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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study evaluated the overall survival after AIDS diagnosis of 1,014 patients reported to the Italian AIDS Registry as resident in Tuscany, stratified by age, gender, year of diagnosis, HIV transmission category, initial AIDS-defining disease and CD4+ cells count. The study was a population-based survival analysis, carried out through Kaplan-Meier method (mean survival times-MST-, 1, 2 and 3-year observed survival) and Cox models (crude and adjusted relative risk-RR). The MST was 12.4 months for all cases, increasing from 4-7 months in 1985-1987 to 14 months in 1991-1992. The observed survival was 51.4% at the first year of follow-up, 28.4% at the second year and 14.5% at the third year. The multivariate analysis showed an independent prognostic effect of age, year of diagnosis, initial AIDS-defining disease and CD4+ cells count. The prognosis was worse in cases aged over 44 (reference: 25-29), diagnosed before 1988 (reference: 1991) and with wasting syndrome, toxoplasmosis, HIV encephalopathy or multiple diseases (reference: PCP alone); and better in cases with more than 100 CD4+ cells/mm3 (reference: < or = 50 cells/mm3). The differences in gender and among HIV transmission categories disappeared after age-adjustment. The study confirmed, in an European population-based series, the poor long-term AIDS prognosis and, once AIDS has became clinically manifest, the prognostic value of some clinical and demographic variables.
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PMID:Survival after AIDS diagnosis in Tuscany (Italy), 1985-1992. 908 93

Neurologic problems in AIDS are usually caused by opportunistic infections or secondary malignancy of the central nervous system (CNS), but brain damage occurs primarily as the result of HIV infection in CNS. In one of the typical opportunistic virus infections of CNS, progressive multifocal leukoencephalopathy (PML), oligodendroglial cells which maintain and support myelin sheaths are specifically attacked by JC virus. As the consequence, demyelination occurred, which could well explain the neuronal deficits. In contrast, in HIV the viral target cells are not neuronal cells, but infiltrating macrophages in CNS. Thus, the indirect injury such as HIV-related neurotoxic substances and macrophage-released cytokines would be augmented to induce diffuse neuronal damage in HIV infected brains. Recent discovery of co-receptor, chemokine receptor (CCR5) which is expressed in macrophages, may give a clue to understand the mechanism of HIV encephalopathy more precisely.
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PMID:[Mechanism of neuronal damage in AIDS]. 908 61

The neurologic disease most frequently seen during acquired immunodeficiency syndrome (AIDS) is AIDS dementia complex (ADC) or HIV encephalopathy, which is a direct consequence of HIV-1 infection of the central nervous system (CNS). A limited expression of HIV-1 in CNS and peripheral nervous system (PNS) tissue of AIDS patients in contrast to widespread functional and pathologic abnormalities suggests indirect or immunopathogenetic mechanisms of ADC and HIV-1-associated predominantly sensory neuropathy. Proposed mechanisms include injury of oligodendrocytes by tumor necrosis factor-alpha (TNF-alpha) released from macrophages, calcium dependent excitoneurotoxicity induced by gp120 HIV-1 envelope protein, N-methyl-D-aspartate (NMDA) receptor-mediated neurotoxicity by quinolinic acid, cell injury by HIV-1-specific cytotoxic T cells, and apoptosis of oligodendrocytes or neurons. The amplification of cellular activation by cytokine network and cell-to-cell contact between activated macrophages and neural cells by upregulation of adhesion molecules dramatically enhance toxic effect of macrophage products.
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PMID:[Pathogenesis of HIV-1-associated-neurologic diseases]. 910 91

Chance of opportunistic infections in hospitals is increasing year by year, because of the steady increase in the number of compromised hosts. Opportunistic infections in the nervous system include fungal, protozoal, bacterial and viral infections. Cytomegalovirus and herpes virus (HSV1 and HSV2) cause encephalitis, myelitis and radiculoneuritis. Varicella-zoster virus (VZV) often causes herpes zoster, which sometimes disseminates when immunodeficiency is severe. VZV also causes encephalitis. Progressive multifocal leukoencephalopathy (PML) is caused by JC virus in severely compromised hosts. HIV encephalopathy or AIDS dementia complex is one of late stage complications of HIV infection. Prevalence of PML and HIV encephalopathy among AIDS patients tend to increase as other opportunistic infections became controllable recently. Primary CNS lymphoma in immunocompromised hosts is supposed to be caused by EB virus and/or Kaposi's sarcoma-associated herpes virus (KSHV, HHV8). In this sense, CNS lymphoma and Kaposi's sarcoma can be defined as virus infection-related condition.
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PMID:[Virus-related neurological disorders complicating in compromised hosts]. 910

