Lymphocytic choriomeningitis virus induces a chronic wasting disease in mice lacking class I major histocompatibility complex glycoproteins

Lymphocytic choriomeningitis virus (LCMV) induces a chronic, wasting syndrome when injected intracerebrally into H-2^b mice homozygous for a β2-microglobulin (β2-m (-/-)) gene disruption. These mice have very few CD8⁺ T cells and express little class I MHC glycoprotein, though minimal levels of the H-2D^b molecule have been detected on in vitro cultured β2-m (-/-) cells. The inderlying immunopathological process in these β2-m (-/-) mice is mediated by virus immune CD4⁺ effectors. However, adoptively transferred CD8⁺ T cells from normal, LCMV-infected H-2D^b compatible donors induce significant (but low level) meningitis in β2-m (-/-) recipients. Such mice develop neither the neurological disease characteristic of LCM nor the persistent, though generally non-fatal, debility that occurs when only the CD4⁺ T cell subset is involved.