Linked Life Data

1845771

Source:http://linkedlifedata.com/resource/pubmed/id/1845771

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-1-22
pubmed:abstractText
An early host defense against infection by RNA or DNA viruses is the induction, within infected cells, of tumor necrosis factor-alpha (TNF-alpha) gene transcription. The protein product of the TNF-alpha gene alone, or together with different types of interferons, inhibits viral propagation in diverse cell types. In this study, the effect of acute and chronic human immunodeficiency virus type 1 (HIV-1) infection on the transcription of the TNF-alpha and interferon-beta (IFN-beta) genes was examined in susceptible monocyte and T-cell lines as well as in primary human mononuclear phagocytes. Although Sendai virus, a prototypic inducer of TNF-alpha and IFN-beta mRNA, induced the transcription of both genes in the monocyte cell lines and TNF-alpha in the T-cell line and in primary mononuclear phagocytes, transcription of these genes was not inducible by HIV-1. Therefore, HIV-1 was able to infect these cells without triggering the transcription of genes encoding proteins important in immediate antiviral cellular defenses. These results may explain in part how HIV-1 is able to establish persistent intracellular infections and escape acute host responses that have evolved to combat viral infection.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0894-9255
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
41-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
HIV-1 infection does not induce tumor necrosis factor-alpha or interferon-beta gene transcription.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't