Linked Life Data

21161615

Source:http://linkedlifedata.com/resource/pubmed/id/21161615

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-2-9
pubmed:abstractText
While the hallmark of HIV-1 infection is the progressive depletion of CD4(+) T cells, extensive B-cell dysfunction ensues that impairs the quality of the humoral response. HIV-1 infection causes hypergammaglobulinemia, polyclonal activation, loss of memory B-cell subsets, B-cell exhaustion, aberrant B-cell surface markers, and impaired humoral responses against infections and vaccinations. The totality of the mechanisms that contribute to B-cell dysfunction in vivo is unknown, although roles for HIV proteins (Env, Tat, and Nef) and virions binding to CD21 on B cells have been identified. Recent studies suggest that early antiretroviral therapy, that minimizes virus replication, can profoundly preserve the early B-cell response to HIV-1. Thus, it is clear that there is an intricate interplay between HIV replication and stimulation of the host B-cell response to infection. A better understanding of how HIV-1 subverts a productive B-cell response is needed to inform vaccine strategies that aim to elicit long-lived plasma cells and memory B-cell responses that can act quickly upon antigen stimulation.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1548-3576
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
23-30
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Alterations of the B-cell response by HIV-1 replication.
pubmed:affiliation
Department of Surgery, Duke Human Vaccine Institute, Duke University Medical Center, Durham, NC 27710, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural