Characterization of the endogenous nonecotropic murine leukemia viruses of NZB/BINJ and SM/J inbred strains

1992 ◽  
Vol 2 (2) ◽  
pp. 110-122 ◽  
Author(s):  
Wayne N. Frankel ◽  
Barbara K. Lee ◽  
Jonathan P. Stoye ◽  
John M. Coffin ◽  
Eva M. Eicher
Virology ◽  
1985 ◽  
Vol 141 (2) ◽  
pp. 319-321 ◽  
Author(s):  
Robert A. Yetter ◽  
Wallace Y. Langdon ◽  
Herbert C. Morse

1983 ◽  
Vol 158 (2) ◽  
pp. 353-364 ◽  
Author(s):  
W P Rowe ◽  
J W Hartley

An assessment of the importance of mink cell focus-inducing (MCF)-type recombinant murine leukemia viruses in spontaneous thymic lymphomagenesis and of the genetic factors affecting its occurrence was carried out with F1 hybrids between AKR and various other inbred strains. There was generally close agreement between the frequency of detection of MCF virus, of thymocyte antigenic amplification in the preleukemic period, and of spontaneous lymphoma. Also, hybrid combinations with moderate to high spontaneous lymphoma were uniformly susceptible to lymphoma induction by neonatal inoculation of MCF 247 virus, while lower leukemic hybrids were at least partially resistant to the induced disease. At least four resistance genes can be identified as affecting the disease in the various hybrids: Fv-1, Rmcf, an unidentified gene carried by the C57 series of mice and SJL, and an unidentified minor gene carried by several other strains.


2002 ◽  
Vol 76 (5) ◽  
pp. 2279-2286 ◽  
Author(s):  
Tiyun Wu ◽  
Chun G. Lee ◽  
Alicia Buckler-White ◽  
Christine A. Kozak

ABSTRACT Mice contain a serum factor capable of inactivating some subgroups of murine leukemia viruses. This leukemia virus-inactivating factor (LVIF) is distinct from immunoglobulin and complement; it has been associated with lipoprotein serum fractions and may be an apolipoprotein. The present study demonstrates that some Swiss-derived inbred strains are LVIF negative. Genetic crosses show this factor to be under control of a single gene that maps to distal chromosome 10 at or near the gene encoding a minor serum apolipoprotein, apolipoprotein F (ApoF). To evaluate this gene as a potential candidate for LVIF, the mouse ApoF gene was cloned and sequenced and its expression was assessed in LVIF-positive and -negative mice; no obvious differences were detected, suggesting that LVIF is under the control of a distinct linked gene.


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