Neuronal loss in HIV encephalopathy remains a mystery since HIV-1 productively infects macrophage and microglia and only rarely infects neurons in the central nervous system. Apoptosis is a mechanism which may account for the loss of neurons in HIV-1 infected brain. Putative toxic factors that result in neuronal cell death in HIV-1 infection include the regulatory protein Tat, since this protein is known to be released from HIV-1 infected cells. Here we show that Tat induces cell death by apoptosis in cultured human fetal neurons producing characteristic morphological and biochemical features associated with apoptosis. These findings suggest that Tat may play an important role as a secreted, soluble neurotoxin in HIV-1 associated dementia.
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PMID:Human immunodeficiency virus type 1 Tat protein induces death by apoptosis in primary human neuron cultures. 911 Nov 79

To delineate the demographic features and clinical profile of male and female individuals utilizing a respite, rehabilitation and hospice centre in London, a retrospective study of patient notes was undertaken. The subjects were 59 male and 59 female HIV patients at first admission to the hospice. The study revealed clinically important differences between men and women and also identified special problems for African women and intravenous drug users. Women experienced more constipation, headache and musculoskeletal pain than men. Men suffered more neuropathic pain and visual loss. Lower respiratory tract infections were more common in women, especially in those with a history of injection drug use. Gynaecological morbidity was common. There was no difference in AIDS diagnoses between men and women. HIV encephalopathy developed in 23% of the cohort during the follow-up period which has implications for provider units. There are increasing numbers of HIV-positive women and injection drug users being referred for palliative care services. Multidisciplinary teams should be aware of the particular symptom profile of these groups.
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PMID:HIV infection: the spectrum of symptoms and disease in male and female patients attending a London hospice. 915 12

The characteristic trait of the family of lentiviruses (Retroviridae) which includes the human immune deficiency virus (HIV), is the tendency to cause a subacute neurologic disease in their animal host. The neuraxis can be inflicted at all its levels. In the advanced stage of HIV disease, more than 60 percent of patients suffer from a clinically evident neurological dysfunction. Neuropathologic changes are demonstrated in 75 - 90 percent of them at autopsy. HIV enters the CNS during the early phase of infection. HIV replicates predominantly in the nervous tissue macrophages which serve also as intrathecal reservoirs of infection. HIV isolated from the CNS is usually macrophagotropic. Neural cells are not susceptible to a productive HIV infection, contrasting with the permissivity of activated astroglial cells. The neuropathological picture of the brain involvement is typical by the giant multinuclear cells, i.e. fused monocytes/macrophages, then neuronal loss and changes in the white matter. The clinical manifestations of CNS involvement (AIDS encephalopathy) in HIV disease are variable protean, frequently associated with dementia. The pathogenesis of the neurological disease remains elusive. The cells supporting the HIV replication in the CNS (microglia, monocytes, astroglia) do not play a major role in dementia development. The neurotoxicity of viral glycoproteins, virus-induced cytokines and neurotoxin produced by CNS macrophages infected with particularly efficiently replicating HIV strains are being intensively studied. Dementia is associated with an increased virus load in the brain in the advanced stage of HIV disease. Neurotoxicity associated with HIV-infected microglial cells and macrophages activity remain to be considered, for the time being, as the most likely pathogenetic mechanism of neural dysfunction and injury. Our investigations have demonstrated that HIV infection of macrophages stimulate considerably the synthesis of MIP-1-alpha, MIP-1-beta RANTES chemokines (subgroup CC). These substances by their chemoattractant and activating properties may participate in the pathogenesis of HIV/AIDS encephalopathy, contributing to leukocytosis and inflammation, increasing thus the population of HIV-susceptible cells, facilitating their infection and enhancing finally the intrathecal spread of virus. (Tab. 2, Ref. 22.)
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PMID:[Encephalopathy in AIDS--increased formation of beta-chemokines in monocytes after HIV-1 virus infection: mechanisms of CNS involvement]. 933 24

While progress has been made in our knowledge of the natural history of HIV infections, an understanding of the molecular pathogenesis of AIDS encephalopathy remains to be determined. Previously we demonstrated that apoptosis and a deficiency of natural killer (NK) cell activity may play significant roles in the progression of HIV infections. We also reported that intracerebral co-injection of a recombinant HIV-1 fusion protein plus an excitatory amino acid agonist into neonatal rats synergistically produced brain pathology. Here we examine: 1) the effects of the HIV-1 envelope protein, gp-120, on neonatal rat astrocytes in vitro; 2) the spontaneous apoptosis of human neonatal and adult mononuclear leukocytes and, 3) the selective inhibition of NK activity cell from adult AIDS patients by the HIV-1 protein that caused brain pathology in neonatal rats. We demonstrate that gp-120 suppresses fas gene expression, a marker for apoptosis, by neonatal rat astrocytes. Neonatal human mononuclear leukocytes manifest spontaneous apoptosis as measured by DNA ladder formation while cells from adult donors do not. Direct addition of the HIV-1 protein to mononuclear cells in vitro selectively suppressed the NK cell activity from AIDS patients. These results support our premise that HIV-1 proteins are involved in the pathogenesis of AIDS encephalopathy.
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PMID:Molecular mechanisms in the pathogenesis of AIDS encephalopathy. 944 25

HIV type 1 viral quasispecies were amplified by polymerase chain reaction (PCR) in the hypervariable V3 region of gp120 from six different regions of the brain (right and left frontal; right and left parietal; and right and left occipital) and from the peripheral blood mononuclear cells (PBMCs) of a patient who died of AIDS dementia complex (ADC). Cloning and sequencing of the entire V3 region suggested the presence of genetically unique sequences in different regions of the brain. In contrast, the blood-derived viral quasispecies carried homogeneous sequences that were characterized by a single octapeptide crest motif (HLGPGSAF), a motif important in viral fusion. The brain-derived viral strains showed extensive sequence heterogeneity and the presence of seven different octapeptide and four different tetrapeptide crest motifs (HIGPGRAF, RIGPGRAF, HIGPGSAI, HLGPGSAF, HIGPESAI, HLGPESAI, and YLRPGSAF). In addition, the brain-derived strains were also characterized by variable net V3 loop charge and hydrophilicity, along with distinct amino acid changes specific to different brain regions. Together, the sequence and phylogenetic analyses are unique in identifying the complexity of a viral quasispecies and its independent regional evolution within the brain compartment. Uniquely divergent viral strains were identified in the frontal regions and their presence was further supported by the presence of multinucleated giant cells (characteristic of HIV encephalopathy) predominantly in the left and right frontal regions. In summary, these analyses suggest that genetically different populations of HIV-1 may be present in different brain compartments and confirm that specific neurotropic variants may exist.
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PMID:Unique HIV type 1 V3 region sequences derived from six different regions of brain: region-specific evolution within host-determined quasispecies. 945 48

The authors assessed 72 human immunodeficiency virus (HIV)-infected patients with a self-rating slowness scale (SRSS) concerning mental and motor slowness in their activities of daily living. In order to understand the relationship between complaints of slowness and predictor variables, the investigators developed a preliminary model using multiple regression analysis. Reports of slowness on the SRSS were independently associated with self-reported cognitive and neurological symptoms and with peripheral neurological syndromes (e.g., neuropathy, myopathy). Lesser contributions to self-perceived mental and motor slowness were found for neuropsychological measures of information processing speed, severity of the infection, depression, HIV encephalopathy, and sociodemographic factors (e.g., age, education). The relationship among the predictor variables showed that complaints of slowness reflect neurological, psychiatric/psychological, and cognitive symptomatology of the HIV infection.
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PMID:Neurobehavioral correlates of perceived mental and motor slowness in HIV infection and AIDS. 970 43


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