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-Deficient Mice Infected with Lymphocytic Choriomeningitis Virus1
*
Institute of Medical Microbiology and Immunology and
Medical Anatomy, University of Copenhagen, Copenhagen, Denmark
To define the role of IFN-
in the control of acute infection
with a noncytopathogenic virus, mice with targeted defects of the genes
encoding IFN-, perforin, or both were infected i.v. with two strains
of lymphocytic choriomeningitis virus differing markedly in their
capacity to spread in wild-type mice. Our results reveal that IFN-
is pivotal to T cell-mediated control of a rapidly invasive stain,
whereas it is less important in the acute elimination of a slowly
invasive strain. Moreover, the majority of mice infected with the
rapidly invasive strain succumb to a wasting syndrome mediated by
CD8+ effector cells. The primary effector mechanism
underlying this disease is perforin-dependent lysis, but other
mechanisms are also involved. Wasting disease can be prevented if naive
CD8+ cells from mice transgenic for an MHC class
I-restricted lymphocytic choriomeningitis virus-specific TCR are
adoptively transferred before virus challenge, indicating that the
disease is the result of an unfortunate balance between virus
replication in internal organs, e.g., liver and spleen, and the host
response; resetting this balance by increasing host responsiveness will
again lead to a rapidly controlled infection and limited tissue damage.
Thus, the presence or absence of IFN- determines whether CTLs will
clear infection with this noncytopathogenic virus or induce severe
immunopathology.
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