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IF A VIRUS CAUSES DIABETES, WHAT ARE THE IMPLICATIONS FOR GENETIC PREDISPOSITION AND AUTOIMMUNITY?.
Wm. Klitz ¹ and Bo Niklasson ². ¹ Public Health, Univ Calif, Berkeley, USA and ² Apodemus AB, Stockholm, Sweden .

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A variety of evidence points to the role of Ljungan virus (LV), a recently discovered picornavirus, in diabetes and reproductive diseases. LV has been found in the native mammals of Sweden, and governs the population cycles of several rodent species in northern Sweden. LV is also present in North American rodents. In native voles and laboratory mice, LV causes a variety of symptoms mimicking T1D and T2D. Kochs postulates for pathogen transmission have been satisfied in lab mice. Antiviral therapy reduces the frequency of diabetes in lab mice.
In humans the incidence of new cases of T1D, gestational diabetes, preeclampsia and intrauterine fetal death (IUFD) in northern Sweden is correlated with rodent population cycles, showing that the attributable risk due to the underlying factor must be substantial. These diseases are found concurrently in individuals far in excess of random expectations. Antisera and IHC (immunohistochemistry) assays show an excess frequency of LV in T1D patients and LV in samples of IUFD from several organs and from placentas of women with preeclampsia, resp. RT-PCR confirms the presence of LV in preeclampsia placenta, and the IHC assay is positive for LV only in preeclampsia cases.
At last, an often posited environmental factor in autoimmunity may be at hand. If LV causes these diseases, then how can genetic predisposition and autoimmunity be explained? The diverse genetic associations of T1D, T2D and gestational diabetes suggest that physiological predisposition to specific metabolic processes of each disease must underlie these relationships, rather than reflecting response to a specific pathogen. The variability among individuals for disruption of metabolism in differing tissues by LV requires much further exploration.