Document 0585
 DOCN  M9590585
 TI    Is alcohol consumption a cofactor in the development of acquired
       immunodeficiency syndrome?
 DT    9509
 AU    Wang Y; Watson RR; Nutritional Sciences Program, University of Arizona
       College of; Medicine, Tucson 85724, USA.
 SO    Alcohol. 1995 Mar-Apr;12(2):105-9. Unique Identifier : AIDSLINE
       MED/95290098
 AB    Excessive alcohol (EtOH) consumption and acquired immunodeficiency
       syndrome (AIDS) are two major public health problems in the United
       States. Overwhelming evidence is showing that heavy EtOH ingestion
       broadly suppresses the various arms of immune response, seriously
       impairing the body's normal host defense to invading microbes and
       tumorigenesis. The onset of clinical symptoms of AIDS (low CD4+ T cells
       count, opportunistic infections, and tumors) is quite variable among
       HIV+ individuals with a mean incubation time 3-10 years following
       seroconversion. Because of the deleterious effects of chronic EtOH
       consumption on cytokine release, immune response, host defense,
       nutritional status, and oxidative stress, it has been believed to be a
       possible cofactor that could enhance the host's susceptibility to
       infections, and subsequently increase the rate of AIDS development. The
       purpose of this review is to present evidence indicating clinical
       disorders during EtOH ingestion in murine AIDS. These EtOH-induced
       abnormalities may promote a more rapid development of AIDS in
       HIV-infected individuals.
 DE    Acquired Immunodeficiency Syndrome/*ETIOLOGY  *Alcohol Drinking  Animal
       Cytokines/PHYSIOLOGY  Human  Immunity  Mice  Support, U.S. Gov't, P.H.S.
       JOURNAL ARTICLE  REVIEW  REVIEW, TUTORIAL

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