Interference by a Non-Interferon-Inducing Subvariant of Benign Encephalomyocarditis Virus-B with the Ability of EMCV-D to Produce Insulin-Dependent Diabetes Mellitus in ICR Swiss Male Mice

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Abstract
The D variant of encephalomyocarditis virus (EMCV-D) produces a disease syndrome that mimics insulindependent diabetes mellitus (IDDM) in certain mouse strains. Benign EMCV-B interferes with the ability of EMCV-D to produce IDDM. Because EMCV-B induces the production of relatively large amounts of interferon (IFN), it has been hypothesized that the interference by EMCV-B with the pathogenesis of EMCV-D is due to IFN. However, we have previously reported that in outbred ICR Swiss and inbred BALB/cByJ mice, interference by EMCV-B with the development of IDDM in response to infection with EMCV-D does not appear to involve IFN. We have isolated a subvariant of EMCV-B (EMCV-B1) which, preliminary experiments indicate, does not induce the production of detectable levels of IFN in cell culture. Studies were initiated using this subvariant to determine more conclusively if IFN is involved in interference by EMCV-B with the pathogenesis of EMCV-D. The data in the present study show that EMCV-B1 does not induce the production of detectable levels of IFN either in cell culture or in mice, but retains other reported characteristics of the parent EMCV-B, including the ability to interfere with the production of IDDM by EMCV-D in ICR Swiss male mice. These observations strengthen the hypothesis that protection of pancreatic beta cells in ICR Swiss mice by EMCV-B occurs by a mechanism other than IFN.