Document 0163
 DOCN  M9580163
 TI    CD8+ T lymphocytes in the lung of acquired immunodeficiency syndrome
       patients harbor human immunodeficiency virus type 1.
 DT    9506
 AU    Semenzato G; Agostini C; Ometto L; Zambello R; Trentin L; Chieco-Bianchi
       L; De Rossi A; Padua University School of Medicine, Institutes of
       Clinical; Medicine and Oncology, Italy.
 SO    Blood. 1995 May 1;85(9):2308-14. Unique Identifier : AIDSLINE
       MED/95244849
 AB    Human immunodeficiency virus-1 (HIV-1) infection of CD8+ lymphocytes has
       been described in several in vitro culture systems, but whether CD8+
       cells are a target and also serve as a reservoir for infection in vivo
       as yet is unknown. We addressed this issue in patients with acquired
       immunodeficiency syndrome (AIDS)-related lower respiratory tract chronic
       inflammation, which is characterized by a massive influx of CD8+
       HIV-1-specific cytotoxic T lymphocytes (CTL). Proviral load in lung T
       lymphocytes and their subpopulations was evaluated by using the
       DNA-polymerase chain reaction (PCR) technique on cells retrieved by
       bronchoalveolar lavage. To avoid the possibility that the presence of
       HIV-1 DNA could be caused by contaminating CD4+ cells, serial dilutions
       of highly purified CD8+ cells were also analyzed by PCR. Our findings
       showed that lung CD8+ cells harbor and express HIV-1. To explore the
       possible mechanisms leading to pulmonary CD8+ lymphocyte infection, we
       evaluated CD4 gene expression on highly purified CD8+ cells by means of
       reverse transcriptase PCR. Despite the lack of membrane CD4 reactivity,
       we could show that CD8+ cells may express CD4 RNA. Coinfection of lung
       CD8+ cells harboring proviral HIV-1 sequences by viral agents capable of
       inducing CD4 expression (ie, HHV-6) was not detected. Our data indicate
       that not only CD4+ T lymphocytes and macrophages, but also CD8+ cells,
       may represent a target and/or a reservoir for HIV-1 in vivo, and suggest
       that lung CD8+ lymphocytes could derive from precursors equipped with
       enough CD4 molecules to become HIV-1 permissive. Aside from the
       cell-to-cell contact between activated HIV-1 specific CTL and relevant
       targets, the infection of precursors could represent an additional
       mechanism accounting for the infection of pulmonary CD8+ cells and their
       functional impairment.
 DE    Acquired Immunodeficiency Syndrome/PATHOLOGY/*VIROLOGY  Adult  Antigens,
       CD4/BIOSYNTHESIS  Bronchoalveolar Lavage Fluid  Cell Separation  Cells,
       Cultured  CD8-Positive T-Lymphocytes/METABOLISM/*VIROLOGY  DNA,
       Viral/ANALYSIS  Female  Human  HIV-1/*ISOLATION & PURIF/PHYSIOLOGY
       Lung/PATHOLOGY/*VIROLOGY  Macrophages, Alveolar/VIROLOGY  Male  Middle
       Age  Models, Biological  Polymerase Chain Reaction  Proviruses/ISOLATION
       & PURIF  RNA, Messenger/ANALYSIS  Support, Non-U.S. Gov't
       T-Lymphocytes, Cytotoxic/METABOLISM/VIROLOGY  Virus Replication  JOURNAL
       ARTICLE

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