Theiler's murine encephalomyelitis virus (TMEV) subgroup strain-specific infection in neural and non-neural cell lines

Citation
M. Obuchi et al., Theiler's murine encephalomyelitis virus (TMEV) subgroup strain-specific infection in neural and non-neural cell lines, MICROB IMMU, 43(9), 1999, pp. 885-892
Citations number
24
Categorie Soggetti
Microbiology
Journal title
MICROBIOLOGY AND IMMUNOLOGY
ISSN journal
03855600 → ACNP
Volume
43
Issue
9
Year of publication
1999
Pages
885 - 892
Database
ISI
SICI code
0385-5600(1999)43:9<885:TMEV(S>2.0.ZU;2-9
Abstract
GDVII subgroup strains of Theiler's murine encephalomyelitis virus (TMEV) a re highly virulent and produce acute polioencephalomyelitis in mice, Neithe r viral persistence nor demyelination is demonstrated in the few surviving mice. In contrast, DA subgroup strains are less virulent and establish a pe rsistent central nervous system infection which results in demyelinating di sease. We previously reported a subgroup-specific infection in a macrophage -like cell line, J774-1 cells; i.e., GDVII strain does not replicate in J77 4-1 cells, whereas the DA strain actively replicates in these cells, In add ition, this subgroup-specific virus growth is shown to be related to the pr esence of L* protein, a 17 kDa protein translated out-of-frame of the viral polyprotein from an AUG located 13 nucleotides downstream from the polypro tein's AUG. The present paper demonstrated that this subgroup-specific infe ction is observed in murine monocyte/macrophage lineage cell lines, but not in other murine cell lines including neural cells. An RNase protection ass ay also suggested that L* protein-related virus grow th is regulated at the step of viral RNA replication. As macrophages are reported to be the major cell harboring virus during the chronic demyelinating stage, the activity of L* protein with respect to virus growth in macrophages may be a key fact or in clarifying the mechanism(s) of TMEV persistence, which is probably a trigger to spinal cord demyelination.