Document 0838
 DOCN  M9470838
 TI    Human immunodeficiency virus (HIV)-infected human blood monocytes and
       peritoneal macrophages have reduced anticryptococcal activity whereas
       HIV-infected alveolar macrophages retain normal activity.
 DT    9409
 AU    Cameron ML; Granger DL; Matthews TJ; Weinberg JB; Division of Infectious
       Diseases, Duke University Medical Center,; Durham, NC 27710.
 SO    J Infect Dis. 1994 Jul;170(1):60-7. Unique Identifier : AIDSLINE
       MED/94284662
 AB    Human immunodeficiency virus type 1 (HIV-1) infection causes immune
       dysfunction. Mononuclear phagocytes (MNP) are immune effector cells
       against some intracellular pathogens and reservoirs for HIV-1. This
       study determined effects of HIV-1 on MNP-mediated antifungal function.
       MNP from seronegative volunteers were inoculated with HIVBal or HIVIIIB.
       MNP were infected with an avirulent clone of Cryptococcus neoformans; 48
       h later, MNP were lysed and yeasts were counted. Viral replication was
       determined by reverse transcriptase and by visualization of cytopathic
       effects. Monocytes and peritoneal macrophages exhibited reduced
       anticryptococcal activity 14 days after infection with HIVBal but
       retained normal activity when infected with HIVIIIB. Loss of
       anticryptococcal activity correlated with viral replication. Alveolar
       macrophages retained normal anticryptococcal activity whether infected
       with HIVBal or HIVIIIB. In vitro MNP-mediated antifungal activity may be
       altered by HIV-1 infection; this altered activity appears to depend on
       viral tropism, viral replication, and MNP tissue origin.
 DE    Cell Survival  Cells, Cultured  Comparative Study  Cryptococcus
       neoformans/*IMMUNOLOGY  Human  HIV-1/*IMMUNOLOGY/PHYSIOLOGY
       Macrophages, Alveolar/CYTOLOGY/IMMUNOLOGY/*MICROBIOLOGY  Macrophages,
       Peritoneal/CYTOLOGY/IMMUNOLOGY/*MICROBIOLOGY
       Monocytes/CYTOLOGY/IMMUNOLOGY/*MICROBIOLOGY  Phagocytosis  Support, U.S.
       Gov't, Non-P.H.S.  Support, U.S. Gov't, P.H.S.  Virus Replication
       JOURNAL ARTICLE

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