Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1984-12-7
pubmed:abstractText
Visna-maedi of sheep and arthritis encephalitis of goats are slowly progressive diseases caused by serologically related lentiviruses. Lesions are inflammatory and can occur at one or many sites including the central nervous system, lungs, joints, and mammary glands. The viruses replicate in macrophages, and in the animal large numbers of infected macrophages can be obtained from inflamed tissues. To study virus-macrophage interactions we transformed sheep alveolar macrophages, which are natural virus target cells, with simian virus 40 and produced a macrophage cell line. The transformed cells grew into density-dependent monolayers and were subcultured after trypsin dissociation. They maintained histochemical and physiologic properties of macrophages as well as the ability to support replication of the lentiviruses. Rabbit antisera to these cells reacted with blood monocytes and only selected populations of tissue macrophages, including those in lung, synovium, mammary gland, and spleen. Microglia, Kupffer cells, and connective tissue histiocytes were not recognized by the sera. Since the tissues in which virus localizes in infected animals are the same as those recognized by the sera, the antimacrophage serum may provide an immunologic marker for virus-susceptible macrophages in the animal.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0023-6837
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
547-55
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Slow virus-macrophage interactions. Characterization of a transformed cell line of sheep alveolar macrophages that express a marker for susceptibility to ovine-caprine lentivirus infections.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.