Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The increase of HIV infected population reaching worldwide 10 million of cases leads to a great number of infected women in reproductive age. Finally the perinatally acquired HIV infection has become a great problem. The number of infants with AIDS is estimated at about 160,000. The diagnosis and evaluation of significant clinical symptoms of HIV infection in infants are briefly described in this study. The nervous system being one of targets of HIV infection the neurological manifestation occurring in infants were more extensively discussed. Microencephaly or brain atrophy and psycho-motor developmental delay resulting in progressive or static encephalopathy syndromes were presented.
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PMID:[Central nervous system changes in infants with HIV infection. Epidemiology and neurology]. 752 41

Mice infected with the LP-BM5 murine leukemia virus mixture develop severe immunosuppression and an encephalopathy characterized by spatial learning deficits. Twelve weeks after infection of C57BL/6J mice with LP-BM5, significant (50-60%) reductions in Met-enkephalin and substance P levels were observed in the striatum, whereas somatostatin levels were unchanged. In addition, a 39% decrease in hypothalamic substance P concentrations was observed, with no alteration in Metenkephalin levels. The apparent selectivity of the decrease in neuropeptide concentrations indicates that a functional alteration of the primary striatal efferent neurons occurs in this infection, which may contribute to the impairment of spatial learning observed in these mice. Moreover, this decrease in striatal neuropeptide levels is similar to the neuropathological changes in basal ganglia observed in HIV-infected individuals and is consistent with previous studies suggesting that the LP-BM5-infected mouse may serve as a useful model of AIDS dementia.
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PMID:Striatal met-enkephalin and substance P levels are decreased in mice infected with the LP-BM5 murine leukemia virus. 753 38

The transmission, diagnosis, and clinical manifestations of human immunodeficiency virus (HIV) infection in children up to 13 years of age are reviewed, and maintenance and prophylactic drug therapies for these patients are discussed. HIV can be transmitted from mother to infant in utero, during delivery, or through breast milk. Perinatal transmission accounts for almost 90% of all pediatric HIV infections. HIV infection can be diagnosed with HIV culturing, polymerase chain reaction testing, the enzyme-linked immunosorbent assay, the Western blot antibody assay, or the p24 core-antigen assay. Testing should begin as soon as possible after the at-risk child reaches one month of age. CD4+ lymphocyte counts are also used in diagnosis and monitoring. The median age at diagnosis of AIDS in children with perinatally acquired HIV infection is 12-24 months. Among the many possible clinical features are Pneumocystis carinii pneumonia (PCP), cytomegalovirus infection, failure to thrive, encephalopathy, recurrent bacterial infection, thrush, lymphoid interstitial pneumonitis, lymphadenopathy, pancreatis, hepatitis, anemia, and thrombocytopenia. Zidovudine is considered the drug of choice for initial therapy in HIV-infected children and is indicated for asymptomatic infection, early symptomatic disease, and advanced disease. However, new research is questioning the role of zidovudine monotherapy. Didanosine is the only agent with FDA-approved labeling for use as second-line therapy in children who do not respond to or become resistant to zidovudine. Agents under investigation for pediatric use are zalcitabine, stavudine, lamivudine, and nevirapine. Drug combinations, such as zidovudine plus didanosine, are also being examined. Zidovudine appears to reduce the rate of maternal transmission of HIV. Agents used prophylactically against PCP in children are trimethoprim-sulfamethoxazole, dapsone, and inhaled or i.v. pentamidine. HIV-infected children should also received prophylaxis against recurrent bacterial infections. The standard pediatric immunization schedule is used, but inactivated injectable poliovirus vaccine must be given instead of the live oral vaccine. Zidovudine remains the first-line agent for treating HIV infection in children. Alternatives are available for those who do not respond to zidovudine.
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PMID:Human immunodeficiency virus infection in children. 764 Oct 35

Eight of 13 children pre- or perinatally infected with the HIV virus subsequently developed neurological symptoms. Three children also had other nonspecific symptoms (fever, lymphadenopathy, diarrhoea, hepatosplenomegaly, failure to thrive and mucocutaneous thrush). Five children developed illnesses associated with AIDS (opportunistic infections, cachexia and lymphocytic interstitial pneumonia). The neurological abnormalities predominantly affected motor functions, only later also involving sensory ones. Motor, cognitive and language development was impaired in all eight children. A loss of developmental milestones occurred in three children with HIV encephalopathy: they have since died. In all the children the HIV infection caused symptoms within the first year, progressing more quickly in the three with encephalopathy. There were no discernible risk factors to account for the difference in the course of the disease.
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PMID:[Cerebral symptoms in pre- or perinatally HIV-infected children]. 768 71

