The M variant of encephalomyocarditis(EMC-M) virus produces intermittently diabetes in mice by infecting and destroying pancreatic beta cells. One highly diabetogenic D variant(EMC-D) and the other nondiabetogenic B variant(EMC-B) were isolated
from
EMC-M, EMC-D scarcely induces interferon, whereas EMC-B is a good inducer for interferon. In contrast to the biological differences. EMC-D and EMC-B are almost indistinguishable in several physicochemical and immunological properties. So the
diabetogenicity of EMC virus was considered to be related to the ability of interferon induction.
We isolated new variants EMC-DV(EMC-D3/1 and EMC-D4/1B) from EMC-D. EMC-DV is neither diabetogenic nor inducing interferon. EMC-D is considered to have a attachment site to pancreaticβcell with high affinity but EMC-DV and EMC-B is to have the
same
attachment site with low affinity by single point mutation from EMC-D However EMC-D, DV and B can be infected toβcell in vivo and in vitro. These observations suggest that some mechanisms other than interferon and attachment system are involved
in
determining the ability of the viruses to infect and destroyβcells. We presumed that EMC-B and EMC-DV induce some viral inhibitory factors from phagocytic cell or lymphocyte and then they are nondiabetogenic. We infected BALB/c mice with EMC-B
and
fused the splenocytes with myeloma cells. We obtained the hybridoma 12D8 releasing viral inhibitory substance(VIS) that must be neither immunoglobulin nor interferon. VIS had inhibiory effects on EMC-D at L(mouse fibroblast-like), BMP (baby mouse
pancreas), Vero(African green monkey kidney), WⅠ-38(human lung) and other cell lines. And VIS had inhibitory effects on EMC-D, EMC-B, coxsackie B4, reovirus and vesicular stomatitis virus at L cell. VIS appeared to act directly on host cell. VIS
had
strong preventive effect(100%) on diabetes induced with EMC-D at SJL/J and DBN/2N mice.
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