Linked Life Data

8623557

Source:http://linkedlifedata.com/resource/pubmed/id/8623557

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-6-19
pubmed:abstractText
The emergence of syncytium-inducing (SI) HIV-1 isolates in infected individuals precedes an accelerated CD4+ T cell decline and is associated with high virus load and rapid disease progression. The exact mechanism by which SI HIV-1 variants may cause this enhanced clinical progression is unknown. Here we demonstrate that an SI HIV-1 isolate had a broader tropism for CD4+ T cell clones (TCC) compared to a macrophage-tropic non-syncytium-inducing (NSI) HIV-1 isolate. Whereas the NSI isolate replicated poorly in 6 of 12 TCC and completely failed to replicate in 3 of 12 TCC, the SI isolate replicated efficiently in all 12 TCC tested. Restriction for replication occurred early in the viral replication cycle, before provirus formation. Infection of TCC with the SI but not with the NSI HIV-1 isolate resulted in massive death of T cells, independent of the extent of virus replication and proportion of infected cells. The high cytopathicity and broader tropism of the SI isolate for primary CD4+ T cells may be directly related to the increased rate of CD4 cell decline and rapid disease progression in carriers of SI variants.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
219
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-95
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Broader tropism and higher cytopathicity for CD4+ T cells of a syncytium-inducing compared to a non-syncytium-inducing HIV-1 isolate as a mechanism for accelerated CD4+ T cell decline in vivo.
pubmed:affiliation
Department of Clinical Viro-Immunology, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't