Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-8-18
pubmed:abstractText
HIV-1 infection of the CNS plays a direct role in the pathogenesis of AIDS dementia that frequently accompanies systemic AIDS. Both adult and pediatric AIDS are characterized by a high proportion of CNS disease. However, the pathogenic mechanisms responsible for AIDS dementia are not understood. A transgenic mouse model using the LTRs of two CNS-derived strains of HIV-1 (HIV-1JR-CSF and HIV-1JR-FL) has been developed to study HIV-1 gene expression in vivo. Analyses of expression in adult transgenic mice revealed expression in neurons in the CNS (J. R. Corboy, J. M. Buzy, M. C. Zink, and J. E. Clement, Science 258, 1804-1808, 1992). In this study, developmental analyses of HIV-1-directed gene expression in embryonic and newborn transgenic mice derived from the above lines revealed strikingly different levels and patterns of expression in the CNS and spinal cord compared with adult mice. Increased expression was observed in the newborn brain compared to the adult, and the neuroanatomical pattern of expression was markedly different than that observed in adult brain. Transient expression was detected in the dorsal root ganglia and spinal cord in embryos and newborns up to Day 14. In contrast to the expression in neurons in adult CNS, HIV-1-directed gene expression in the newborn brain was observed in neurons, endothelial cells, and macrophages. This difference in expression during development probably reflects temporally regulated cellular transcription factors in the CNS. This transgenic model suggests that HIV-1 replication in the CNS may use cellular transcription factors different from those in nonneural tissues. Studies are in progress to identify cellular transcription factors that may be responsible for the differential expression of the LTRs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
210
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
361-71
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7618273-AIDS Dementia Complex, pubmed-meshheading:7618273-Animals, pubmed-meshheading:7618273-Animals, Newborn, pubmed-meshheading:7618273-Base Sequence, pubmed-meshheading:7618273-Central Nervous System, pubmed-meshheading:7618273-Endothelium, pubmed-meshheading:7618273-Eye, pubmed-meshheading:7618273-Gene Expression Regulation, Developmental, pubmed-meshheading:7618273-Gene Expression Regulation, Viral, pubmed-meshheading:7618273-Genes, Reporter, pubmed-meshheading:7618273-HIV Long Terminal Repeat, pubmed-meshheading:7618273-HIV-1, pubmed-meshheading:7618273-Macrophages, pubmed-meshheading:7618273-Mice, pubmed-meshheading:7618273-Mice, Transgenic, pubmed-meshheading:7618273-Microglia, pubmed-meshheading:7618273-Molecular Sequence Data, pubmed-meshheading:7618273-Neurons, pubmed-meshheading:7618273-RNA, Messenger, pubmed-meshheading:7618273-Virus Replication, pubmed-meshheading:7618273-beta-Galactosidase
pubmed:year
1995
pubmed:articleTitle
HIV-1 in the developing CNS: developmental differences in gene expression.
pubmed:affiliation
Agency for International Development, USAID, Arlington, Virginia 22209, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.