Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 13, Pages 7274-7279Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00250-07
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Funding
- NCI NIH HHS [R01 CA083823, CA83823, CA33771, R01 CA033771] Funding Source: Medline
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Infection with a recombinant murine-feline gammaretrovirus, MoFe2, or with the parent virus, Moloney murine leukemia virus, caused significant reduction in B-lymphoid differentiation of bone marrow at 2 to 8 weeks postinfection. The suppression was selective, in that myeloid potential was significantly increased by infection. Analysis of cell surface markers and inummoglobulin H gene rearrangements in an in vitro model demonstrated normal B-lymphoid differentiation after infection but significantly reduced viability of differentiating cells. This reduction in viability may confer a selective advantage on undifferentiated lymphoid progenitors in the bone marrow of gammaretrovirus-infected animals and thereby contribute to the establishment of a premalignant state.
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