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      Effects of Alcohol and HIV Infection on the Central Nervous System

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          Abstract

          Many people at risk for or infected with the human immunodeficiency virus (HIV) are heavy drinkers. Both HIV infection and heavy alcohol use adversely affect the immune system and central nervous system (CNS) function. However, little research has addressed the effects of heavy alcohol use on the severity and progression of HIV disease, including the development of HIV-associated CNS disease. Animal and in-vitro studies suggest that alcohol impairs various aspects of the immune system and increases the susceptibility to HIV infection, but may not accelerate progression of HIV disease. However, heavy alcohol use may interfere with the patient’s adherence to antiretroviral treatment regimens. Neuropathological and neuropsychological studies have indicated that certain brain areas are affected by both HIV-infection and chronic alcohol abuse. Magnetic resonance spectroscopy studies of both HIV-positive and HIV-negative people who were either heavy or light drinkers found that chronic alcohol abuse exacerbates some metabolic injury in the brains of HIV-infected people, although this effect may be less pronounced in patients receiving effective antiretroviral therapy.

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          Most cited references27

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          The brain in AIDS: central nervous system HIV-1 infection and AIDS dementia complex.

          Infection with human immunodeficiency virus type 1 (HIV-1) is frequently complicated in its late stages by the AIDS dementia complex, a neurological syndrome characterized by abnormalities in cognition, motor performance, and behavior. This dementia is due partially or wholly to a direct effect of the virus on the brain rather than to opportunistic infection, but its pathogenesis is not well understood. Productive HIV-1 brain infection is detected only in a subset of patients and is confined largely or exclusively to macrophages, microglia, and derivative multinucleated cells that are formed by virus-induced cell fusion. Absence of cytolytic infection of neurons, oligodentrocytes, and astrocytes has focused attention on the possible role of indirect mechanisms of brain dysfunction related to either virus or cell-coded toxins. Delayed development of the AIDS dementia complex, despite both early exposure of the nervous system to HIV-1 and chronic leptomeningeal infection, indicates that although this virus is "neurotropic," it is relatively nonpathogenic for the brain in the absence of immunosuppression. Within the context of the permissive effect of immunosuppression, genetic changes in HIV-1 may underlie the neuropathological heterogeneity of the AIDS dementia complex and its relatively independent course in relation to the systemic manifestations of AIDS noted in some patients.
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            Consequences of alcohol consumption on host defence.

            B Szabo (2015)
            This communication reviews recent literature and summarizes current views on the immunomodulatory effects of acute and chronic alcohol consumption. Chronic and even acute, moderate alcohol use can increase host susceptibility to infections caused by bacterial and viral pathogens. Impaired host defence after alcohol exposure appears to be linked to a combination of decreased inflammatory response, altered cytokine production, and abnormal reactive oxygen intermediate generation. Furthermore, cellular immunity, particularly antigen-specific immune response, is impaired by both acute and chronic alcohol use. Although T lymphocyte functions can be directly affected by ethanol, decreased antigen presenting cell function appears to be a key element in the ethanol-induced decrease in cell-mediated immunity. In addition, a preferential induction of Th2 vs Th1 immune response has been suggested, based on the increased immunoglobulin levels seen in chronic alcoholics. The effects of chronic and acute alcohol consumption in humans, animal models and in vitro systems on host defence and immunity are discussed in the context of the functional abnormalities of T and B lymphocytes, natural killer cells and monocytes/macrophages resulting in the altered immune response seen after alcohol use.
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              Brain shrinkage in alcoholics: a decade on and what have we learned?

              Brain atrophy in alcoholics has been identified using both radiological and pathological techniques. However the magnitude and topography of the atrophy, and the factors which contribute to it, are unclear. This review compares the results of imaging and pathological studies in alcoholics examining variables which may contribute to any discrepancies. We conclude that significant brain damage does occur as a result of alcohol abuse per se, that the damage is regionally specific with the frontal lobes being particularly affected, and that both grey matter and white matter components are damaged.
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                Author and article information

                Journal
                Alcohol Res Health
                Alcohol Res Health
                Alcohol Research & Health
                National Institute on Alcohol Abuse and Alcoholism
                1535-7414
                1930-0573
                2001
                : 25
                : 4
                : 288-298
                Affiliations
                Dieter J. Meyerhoff, Ph.D., is an associate professor in the Department of Radiology and Department of Veterans’ Affairs Medical Center, University of California San Francisco, San Francisco, California
                Article
                arcr-25-4-288
                6705701
                11910707
                8fc00acc-3167-40a3-b6aa-41eacb384990
                Copyright @ 2001

                Unless otherwise noted in the text, all material appearing in this journal is in the public domain and may be reproduced without permission. Citation of the source is appreciated.

                History
                Categories
                Articles

                hiv infection,central nervous system,immune system,heavy aod (alcohol and other drug) use,chronic aode (effects of aod use, abuse, and dependence),drug therapy,patient compliance,brain damage,neuropathy

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