       Document 0132
 DOCN  M9630132
 TI    Quinolinic acid levels in a murine retrovirus-induced immunodeficiency
       syndrome.
 DT    9603
 AU    Sei Y; Paul IA; Saito K; Layar R; Hartley JW; Morse HC 3rd; Skolnick P;
       Heyes MP; Laboratory of Neuroscience, National Institute of Diabetes,;
       Digestive and Kidney Diseases, National Institutes of Health,; Bethesda,
       Maryland, USA.
 SO    J Neurochem. 1996 Jan;66(1):296-302. Unique Identifier : AIDSLINE
       MED/96102947
 AB    Mice infected with the retrovirus mixture designated LP-BM5 murine
       leukemia virus (MuLV) develop an immunosuppressive disease. Quinolinic
       acid (QUIN) is an endogenous neurotoxic N-methyl-D-aspartate agonist
       that may contribute to the pathogenesis of HIV-associated neurologic
       disease. In the present study, the levels of QUIN in brain and blood
       were measured in mice infected with LP-BM5 MuLV and compared with those
       in uninfected mice and mice infected with the nonpathogenic strain of
       ecotropic MuLV (helper component of LP-BM5 MuLV). Infection with LP-BM5
       MuLV resulted in progressive increases in blood QUIN levels beginning 2
       weeks after inoculation that peaked by 16 weeks postinfection. QUIN
       levels were also increased in cerebral cortex, hippocampus, and
       striatum. In systemic tissues, QUIN levels were increased in lung,
       liver, and spleen. In contrast, infection with the ecotropic viral
       component of the LP-BM5 MuLV mixture was not associated with any changes
       in brain, blood, or systemic tissue QUIN levels, even though helper
       virus burdens were comparable to those in mice infected with LP-BM5
       MuLV. Treatment of LP-BM5 MuLV-infected mice with the antiretroviral
       agent zidovudine (azidothymidine) significantly reduced blood and brain
       QUIN levels in association with reductions in viral load in brain and
       spleen. These observations suggest that elevated QUIN production is not
       attributable to productive infection with retrovirus per se but occurs
       in response to an agent or agents, such as cytokines, that are produced
       by the host in response to virus infection.
 DE    Animal  *AIDS Dementia Complex  *Brain Chemistry  Comparative Study
       Cytokines/PHYSIOLOGY  Defective Viruses/PATHOGENICITY  *Disease Models,
       Animal  Helper Viruses/PATHOGENICITY  Human  Leukemia Viruses,
       Murine/PATHOGENICITY  Mice  Mice, Inbred C57BL  Murine Acquired
       Immunodeficiency Syndrome/*METABOLISM  Quinolinic Acid/*ANALYSIS/BLOOD
       Viscera/CHEMISTRY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

