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. 1986 Oct;59(2):261–267.

Immune response to foot-and-mouth disease virus in a murine experimental model: effective thymus-independent primary and secondary reaction.

M V Borca, F M Fernández, A M Sadir, M Braun, A A Schudel
PMCID: PMC1453162  PMID: 3490436

Abstract

The immune response against foot-and-mouth disease virus (FMDV) was studied in a murine model. In untreated control mice, the inoculation of 10,000 suckling mouse 50% lethal doses of Ol Campos FMDV i.p. was followed by a burst of viraemia that disappeared in less than 4 days, i.e. when the neutralizing antibodies (NAb) reached titres above one neutralizing unit. In mice treated with cyclophosphamide, the curves of viraemia and NAb were significantly delayed. Nu/nu mice injected with FMDV had curves of viraemia and NAb identical to those of their nu/t littermates. We then studied the secondary (memory) immune reaction in the same model. In order to investigate which preimmunized cells participate in the elimination of actively replicating FMDV, mice were irradiated, then infected with FMDV, and 24 hr later repopulated with cells obtained from either donor mice that had been previously immunized by infection with live virus, or non-infected controls. The transfer of control (non-immunized) lymphoid cells was unable to eliminate the viraemia in recipient animals at times significantly different from those observed with irradiated recipients receiving no cells, while repopulation of recipients with 10(8) immune lymphoid cells (obtained from pooled thymus, blood, peritoneal exudate, spleen and lymph nodes of preinfected donor mice) led to undetectable titres of viraemia at Day 5 post-infection (p.i.). High doses of thymus cells were totally inactive, while a few as 10(7) donor spleen cells were able to abort viraemia at 6 days p.i. When enriched preparations of B or T spleen cells were adoptively transferred, only B cells were able to abort viraemia in irradiated recipients. It is concluded that, in the murine model of FMDV infection, B cells are mainly responsible for primary response and short-term immunological memory. In both cases the protective immune reaction is T-independent.

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Selected References

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