T cell immunodeficiency involved in pathogenicity of attenuated MHV3 mutants

Abstract

Viral pathogenicity results when there is an imbalance between viral replication and the host's immune defenses. The immune system plays and important role in the outcome of an acute disease induced by the mouse hepatitis virus type 3 (MHV3). Of use in the study of the role of viral properties involved in its pathogenicity is the attenuated escape mutants. We reported that two MHV3 escape mutants were attenuated in their ability to deplete T cell subpopulations in the spleen in BALB/c mice according to inoculation route and time postinfection. The highly attenuated CL12 mutant cannot induce depletion in T cells following intraperitoneal (i.p.) or intranasal (i.n.) inoculations, at three days postinfection (p.i.). The less attenuated 51.6 mutant, however, maintained the ability to deplete T cells following i.p. inoculation, as described for the pathogenic MHV3. In contrast, no depletion of T cells following i.n. inoculation was induced with this mutant. The use of such mutants enables us to dissect the role of each compartment of the immune system.