Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
CD8+ T lymphocytes in the lung of acquired immunodeficiency syndrome patients harbor human immunodeficiency virus type 1.
Blood. 1995 May 1;85(9):2308-14. Unique Identifier : AIDSLINE MED/95244849 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.
Abstract:
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.
Keywords: 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 950830
M9580950
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Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