The human immunodeficiency virus type 1 (HIV-1) protein Tat is known to be released from HIV-1-infected cells. We show that micromolar concentrations of Tat depolarized young rat and adult human neurons. In addition, Tat, at similar concentrations, was toxic to human fetal neurons in culture. Tat-induced responses were insensitive to the Na+ channel blocker tetrodotoxin, suggesting a direct effect of Tat on neurons. Tat-induced depolarizations and cytotoxicity were blocked by the excitatory amino acid antagonist kynurenate. The N-methyl-D-aspartate receptor antagonist D-2-amino-5-phosphonovalerate had little effect on Tat-induced depolarizations but did provide protection from Tat neurotoxicity. These results suggest that Tat, released from HIV-1-infected cells, may be an important mediator of neurotoxicity observed in HIV-1 encephalopathy.
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PMID:Human immunodeficiency virus type 1 tat activates non-N-methyl-D-aspartate excitatory amino acid receptors and causes neurotoxicity. 769 37

Microglial cell activation, myelin alteration, and abundant tumor necrosis factor (TNF)-alpha message have been observed in the brains of some human immunodeficiency virus type 1 (HIV-1)-infected and demented patients. We therefore used cultures of purified human microglia and oligodendrocytes derived from adult human brain to examine the role of TNF-alpha in HIV-1 encephalopathy. Human microglia synthesize TNF-alpha message and protein in vitro. When these cells were infected with HIV-1 JrFL and maintained in the presence of TNF-alpha antibodies, soluble TNF-alpha receptors, or the TNF-alpha inhibitor pentoxifylline, viral replication was delayed or strongly inhibited. Both human microglia and oligodendrocytes express the two TNF receptors, TNF-R1, which has been implicated in cytotoxicity, and TNF-R2. While TNF-alpha may enhance HIV-1 replication in an autocrine manner, it is not toxic for microglia. In contrast, recombinant human TNF-alpha causes oligodendrocyte death in a dose-dependent manner. In situ detection of DNA fragmentation in some cells indicated that oligodendrocyte death may occur by apoptosis. Addition of live microglia or medium conditioned by these cells also resulted in 30 to 40% oligodendrocyte death, which was largely prevented by TNF-alpha inhibitors. We propose that TNF-alpha plays a dual role in HIV-1 encephalopathy, enhancing viral replication by activated microglia and damaging oligodendrocytes. Thus, TNF-alpha inhibitors may alleviate some of the neurological manifestations of acquired immunodeficiency syndrome.
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PMID:In vitro evidence for a dual role of tumor necrosis factor-alpha in human immunodeficiency virus type 1 encephalopathy. 766 40

The Czech Republic is characterized here as both a low HIV prevalence area (1.64 registered positivity per 10(5) population and 45 AIDS patients notified in the 1986-93 period) and a low tuberculosis prevalence area (mortality rate 0.8, incidence of bacillary pulmonary cases 11.3 per 10(5) population and risk of infection 0.04 in 1990). From 1986 to 1993 a total of 10 cases of mycobacterial infections complicating AIDS or ARC disease were registered in the Czech Republic in 9 male patients aged from 29 to 55, 8 homosexuals, and one woman aged 48. Classical pulmonary tuberculosis caused by M. tuberculosis was diagnosed in one male patient and was controlled by antituberculosis chemotherapy. The remaining mycobacterial infections were caused by the following opportunistic mycobacterial pathogens. (a) M. avium in five individuals, four of them died of a disseminated disease; (b) M. kansasii--in two patients, one died of a disseminated infection; (c) M. xenopi--involved in a fatal generalized CMV, and cryptococcal and mycobacterial infection; (d) M. fortuitum caused a generalized disease in a case of exhaustive multifocal encephalopathy. Authors conclude that under conditions of low prevalence of both HIV and tuberculosis infection the risk to AIDS patients of contracting classical tuberculosis is low. A relatively frequent occurrence of non-tuberculosis mycobacterial disease in AIDS patients afflicted with the impaired immunity is explained by transmission of opportunistic mycobacteria from the environment.
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PMID:Mycobacterial infections in patients with AIDS in a low HIV prevalence area. 769 15

