Linked Life Data

21814282

Source:http://linkedlifedata.com/resource/pubmed/id/21814282

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7358
pubmed:dateCreated
2011-8-4
pubmed:abstractText
Natural killer (NK) cells have an important role in the control of viral infections, recognizing virally infected cells through a variety of activating and inhibitory receptors. Epidemiological and functional studies have recently suggested that NK cells can also contribute to the control of HIV-1 infection through recognition of virally infected cells by both activating and inhibitory killer immunoglobulin-like receptors (KIRs). However, it remains unknown whether NK cells can directly mediate antiviral immune pressure in vivo in humans. Here we describe KIR-associated amino-acid polymorphisms in the HIV-1 sequence of chronically infected individuals, on a population level. We show that these KIR-associated HIV-1 sequence polymorphisms can enhance the binding of inhibitory KIRs to HIV-1-infected CD4(+) T cells, and reduce the antiviral activity of KIR-positive NK cells. These data demonstrate that KIR-positive NK cells can place immunological pressure on HIV-1, and that the virus can evade such NK-cell-mediated immune pressure by selecting for sequence polymorphisms, as was previously described for virus-specific T cells and neutralizing antibodies. NK cells might therefore have a previously underappreciated role in contributing to viral evolution.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1476-4687
pubmed:author
pubmed:issnType
Electronic
pubmed:day
4
pubmed:volume
476
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
96-100
pubmed:dateRevised
2011-10-17
pubmed:meshHeading
pubmed-meshheading:21814282-Adaptation, Physiological, pubmed-meshheading:21814282-Antibodies, Neutralizing, pubmed-meshheading:21814282-CD4-Positive T-Lymphocytes, pubmed-meshheading:21814282-Decision Trees, pubmed-meshheading:21814282-Evolution, Molecular, pubmed-meshheading:21814282-Genotype, pubmed-meshheading:21814282-HIV Infections, pubmed-meshheading:21814282-HIV-1, pubmed-meshheading:21814282-Host-Pathogen Interactions, pubmed-meshheading:21814282-Human Immunodeficiency Virus Proteins, pubmed-meshheading:21814282-Humans, pubmed-meshheading:21814282-Immune Evasion, pubmed-meshheading:21814282-Killer Cells, Natural, pubmed-meshheading:21814282-Polymorphism, Genetic, pubmed-meshheading:21814282-Receptors, KIR, pubmed-meshheading:21814282-Receptors, KIR2DL2, pubmed-meshheading:21814282-Viral Regulatory and Accessory Proteins, pubmed-meshheading:21814282-Virus Replication, pubmed-meshheading:21814282-env Gene Products, Human Immunodeficiency Virus
pubmed:year
2011
pubmed:articleTitle
HIV-1 adaptation to NK-cell-mediated immune pressure.
pubmed:affiliation
Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02129, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural, Research Support, N.I.H., Intramural