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CD8+ T lymphocytes in the lung of acquired immunodeficiency syndrome
patients harbor human immunodeficiency virus type 1
G Semenzato, C Agostini, L Ometto, R Zambello, L Trentin, L Chieco-Bianchi and A De Rossi
Padua University School of Medicine, Institutes of Clinical Medicine and
Oncology, Italy.
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.
Volume 85,
Issue 9,
pp. 2308-2314,
05/01/1995
Copyright © 1995 by The American Society of Hematology
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