Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1995-5-31
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
85
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2308-14
pubmed:dateRevised
2006-11-15
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
pubmed:year
1995
pubmed:articleTitle
CD8+ T lymphocytes in the lung of acquired immunodeficiency syndrome patients harbor human immunodeficiency virus type 1.
pubmed:affiliation
Padua University School of Medicine, Institutes of Clinical Medicine and Oncology, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't