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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
1995-5-31
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pubmed:abstractText |
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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2308-14
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7727764-Acquired Immunodeficiency Syndrome,
pubmed-meshheading:7727764-Adult,
pubmed-meshheading:7727764-Antigens, CD4,
pubmed-meshheading:7727764-Bronchoalveolar Lavage Fluid,
pubmed-meshheading:7727764-CD8-Positive T-Lymphocytes,
pubmed-meshheading:7727764-Cell Separation,
pubmed-meshheading:7727764-Cells, Cultured,
pubmed-meshheading:7727764-DNA, Viral,
pubmed-meshheading:7727764-Female,
pubmed-meshheading:7727764-HIV-1,
pubmed-meshheading:7727764-Humans,
pubmed-meshheading:7727764-Lung,
pubmed-meshheading:7727764-Macrophages, Alveolar,
pubmed-meshheading:7727764-Male,
pubmed-meshheading:7727764-Middle Aged,
pubmed-meshheading:7727764-Models, Biological,
pubmed-meshheading:7727764-Polymerase Chain Reaction,
pubmed-meshheading:7727764-Proviruses,
pubmed-meshheading:7727764-RNA, Messenger,
pubmed-meshheading:7727764-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:7727764-Virus Replication
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pubmed:year |
1995
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pubmed:articleTitle |
CD8+ T lymphocytes in the lung of acquired immunodeficiency syndrome patients harbor human immunodeficiency virus type 1.
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pubmed:affiliation |
Padua University School of Medicine, Institutes of Clinical Medicine and Oncology, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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