Roy S. Jamron holds a B.S. in Physics from the University of Michigan and an M.S. in Engineering Applied Science from the University of California at Davis, and independently investigates the latest research on celiac disease and related disorders.
Celiac.com 10/30/2006 - Two recent scientific publications have now shown that a rotavirus protein may be linked to celiac disease through a molecular mimicry mechanism and that the risk of developing celiac disease appears to increase in children in relation to the number of rotavirus infections. What does this mean? Does rotavirus cause celiac disease?
Research has not yet determined the exact role of rotavirus in celiac disease. Researchers found, in active celiac disease, a subset of anti-tTG IgA antibodies recognize the rotavirus protein, VP-7. This means, in celiacs, that the immune system appears to respond to the rotavirus protein the same as it would to a gluten peptide. Hence, a rotavirus infection might, in part, look just like a large dose of ingested gluten in individuals predisposed to celiac disease.
In the study, children genetically susceptible to celiac disease seemed to develop celiac disease in greater numbers after experiencing rotavirus infections than did those children who did not have rotavirus infections. Note that children NOT experiencing a rotavirus infection STILL developed celiac disease. Hence, some OTHER mechanism must be the actual CAUSE of celiac disease, NOT rotavirus. The fact is, the study does NOT show whether the children having rotavirus infections would have eventually developed celiac disease if they were NOT infected with rotavirus (and no study would be able to do so.) The study followed the children from infancy. The study needs to follow the children for many more years to see if the risk rates of children developing celiac disease who experience or do not experience rotavirus infections eventually match. This would eliminate rotavirus as a significant risk factor.
Think of it this way. If instead of experiencing rotavirus infection, some children were fed large quantities of gluten and some children were fed small amounts of gluten, wouldnt it be expected that children fed MORE gluten would be more likely to develop celiac disease SOONER than the children receiving LESS gluten? Now, due to molecular mimicry, think of a rotavirus infection as being a large daily feeding of gluten. Hence, children experiencing rotavirus infections would be more likely to develop celiac disease SOONER than those children who are uninfected. Eventually, ALL children who would have developed celiac disease, sooner or later, would develop the disease.
A previous study found a molecular mimicry mechanism may associate a rotavirus protein with celiac disease. Now a new study of rotavirus antibodies in 1,931 children carrying HLA alleles for celiac disease in the Denver metropolitan area seems to show that the risk of developing celiac disease increases as the frequency of rotavirus infection increases. The study followed children from infancy, taking blood samples at 9, 15, and 24 months and annually, thereafter. 54 children developed celiac disease at a median age of 4.4 years. The study found "Frequent rotavirus infections predicted a higher risk of celiac disease autoimmunity (compared with zero infections, rate ratio 1.94, 95% confidence interval [CI] 0.39-9.56, for one infection and rate ratio 3.76, 95% CI 0.76-18.7, for 2 or more infections, rate ratio for trend per increase in number of infections = 1.94, 95% CI 1.04-3.61, p= 0.037)."
Could rotavirus infection as an adult trigger celiac disease? Not likely. Though symptoms and diagnosis of celiac disease may come late in life, it has been shown celiac disease begins in early childhood. The prevalence of celiac disease in studies of children is the same as the prevalence of celiac disease in adults and does not increase with age.
Am J Gastroenterol. 2006 Oct;101(10):2333-40.
Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: a longitudinal study.
Stene LC, Honeyman MC, Hoffenberg EJ, Haas JE, Sokol RJ, Emery L, Taki I, Norris JM, Erlich HA, Eisenbarth
GS, Rewers M.
Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, Colorado.
PLoS Medicine Volume 3, Issue 9, SEPTEMBER 2006
In Celiac Disease, a Subset of Autoantibodies against Transglutaminase Binds Toll-Like Receptor 4 and Induces Activation of Monocytes
Giovanna Zanoni, Riccardo Navone, Claudio Lunardi, Giuseppe Tridente, Caterina Bason, Simona Sivori, Ruggero Beri, Marzia Dolcino, Enrico Valletta, Roberto Corrocher, Antonio Puccetti