Suppression of the Primary Antibody Plaque Response of Mice Following Infection with Friend Disease Virus.

Ceglowski, Walter S.; Friedman, Herman

doi:10.3181/00379727-126-32533

Cited by 34 publications

(6 citation statements)

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“…This FLV-induced immunosuppression has been shown to affect B-cell function (12,37,40), T-cell function (14,33,34,38,39), macrophage function (9,30), natural killer cell function (20,35), leukocyte migration (19), and suppressor cell generation (25). A number of studies have shown that FLV infection suppresses cellular (38) and humoral (11,12, 37, 40) responses to nominal antigens such as purified protein derivative and sheep erythrocytes. The effect of FLV-induced immunosuppression on the immune response to pathogenic organisms, however, has not been extensively investigated.…”

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confidence: 99%

Effect of Friend leukemia virus infection on susceptibility to Candida albicans

et al. 1990

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Previous studies have demonstrated that Friend leukemia virus (FLV) induces a profound immunosuppression in susceptible mice. The studies described in this report indicate that mice infected with FLV have an increased susceptibility to subsequent infection with the opportunistic pathogen Candida albicans, as measured by increased numbers of C. albicans CFU in the kidneys of FLV-infected mice relative to uninfected controls. Experiments in which the NB-tropic and N-tropic strains of FLV were used suggest that virus replication or the resulting virus burden may be important in the observed increased susceptibility to C. albicans. Since neutrophils are believed to be important in the response of mice to systemic Candida infections, the effect of FLV infection on neutrophil candidacidal activity was investigated. The percentage of neutrophils present in unfractionated Proteose Peptone-elicited peritoneal exudates of mice infected with FLV for 14 days was significantly lower than in uninfected control mice or mice infected with FLV for 6 or 10 days. When neutrophils from FLV-infected and control mice were purified, adjusted to equal concentrations, and tested for in vitro candidacidal activity, neutrophils from mice infected with FLV for 14 days were deficient in their ability to kill C. albicans relative to normal controls and mice infected with FLV for 6 or 10 days. Addition of normal mouse serum increased killing in all groups but did not restore candidacidal activity of neutrophils from mice infected with FLV for 14 days to levels of control neutrophils or neutrophils from mice infected for 6 or 10 days with the virus. These results suggest a defect in neutrophil function, at the later stages of FLV infection, involving in vitro candidacidal activity. In addition, neutrophils from FLV-infected mice may be deficient in in vivo chemotactic activity. These defects in neutrophil function could account, at least in part, for the observed increased susceptibility of FLV-infected mice to C. albicans.

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confidence: 99%

Effect of Friend leukemia virus infection on susceptibility to Candida albicans

et al. 1990

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“…In this case BPFC potentiation would also depend on the availability of cross-reacting antigens, explaining why BPFC that are absent or very few in the normal spleen (such as those to RRC and HuRC) are not induced by infection. This mode of action, however, sharply contrasts with the depression of immunological on September 3, 2020 by guest http://iai.asm.org/ Downloaded from reactivity that characterizes FLC and RPV infections (15,20,29). Cross-reactivity between the viral antigens and the antigens used as targets to detect BPFC is ruled out by previous observations (23) and by the wide diversity of erythrocytes with which cross-reaction should occur to justify the present data.…”

Section: Resultsmentioning

confidence: 95%

“…The differences were significant in the FLC-infected group for BPFC to SRC (P < 0.05) and in the RPVinfected group for BPFC to CRC (P < 0.01). By (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) FLC at day -20 a Geometric mean (in parentheses, the 95% confidence limits). day 20 postinfection BPFC were again at normal levels except those directed to CRC in the FLC-infected group, which were still, though not significantly, potentiated.…”

Section: Resultsmentioning

confidence: 99%

Immunodepression by Rowson-Parr virus in mice: effect of Rowson-Parr virus and Friend leukemia complex infections on background antibody-forming cells to various erythrocytes

Bendinelli¹,

Toniolo²,

Campa³

1975

Infect Immun

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The numbers of background antibody-forming cells (BPFC) toward erythrocytes of various species present in the lymphoid organs of unimmunized susceptible BALB/c and resistant C57BL/6 mice were investigated at various times after infection with Friend leukemia complex (FLC) or Rowson-Parr virus (RPV). Both virus preparations induced an increase of BPFC numbers in both animal strains, but the rate and magnitude of the enhancements produced by RPV were much lower. The degree of potentiation varied with the specificity of the BPFC populations and was more pronounced in the spleen than in the lymph nodes and in BALB/c than in C57BL/6 mice. In the late stage of FLC infection, the numbers of splenic BPFC to some erythrocytes underwent a dramatic fall, which was not observed in RPV-infected mice. BPFC present in BALB/c splenocytes cultured in diffusion chambers implanted in the peritoneal cavity of isogeneic normal mice were not affected by viral infection of the chambers.

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“…Immunosuppression in FV leukemia has been demonstrated repeatedly as decrease in serum hemagglutinin titer (11), serum hemolysin titer (5,(9)(10)(11), and hemolytic plaque response (4,5,9,11). The rationale for repeated injection of sheep erythrocytes in our experiments was to provide an opportunity for the antigen-preparing cells which remain after leukemic infiltration to have maximum contact with the antigen.…”

Section: Discussionmentioning

confidence: 99%

Effect of 7,12-Dimethylbenz[a]anthracene on Phagocytosis and Antibody Formation in Friend Virus Leukemia

Elliott

Schloss

1971

Infect Immun

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BALB/c mice with Friend virus leukemia showed (i) a decreased carbon uptake by spleen and liver, observed histologically and measured by the corrected phagocytic index a, in spite of an increased total carbon clearance measured by the phagocytic index K, and (ii) a decreased serum hemolysin titer. Treatment with 7,12-dimethylbenz[a]anthracene (DMBA) increased the carbon uptake by spleen and liver and the serum hemolysin titer. This corresponds to the previously described effect of DMBA on Friend virus leukemia as expressed in the blood picture and the delay in the neoplastic transformation of the spleen causing a prolonged latent period and survival time and a decreased spleen weight. DMBA alone had no effect on carbon clearance and serum hemolysin titer in normal mice. An inhibitory effect on Friend virus (FV) leukemia by the carcinogenic polycyclic aromatic hydrocarbon 7, 12-dimethylbenz[a]anthracene (DMBA) was recently reported (6, 7). Latent

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Suppression of the Primary Antibody Plaque Response of Mice Following Infection with Friend Disease Virus.

Cited by 34 publications

References 0 publications

Effect of Friend leukemia virus infection on susceptibility to Candida albicans

Effect of Friend leukemia virus infection on susceptibility to Candida albicans

Immunodepression by Rowson-Parr virus in mice: effect of Rowson-Parr virus and Friend leukemia complex infections on background antibody-forming cells to various erythrocytes

Effect of 7,12-Dimethylbenz[a]anthracene on Phagocytosis and Antibody Formation in Friend Virus Leukemia

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