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      Human immunodeficiency virus and the central nervous system

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          Abstract

          The pandemic of HIV/AIDS continues to grow daily. Incident cases among women, intravenous drug users and ethnic minorities comprise the fastest growing segment of the HIV-infected population, and the number of HIV-infected individuals over the age of 50 is growing rapidly. Today, the central nervous system and the immune system are seen as main targets of HIV infection. Significant progress in the knowledge and treatment of AIDS has been obtained in recent years. The neurological manifestations directly related to HIV are acute viral meningitis, chronic meningitis, HIV-associated dementia (HAD), vacuolar myelopathy, and involvement of the peripheral nervous system.

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          The AIDS dementia complex: I. Clinical features.

          Ashleigh R. Price, Lee Jordan, B Navia (1986)
          Of 70 autopsied patients with the acquired immune deficiency syndrome (AIDS), 46 suffered progressive dementia that was frequently accompanied by motor and behavioral dysfunction. Impaired memory and concentration with psychomotor slowing represented the most common early presentation of this disorder, but in nearly one half of the patients either motor or behavioral changes predominated. Early motor deficits commonly included ataxia, leg weakness, tremor, and loss of fine-motor coordination, while behavioral disturbances were manifested most commonly as apathy or withdrawal, but occasionally as a frank organic psychosis. The course of the disease was steadily progressive in most patients, and at times was punctuated by an abrupt acceleration. However, in 20% of patients a more protracted indolent course was observed. In the most advanced stage of this disease, patients exhibited a stereotyped picture of severe dementia, mutism, incontinence, paraplegia, and in some cases, myoclonus. The high incidence and unique clinical presentation of this AIDS dementia complex is consistent with the emerging concept that this complication is due to direct brain infection by the retrovirus that causes AIDS.
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            Chemokines and activated macrophages in HIV gp120-induced neuronal apoptosis.

            Allan Lipton, M Kaul (1999)
            HIV-1 glycoprotein gp120 induces injury and apoptosis in rodent and human neurons in vitro and in vivo and is therefore thought to contribute to HIV-associated dementia. In addition to CD4, different gp120 isolates bind to the alpha- or beta-chemokine receptors CXCR4 and CCR5, respectively. These and other chemokine receptors are on brain macrophages/microglia, astrocytes, and neurons. Thus, apoptosis could occur via direct interaction of gp120 with neurons, indirectly via stimulation of glia to release neurotoxic factors, or via both pathways. Here we show in rat cerebrocortical cultures that recapitulate the type and proportion of cells normally found in brain, i.e., neurons, astrocytes, and macrophages/microglia, that the beta-chemokines RANTES (regulated on activation, normal T cell expressed and secreted) and macrophage inflammatory protein (MIP-1beta) protect neurons from gp120SF2-induced apoptosis. The gp120SF2 isolate prefers binding to CXCR4 receptors, similar to the physiological alpha-chemokine ligands, stromal cell-derived factor (SDF)-1alpha/beta. SDF-1alpha/beta failed to prevent gp120SF2 neurotoxicity, and in fact also induced neuronal apoptosis. We could completely abrogate gp120SF2-induced neuronal apoptosis with the tripeptide TKP, which inhibits activation of macrophages/microglia. In contrast, TKP or depletion of macrophages/microglia did not prevent SDF-1 neurotoxicity. Inhibition of p38 mitogen-activated protein kinase ameliorated both gp120SF2- and SDF-1-induced neuronal apoptosis. Taken together, these results suggest that gp120SF2 and SDF-1 differ in the cell type on which they stimulate CXCR4 to induce neuronal apoptosis, but both ligands use the p38 mitogen-activated protein kinase pathway for death signaling. Moreover, gp120SF2-induced neuronal apoptosis depends predominantly on an indirect pathway via activation of chemokine receptors on macrophages/microglia, whereas SDF-1 may act directly on neurons or astrocytes.
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              Incidence and prevalence of neurological disorders associated with HIV since the introduction of highly active antiretroviral therapy (HAART).

              U Hengge, M. Maschke, O Kastrup … (2000)
              To determine the change of incidence and prevalence of neurological disorders caused by the human immunodeficiency virus (HIV) and opportunistic infections in HIV positive patients under treatment since the introduction of highly active antiretroviral therapy (HAART). The data of all HIV infected patients were retrospectively analysed, who were examined in the HIV outpatients clinic of the neurological department of the University Clinic Essen between 1995 and 1998 (n=563, total number of visits=735). Data from identified patients were divided into two groups according to the time of examination from 1995 to 1996 (334 visits) and from 1997 to 1998 (401 visits). The incidence and prevalence of neurological disorders were statistically compared between both time intervals. Significantly more patients received HAART in 1997-8 (p<0. 001) and mean CD4+ cell count was significantly higher in 1997-8 (p<0.001). The prevalence of HIV associated dementia and HIV associated polyneuropathy were significantly lower in 1997-8 (both: p=0.02) and the incidence of toxoplasma encephalitis decreased from 5.7% in 1995-6 to 2.2% in 1997-8 (p=0.015). Based on the small number of patients significant changes in HIV associated myopathy, progressive multifocal leukoencephalopathy, cryptoccocal meningitis, and cytomegalovirus-encephalitis could not be detected. The prevalence of the most frequent HIV associated neurological disorders and incidence of toxoplasma encephalitis decreased since the introduction of HAART. This may be due to the improvement of immunostatus by HAART as demonstrated by the higher CD4+ cell count in the later time interval. Direct antiretroviral effects within the nervous system may be considered causative as well. The prevalence and incidence of HIV associated neurological disorders and opportunistic CNS infections decreased after introduction of HAART.
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                Author and article information

                Journal
                Journal ID (publisher-id): bjid
                Title: Brazilian Journal of Infectious Diseases
                Abbreviated Title: Braz J Infect Dis
                Publisher: Brazilian Society of Infectious Diseases (Salvador, BA, Brazil )
                ISSN (Print): 1413-8670
                ISSN (Electronic): 1678-4391
                Publication date (Print and electronic): February 2006
                Volume: 10
                Issue: 1
                Pages: 41-50
                Affiliations
                [01] Curitiba PR orgnameUniversidade Federal do Paraná orgdiv1Neurology Unit Brazil
                [02] San Diego CA orgnameUCSD orgdiv1HIV Neurobehavioral Research Center USA
                Article
                Publisher ID: S1413-86702006000100009 Publisher ID: S1413-8670(06)01000109
                DOI: 10.1590/S1413-86702006000100009
                SO-VID: 768a2672-cf10-44b6-aa30-4f9247df6823
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                History
                Date received : 11 September 2005
                Date revision received : 07 January 2006
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 88, Pages: 10
                Product

                SciELO Brazil

                Self URI: Full text available only in PDF format (EN)
                Categories
                Subject: Review Articles

                Keywords: HIV dementia,AIDS,HIV,chemokines,viral load,cerebrospinal fluid,central nervous system
                Data availability:
                Keywords: HIV dementia, AIDS, HIV, chemokines, viral load, cerebrospinal fluid, central nervous system

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