Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-11-18
pubmed:abstractText
HIV-associated dementia (HAD) is a serious neurological disorder affecting about 7% of people with AIDS. In the brain, HIV-1 infects a restricted number of cell types, being primarily present in macrophages and microglial cells, less abundant in astrocytes, and rarely seen in oligodendrocytes and neurons. Lack of a productive HIV-1 infection of neuronal cells suggests the presence of an indirect pathway by which the virus may determine the brain pathology and neuronal dysfunction seen in AIDS patients. Among the participants in this event, viral proteins including gp120 and Tat, along with host factors including cytokines, chemokines, and several signaling pathways have received considerable attention. In this article, we discuss the most recent concepts pertaining to the mechanisms of HIV-1-induced neuronal dysfunction by highlighting the interplay between signal transduction pathways activated by viral and host factors and their consequences in neuronal cell function.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:author
pubmed:day
1
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
114-25
pubmed:dateRevised
2010-8-13
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Cross talk between growth factors and viral and cellular factors alters neuronal signaling pathways: implication for HIV-associated dementia.
pubmed:affiliation
Center for Neurovirology and Cancer Biology, Temple University, 1900 12th North Street, Philadelphia, PA 19122, USA. fperuzzi@temple.edu
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural