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Genotype-limited changes in platelet and erythroid kinetics in Friend-virus-infected allophenic mice
Abstract:
We report here results suggesting that cells of the megakaryocytic lineage or uncommitted precursor cells may be targets for Friend-virus-induced proliferation, and that genetic differences (other than Fv-2) between strains C57BL/6 and DBA/2 affect the susceptibility of these cells to Friend virus. The evidence suggesting this was derived from experiments with C57BL/6 in equilibrium DBA/2 allophenic mice. Within the first few weeks following infection of these mice with the polycythemic NB-tropic strain of Friend virus (FV-P), we observed a rapid shift in the genotypic composition of both red cells and platelets in favor of those of the DBA/2 genotype. Infection with the anemia-inducing strain of Friend virus (FV-A) also resulted in preferential production of DBA/2 strain erythrocytes, but its effect on platelet kinetics was nil. The FV-P- and FV-A-induced change in red cell composition is consistent with the view that erythroid precursors are target cells for Friend virus and that viral infection preferentially stimulates proliferation of susceptible strain (DBA/2) erythroid precursors. As for the platelet shifts induced by FV-P (and not FV-A), we believe the changes in platelet mosaicism also could be caused by viral-induced proliferation of DBA/2 platelet precursors, or more primitive progenitors, over the C57BL/6 ones. Thus, these results implicate the existence of nonerythroid target cells for FV-P-induced proliferation, as well as the existence of genetic differences between strains C57BL/6 and DBA/2 that modulate the responsiveness of such cells to infection.
Insights
Friend virus infection targets megakaryocytic lineage cells, influencing proliferation. Genetic differences between mouse strains C57BL/6 and DBA/2 impact cell susceptibility to Friend virus, affecting red blood cells and platelets.
Area of Science:
- * Hematology
- * Virology
- * Immunogenetics
Background:
- * Friend virus (FV) is known to induce proliferation in hematopoietic cells.
- * Genetic factors, such as the Fv-2 locus, influence susceptibility to FV infection.
- * Previous studies have focused on erythroid precursor cells as primary targets for FV.
Purpose of the Study:
- * To investigate whether megakaryocytic lineage cells or uncommitted precursors are targets for FV-induced proliferation.
- * To determine if genetic differences between C57BL/6 and DBA/2 mice, beyond Fv-2, affect cellular susceptibility to FV.
- * To elucidate the specific effects of different FV strains (FV-P and FV-A) on red blood cell and platelet production.
Main Methods:
- * Experiments utilized C57BL/6 in equilibrium DBA/2 allophenic mice.
- * Mice were infected with either the polycythemic NB-tropic strain of Friend virus (FV-P) or the anemia-inducing strain (FV-A).
- * Genotypic composition of red blood cells and platelets was analyzed post-infection.
Main Results:
- * FV-P infection led to a rapid shift in both red cell and platelet genotypes favoring DBA/2.
- * FV-A infection resulted in preferential production of DBA/2 erythrocytes but had no effect on platelet kinetics.
- * These findings suggest erythroid precursors are target cells for both FV strains, with DBA/2 precursors showing increased proliferation.
Conclusions:
- * Results suggest that megakaryocytic lineage cells or earlier progenitors are targets for FV-P-induced proliferation.
- * Genetic variations between C57BL/6 and DBA/2 mice modulate cellular responses to FV infection.
- * FV-P, but not FV-A, appears to induce proliferation in non-erythroid target cells, impacting platelet production.