scholarly journals Influence of the murine MHC (H-2) on Friend leukemia virus-induced immunosuppression.

1986 ◽  
Vol 163 (2) ◽  
pp. 301-314 ◽  
Author(s):  
R P Morrison ◽  
J Nishio ◽  
B Chesebro
Keyword(s):  
T Lymphocyte ◽  
B Lymphocyte ◽  
Leukemia Virus ◽  
Friend Leukemia ◽  
Virus Complex ◽  
Plasma Antibody ◽  
Antibody Titers ◽  
Partial Suppression ◽  
Friend Leukemia Virus ◽  
Murine Leukemia

Friend murine leukemia virus complex (FV)-induced immunosuppression was studied by assaying splenic anti-SRBC PFC responses and plasma antibody titers in mice at various times after FV inoculation. Genes located within the H-2 complex were found to influence resistance to FV-induced immunosuppression. Near normal responses were observed in mice having the H-2a/b or H-2b/b genotype, whereas mice having the H-2a/a genotype were suppressed. This H-2 effect was observed not only in mice having heterozygous C57BL/10 X A background genes, including Rfv-3r/s, but also was apparent in mice having homozygous A-strain background genes, including Rfv-3s/s. Therefore, the Rfv-3 gene did not appear to convey resistance to FV-induced immunosuppression. The suppression in susceptible H-2a/a mice was characterized by a partial suppression of the IgM response and a profound suppression of both the primary and secondary IgG responses. Neither splenomegaly nor viremia alone appeared to be sufficient for the induction or maintenance of the immunosuppression. The mechanism of suppression was unclear, but both B lymphocyte and T lymphocyte functions appeared to be altered.

Immunotherapy of murine leukemia. I. protection against friend leukemia virus-induced disease by passive serum therapy

1978 ◽  
Vol 21 (1) ◽  
pp. 51-61 ◽  
Author(s):  
Jeffrey J. Collins ◽  
Fred Sanfilippo ◽  
Lynn Tsong-Chou ◽  
Ryo Ishizaki ◽  
Richard S. Metzgar
Keyword(s):  
Leukemia Virus ◽  
Friend Leukemia ◽  
Serum Therapy ◽  
Friend Leukemia Virus ◽  
Murine Leukemia

scholarly journals Erythroleukemia induction by replication-competent type C viruses cloned from the anemia- and polycythemia-inducing isolates of Friend leukemia virus.

1980 ◽  
Vol 151 (6) ◽  
pp. 1493-1503 ◽  
Author(s):  
M E MacDonald ◽  
T W Mak ◽  
A Bernstein
Keyword(s):  
Leukemia Virus ◽  
Kinetic Studies ◽  
Biological Properties ◽  
Erythroid Cells ◽  
Erythroid Progenitor ◽  
Newborn Mice ◽  
Adult Mice ◽  
Friend Leukemia ◽  
Virus Complex ◽  
Friend Leukemia Virus

In this study, the biological properties of the replication-competent viruses, F-MuLVA, present in the anemia-inducing isolate of Friend leukemia virus complex (FV-A); and F-MuLVP, present in the polycythemia-inducing isolate of Friend leukemia virus complex (FV-P) have been examined. BALB/c mice infected as newborns with clonal isolates of F-MuLVA or F-MuLVP become anemic and show splenic enlargement characterized by an increased proportion of cells that resemble immature nucleated erythroid cells. In addition, the spleens of these F-MuLVA- or F-MuLVP-infected mice contain a markedly increased proportion of both erythropoietin-dependent erythroid progenitor cells and spectrin-containing erythroid cells. These results suggest that Friend murine leukemia virus (F-MuLV) by itself can induce an erythroleukemic transformation in newborn BALB/c mice similar to that induced by the anemia-inducing spleen focus-forming virus (SFFVA) in newborn or adult mice. Kinetic studies indicated that the alterations in hemopoietic cell populations induced by F-MuLVA or F-MuLVP in newborn BALB/c mice occurred more slowly than the rapid changes observed after infection with FV-A. In addition, adult BALB/c mice were fully susceptible to the erythroleukemic transformation induced by either SFFVA or SFFVP, whereas only newborn mice were susceptible to F-MuLV. Taken together, these results suggest that, although the replication-defective Friend spleen focus-forming viruses appear to be the major determinant of erythroleukemia induction in adults, the replication-competent helper F-MuLV also have erythroleukemic potential when assayed in newborn animals.

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