Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9283771 | Microbial Pathogenesis | 2005 | 7 Pages |
Abstract
DA subgroup strains of TMEV persist in the CNS of infected mice and induce demyelination. The mechanism(s) of virus persistence and demyelination remains unknown. DA subgroup strains synthesize a 17-kDa protein, called L*, from an initiation site out-of-frame with the polyprotein. The previous study using a mutant virus, DAL*-1 (in which the L* AUG is substituted by an ACG) showed that L* has an anti-apoptotic effect in a macrophage cell line, P388D1. Therefore, we established P388D1 cells that continuatively express L*, in order to confirm its role in TMEV-induced apoptosis. The anti-apoptotic activity of L* may be important in TMEV pathogenesis.
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Authors
Toshiki Himeda, Yoshiro Ohara, Kunihiko Asakura, Yasuhide Kontani, Makoto Sawada,