Source:http://linkedlifedata.com/resource/pubmed/id/10628199
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
46
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pubmed:dateCreated |
2000-1-19
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pubmed:abstractText |
Simultaneous HHV-6A infection can activate HIV-1 latency and promote AIDS progression, but in this process the effects of HHV-6A induced soluble mediators on HIV-1 have not been studied yet. Recently, supernatants of HSB-2 cultures infected with HHV-6A and/or treated with endotoxin have been filtered virus free at time intervals until the cytopathic effect developed. Biological activity of some cytokines which might participate in HIV-1 activation was quantitated. Filtered supernatants were mixed into CEM-ss cultures, which had been HIV-1 infected at 1:1 cell:virus ratio, subsequently HIV-1 replication was quantitated and compared to controls. Supernatants filtered during the first 96 hours of HHV-6A replication without visible cytopathic effect augmented HIV-1 syncytium formation by tenfold, reverse transcriptase activity by threefold, p24 antigen production by 6-fold. Filtered supernatants obtained at onset of HHV-6A cytopathic effect did not modify HIV-1 replication. HSB-2 cultures produced no IL-2, and IFN-gamma induced by endotoxin diminished HIV-1 replication. HHV-6A delayed IFN-gamma release. An increase in the tumour necrosis factor activity upon the effect of HHV-6A and endotoxin was not parallel to HIV-1 activation. The putative mediator, different from those above which characterisation is in progress, might transmit similar transactivating effects between immune cells of lymph nodes and circulation.
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pubmed:language |
hun
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0030-6002
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
14
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pubmed:volume |
140
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2577-80
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pubmed:dateRevised |
2009-10-21
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pubmed:meshHeading | |
pubmed:year |
1999
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pubmed:articleTitle |
[Human herpesvirus 6 A enhances HIV-1 replication in vitro by soluble mediators, this effect is diminished by endotoxin].
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pubmed:affiliation |
Pisai Egyetem, Orvosbiológiai Tanszék, Olaszország.
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pubmed:publicationType |
Journal Article,
In Vitro,
English Abstract,
Review,
Research Support, Non-U.S. Gov't
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