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Nature.
1996 Aug 29;382(6594):826-9.
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Comment in:
Nature. 1996 Aug 29;382(6594):762-3.
Positional cloning of the mouse retrovirus restriction gene Fv1.
Best S
,
Le Tissier P
,
Towers G
,
Stoye JP
.
Division of Virology, National Institute for Medical Research, London, UK.
Vertebrate evolution has taken place against a background of constant retrovirus infection, and much of the mammalian genome consists of endogenous retrovirus-like elements. Several host genes have evolved to control retrovirus replication, including Friend-virus-susceptibility-1, Fv1, on mouse chromosome 4 (refs 3, 4). The Fv1 gene acts on murine leukaemia virus at a stage after entry into the target cell but before integration and formation of the provirus. Although restriction is not absolute, Fv1 prevents or delays spontaneous or experimentally induced viral tumours. In vitro, Fv1 restriction leads to an apparent 50-1,000 fold reduction in viral titre. Genetic evidence implicates a direct interaction between the Fv1 gene product and a component of the viral preintegration complex, the capsid protein CA (refs 7-9). We have now cloned Fv1: the gene appears to be derived from the gag region of an endogenous retrovirus unrelated to murine leukaemia virus, implying that the Fv1 protein and its target may share functional similarities despite the absence of nucleotide-sequence homology.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 8752279 [PubMed - indexed for MEDLINE]
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