Type 1 Diabetes: Virus Infection Or Autoimmune Disease

Type 1 diabetes: virus infection or autoimmune disease?

Type 1 diabetes mellitus (T1DM) may have a stress-activated autoimmune component AND a virus infection component AND an epigenetic component.

In a recent conversation with a person diagnosed with Type 1 Diabetes Mellitus (T1DM), he suggested that the onset of his T1DM was “triggered” by the failure ofhis first romantic relationship. I had never heard of any instances of T1DM being "triggered." Instead, the literature and dogma suggest that Coxsackie B virus contributes to T1DM (see < < and <

My recent research suggests that stress-activated "autovirulence" has a “triggering” role in the etiologies of numerous conditions (e.g., many cancers, most autoimmune syndromes, many neuropsychiatric disorders et al.).Stress-activated autovirulence refers to transmissible and infectious Epstein-Barr virus (EBV) and selected adenovirus secondary (small RNA) particles (e.g., EBV EBER-1 and EBER-2; and, adenovirus VAI and VAII)that lead to transcription and/or translation epigenetic errors (GERRs; see Smith, R 1984 AIDS and 'Slow Viruses', Annals of the NYAS 437, :576-607; also see < and

I then decided to explore whether other instances of T1DM were associated with some trigger event. To my surprise, every person I contacted who has T1DM could cite some (usually stress-related) trigger event. After obtaining a copy of "Type 1 diabetes: virus infection or autoimmune disease?" [Nature Immunology 2002; 3(4), 338-340], it now is evident that T1DM may be caused by a Coxsackie B (or other) virus infection AND some stress-activated autoimmune component AND an epigenetic factor. The article’s subtitle ("What does Coxsackie virus have to do with diabetes? Evidence is emerging that insulin-producing beta cells are highly susceptible to acute infection by Coxsackie virus if their production of interferon is inhibited, resulting in diabetes") reveals the seminal clue. To wit, it is well established that EBV contributes to decreased production of interferons (and especially alpha interferons) and the increased production of competitive acid-labile moieties (cf.Smith, R 1984 AIDS and 'Slow Viruses', Annals of the NYAS437, 576-607; also see < and < alpha interferon should be considered a prototypicGERRand epigenetic byproduct of autovirulence.
I welcome your comments and opinions, and especially if you can cite any instancesof T1DM being triggered by anxiety or stress. If stress-activated T1DM is widespread, then the clinical and laboratory implications may be profound (e.g., in regards to concrete indicators of stress and anxiety; and, assessment of EBV and adenovirus early-antigens). Perhaps more importantautovirulence and epigenetics/epigenomics should receive increased attention especially in regards to ways autovirions effectively change the genetic code for specific gene products (i.e., GERRs), and particularly in view of the “beneath-the-radar” and “hit-and-run” aspects of autovirions.

Roulette Wm. Smith, Ph.D. - Director
Institute for Postgraduate Interdisciplinary Studies
P. O. Box 60846
Palo Alto, CA94306USA
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