Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-10-29
pubmed:abstractText
Podocyte damage induced by HIV-1 is critical to the pathogenesis of HIV-1 associated nephropathy (HIVAN) and is believed to result from productive replication of the virus. Here we demonstrate that HIV-1 readily enters human podocytes by a dynamin-mediated endocytosis but does not establish productive infection. We provide evidence suggesting that viral nucleic acids and proteins detected in podocytes are delivered by viral particles internalized by the cells. Endocytosed HIV-1 is only transiently harbored by podocytes and is subsequently released to the extracellular milieu as fully infectious virus. Similarly, primary podocytes established from normal human urine do not support productive infection by HIV-1 but sustain replication of VSV-G pseudotyped virus that bypasses HIV-1 entry receptors. Moreover, transfected podocytes expressing CD4 and CXCR4 receptors support productive replication of HIV-1. This further confirms that lack of HIV-1 entry receptors is the major barrier preventing productive infection of podocytes in vitro.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1096-0341
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
5
pubmed:volume
408
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
119-27
pubmed:dateRevised
2011-10-5
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Non-productive HIV-1 infection of human glomerular and urinary podocytes.
pubmed:affiliation
Center for AIDS Health Disparities Research, Meharry Medical College, 1005 D. B. Todd Blvd., Nashville, TN 37208, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural