Linked Life Data

9143703

Source:http://linkedlifedata.com/resource/pubmed/id/9143703

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1997-7-29
pubmed:abstractText
In human plasma, HIV activates the complement system, even in the absence of specific antibodies. Complement activation would, however, be harmful to the virus if the reactions were allowed to go to completion, since their final outcome would be virolysis. This is avoided by complement regulatory molecules, which either are included in the virus membrane upon budding from the infected cells (e.g. DAF/CD55) or are secondarily attached to HIV envelope glycoproteins as in the case of factor H. By using this strategy of interaction with complement components, HIV takes advantage of human complement activation for enhancement of infectivity, for follicular localization, and for broadening its target cell range at the same time that it displays an intrinsic resistance against the lytic action of human complement. This intrinsic resistance to complement-mediated virolysis can be overcome by monoclonal antibodies inhibiting recruitment of human factor H to the virus surface, suggesting a new therapeutic principle.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0732-0582
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
649-74
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Role of complement in HIV infection.
pubmed:affiliation
Institut für Hygiene, Innsbruck, Austria. Stoiber.hygiene@uibk.ac.at
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't