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Found 5 results

  1. Celiac.com 01/30/2019 - Children who receive the rotavirus vaccine may be less likely to develop type 1 diabetes than children who remain unvaccinated, a recent Australian study suggests. Rotavirus can cause severe watery diarrhea, vomiting, fever, and abdominal pain. In some cases, the virus can leave kids with dehydration that is serious enough to require a hospital visit. There is some data to indicate that rotavirus infections can accelerate the development of type 1 diabetes, though researchers don’t yet know why. In May, 2007, health officials introduced a routine oral rotavirus vaccine for infants six weeks and older. In the most recent study, the research team compared rates of type 1 diabetes in the eight years before and the eight years after the vaccine was introduced. The data showed that cases of type 1 diabetes cases declined 14 percent among children age four and younger in the period after the vaccine. The same data showed no significant change in type 1 diabetes cases among older kids. The study wasn’t set up to prove that rotavirus causes type 1 diabetes or how vaccination might help minimize this risk. The findings are only preliminary, lead study author Dr. Kirsten Perrett of the University of Melbourne says that “rotavirus vaccination may be one of possibly many as yet unknown protective environmental and modifiable factors against the development of type 1 diabetes in early childhood.” Perrett stresses that diabetes “has not been clearly linked to other modifiable lifestyle factors and cannot be prevented.” Rotavirus can interfere with insulin production in the pancreas, which could promote type 1 diabetes, Perrett said. The study does add more data to support the idea that viral infections likely contribute to autoimmune disorders like type 1 diabetes and celiac disease in otherwise susceptible people, said Dr. Federico Martinon-Torres a researcher at Hospital Clínico Universitario de Santiago and Instituto de Investigacion Sanitaria de Santiago in Spain. All infants who do not have severely compromised immune systems or a history of bowel obstruction should receive the rotavirus vaccine, says Martinon-Torres. The good news about this study is that a vaccine that is routinely given to most infants seems to offer protection against type 1 diabetes. Source: JAMA Pediatrics, online January 22, 2019.
  2. Celiac.com 09/03/2010 - Many patients who show up at hospitals and clinics with non-specific gastrointestinal symptoms have rotavirus infection A team of researchers recently studied a large cohort of adults with non-specific gastrointestinal complaints to see if people with celiac disease had any higher for rotavirus. The research team included Mohammad Rostami-Nejad, BS, Kamran Rostami, MD,PhD, Maryam Sanaei, MSc, Seyed R. Mohebbi, PhD, David Al-Dulaimi, MD, Ehsan Nazemalhosseini-Mojarad, MSc, Pekka Collin, MD, Chris J. Mulder, MD, PhD, Mohammad R. Zali, MD, FACG. They are associated variously with the Research Center of Gastroenterology and Liver Diseases at Shaheed Beheshti University in Tehran, Iran; the School of Medicine of the University of Birmingham, UK, the Department of Gastroenterology at Alexander Hospital in Redditch, UK; the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital in Finland, and with the Department of Gastroenterology at VU University Medical Center in Amsterdam, The Netherlands. The team conducted the study at the Research Center of Gastroentrology and Liver Disease at Taleghani Hospital in Tehran, Iran. For their study, they randomly selected 5176 individuals living in Tehran, Iran between September 2006 and September 2007. Using a questionnaire, they found 670 case of GI symptoms, each of whom was invited for additional study, including stool sampling and blood tests. The researchers screened stool samples for rotavirus using amplification of specific gene (VP6), light microscopy and formalin-ether concentration methods. They also tested subjects for celiac disease including anti-transglutaminase (tTG) antibodies and total immunoglobulin A (IgA). The research team found the VP6 gene in 150 (22.3%) individuals. 22 subjects showed positive results for anti-tissue transglutaminase (tTG-IgA) (95% CI 2.3-5.1), while three patients who were IgA deficient tested positive for the IgGtTG antibody. Eight of 25 patients (32%) showed amplification of VP6 gene, and positive blood screens for celiac disease, while 142 of 645 with negative celiac blood tests (22%) showed amplification of VP6 gene. They found no statistically important difference between the two groups (p=0.2). Unlike earlier studies in children, this adult study shows that rates of active rotavirus infection were about the same for adults who tested positive for tTG antibody as they were for adults who tested negative for tTG antibody. Based on this study, there is no higher rotavirus risk for adults with celiac disease. Source: Saudi Med J 2010; Vol. 31 (8):891-4.
  3. 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. New Study: 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. Previous study: 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
  4. Celiac.com 09/29/2006 - A new study identified a peptide which causes an immune reaction in a majority of active celiac disease patients but no such reaction in any celiac disease patients on a gluten-free diet. Antibodies to this celiac peptide also recognize and bind to the rotavirus protein VP-7 and cause increased intestinal permeability. Antibodies to VP-7 produced in rabbits also increase intestinal permeability. The celiac peptide also binds to Toll-like receptor 4 and activates monocytes (white blood cells active in innate immunity.) IgA and IgG antibodies to rotavirus protein VP-7 are present in a majority of celiac disease patients and to a much lesser percent of the general population. This suggests VP-7 may be involved in the pathogenesis of celiac disease through a molecular mimicry mechanism. Below is the abstract of the study: 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 Methods and Findings: "In our attempt to clarify the pathogenesis of celiac disease, we screened a random peptide library with pooled sera of patients affected by active disease after a pre-screening with the sera of the same patients on a gluten-free diet. We identified a peptide recognized by serum immunoglobulins of patients with active disease, but not by those of patients on a gluten-free diet. This peptide shares homology with the rotavirus major neutralizing protein VP-7 and with the self-antigens tissue transglutaminase, human heat shock protein 60, desmoglein 1, and Toll-like receptor 4. We show that antibodies against the peptide affinity-purified from the sera of patients with active disease recognize the viral product and self-antigens in ELISA and Western blot. These antibodies were able to induce increased epithelial cell permeability evaluated by transepithelial flux of [3H] mannitol in the T84 human intestinal epithelial cell line. Finally, the purified antibodies induced monocyte activation upon binding Toll-like receptor 4, evaluated both by surface expression of activation markers and by production of pro-inflammatory cytokines." Conclusions: "Our findings show that in active celiac disease, a subset of anti-transglutaminase IgA antibodies recognize the viral protein VP-7, suggesting a possible involvement of rotavirus infection in the pathogenesis of the disease, through a mechanism of molecular mimicry. Moreover, such antibodies recognize self-antigens and are functionally active, able to increase intestinal permeability and induce monocyte activation. We therefore provide evidence for the involvement of innate immunity in the pathogenesis of celiac disease through a previously unknown mechanism of engagement of Toll-like receptor 4."
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