We report the results of a hospital-based study of 188 consecutive patients seropositive for the human immune deficiency virus type 1 (HIV-1) who presented in a 4-year period (1988-1991) with possible signs or symptoms of first-ever central nervous system disease. Confirmed diagnoses were cerebral toxoplasmosis in 47 patients (25.0%), HIV-1 encephalopathy in 19 (10.1%), progressive multifocal leucoencephalopathy (PML) in 9 (4.8%), cerebral lymphoma in 1 (0.5%), and other conditions in 9 patients (4.8%). Seventy-three subjects (38.8%) showed focal brain lesions on initial computed tomography or magnetic resonance imaging, which were assessed prospectively. Positive predictivity for toxoplasmosis was 100% if multiple lesions occurred in combination with mass effect or contrast enhancement (23 patients), or if at least one space-occupying or enhancing lesion was located in the basal ganglia or the thalamus (26 patients). Solitary lesions with mass effect or contrast enhancement were seen in 26 patients and were caused by cerebral toxoplasmosis in 22 (84.6%). Eight of the 9 PML patients presented with one or more non-enhancing, non-mass lesions, although the predictive value of this pattern was low (47.1% for PML). Thus, in our epidemiological context, certain imaging findings in HIV-1-seropositive patients were highly predictive of cerebral toxoplasmosis. This may differ from findings from other parts of the world where cerebral toxoplasmosis may be less prevalent among HIV-1-infected individuals.
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PMID:Focal brain lesions in patients with AIDS: aetiologies and corresponding radiological patterns in a prospective study. 770 92

Thirty-three patients with AIDS were subjected to neuropsychological and immunological testing with semi-annual examinations over a two year period. No patient had signs of opportunistic infections or neoplasms in the CNS. Patients who were neuropsychologically impaired at the time of AIDS diagnosis (n = 12) survived for a significantly shorter period than did the non-impaired subjects (n = 21), and neuropsychological function at first test had a significant predictive value concerning survival time. The poor prognosis associated with impaired neuropsychological status was seen also in patients treated with zidovudine (ZDV). Of the 21 patients who started ZDV treatment shortly after the first neuropsychological examination, 12 were retested. Follow-up data showed that this group of patients had a significant improvement in neuropsychological functioning during the first 6 months. However, a decrease in performance was observed at second follow-up. In the group not treated with ZDV (n = 7), two initially normal patients developed signs of HIV-encephalopathy, while none of the initially normal ZDV-treated patients did so. This might suggest a prophylactic effect of ZDV on development of neuropsychological dysfunction. Changes in neuropsychological test results were correlated with changes in serum concentration of neopterin irrespective of ZDV treatment, suggesting that monocyte/macrophage activation may be involved in the pathogenesis of HIV-encephalopathy.
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PMID:A follow-up study of neuropsychological functioning in AIDS-patients. Prognostic significance and effect of zidovudine therapy. 779 39

Neurological manifestations of HIV disease occur in most adults and children with AIDS. Many of those affected will inevitably suffer clinical neurological deficits involving mental function, movement, and sensation. Surprisingly, there are not as yet adequate monitoring systems to predict the onset and/or progression of HIV infection of the CNS. Neurological, neuropsychological, CSF, and magnetic resonance imaging (MRI) analyses cannot accurately detect mental deterioration during advancing HIV disease. Reports suggest that in vivo proton MR spectroscopy (1H MRS) of the brain could be a predictor of virus-induced neurological deterioration. H MRS can measure N-acetylaspartate (NAA), a metabolite present only in neurons. Decreased NAA reflects neuronal loss seen during HIV infection of brain. To uncover possible associations between NAA levels and HIV-induced neurological disease we performed serial 1H MRS brain tests in HIV-infected patients with or at risk for encephalopathy. Serial testing, for 1 year, of 10 patients showed that brain NAA levels decreased in all HIV-infected subjects. The most severe NAA reductions were associated with progressive neurological impairment. These findings suggest that NAA can be used as a noninvasive measure of neuronal loss in patients with HIV disease. Most important, the results suggest that 1H MRS could be used to monitor therapeutics directed against HIV infection within the CNS.
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PMID:Prospective utility of cerebral proton magnetic resonance spectroscopy in monitoring HIV infection and its associated neurological impairment. 781 49


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