunodeficiency virus type 1 infection. 1151 30


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