Linked Life Data

8395116

Source:http://linkedlifedata.com/resource/pubmed/id/8395116

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-9-22
pubmed:abstractText
Results in a previous report established the presence of dominant genetic factor(s) in C3H/BiDa mice which contributed to the unusually high susceptibility of this strain to polyoma virus-induced tumors (Freund et al. (1992) Virology 191, 724-731). Here we show that C57BR/cdJ mice, while identical to C3H/BiDa at the H-2 locus, are almost completely lacking in susceptibility. Analysis of crosses between these two H-2k strains has shown that susceptibility is due to a single dominant autosomal gene, designated Pyvs. On an H-2k background, Pyvs acts in a highly penetrant manner to confer susceptibility to induction of a broad range of tumors by the virus. Analysis of F1 mice between C3H/BiDa and the highly resistant C57BL/6 (H-2b) strain shows that Pyvs can partially overcome the immunologically mediated resistance associated with an H-2b haplotype. Pyvs does not encode cell receptors for the virus, nor does it affect levels of virus replication or anti-viral humoral responses in the host. Studies with early passage embryo fibroblasts in culture show that Pyvs does not affect intracellular events essential for either productive infection or cell transformation by the virus. Pyvs thus determines a generalized susceptibility of the host to polyoma-induced tumors but apparently does not act at the level of target cells for tumor induction.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:volume
196
pubmed:geneSymbol
Pyv<up>s</up>
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
241-8
pubmed:dateRevised
2010-12-3
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Pyvs: a dominantly acting gene in C3H/BiDa mice conferring susceptibility to tumor induction by polyoma virus.
pubmed:affiliation
Harvard Medical School, Department of Pathology, Boston, Massachusetts 02115.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.