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  • Jefferson Adams
    Jefferson Adams

    Enterovirus Infection in Childhood Could Trigger Celiac Disease

      A new study shows that early childhood infection with enterovirus is associated with later celiac disease.

    Caption: Image: CC--Jacqui Brown

    Celiac.com 02/18/2019 - Many researchers have suspected that childhood infections with certain viruses may open the door for the development of celiac disease. Celiac.com has covered the connection in previous articles, such as Can Viruses Trigger Celiac Disease? and Is a Reovirus Infection a Prime Cause of Celiac Disease? Now there is even more evidence to support such a connection.

    A team of Norwegian researchers recently set out to learn whether early exposure to common intestinal viruses, specifically human enterovirus or adenovirus, are factors in the later development of celiac disease.

    The research team included Christian R Kahrs,  Katerina Chuda,  German Tapia,  Lars C Stene,  Karl Mårild,  Trond Rasmussen,  Kjersti S Rønningen,  Knut E A Lundin,  Lenka Kramna,  Ondrej Cinek, professor,  and Ketil Størdal. 

    Study Methods

    For their case-controlled study, nested within Norwegian birth cohort, the team reviewed data for patients recruited between 2001 and 2007, which were followed through September 2016. The team specifically looked at data for children carrying the HLA genotype DR4-DQ8/DR3-DQ2, which increases risk of celiac disease. The team detected enterovirus and adenovirus in real time using polymerase chain reaction in monthly stool samples from age 3 to 36 months. Celiac disease diagnoses were made using standard criteria. 

    The team looked for celiac disease antibodies in blood samples taken at age 3, 6, 9, and 12 months and then annually. To determine the connection between viral infections before appearance of celiac disease antibodies and celiac disease, the team calculated adjusted odds ratios using a mixed effects logistic regression model.

    Study Findings

    This study showed that exposure to Enterovirus A and Enterovirus B during early childhood is associated with later celiac disease. Interestingly, The connection was only for infections after introduction of gluten into the infant diet.They found no connection between adenovirus and later celiac development. This study strengthens the idea that early childhood exposure to a viral infection likely plays a role in the development of celiac disease.

    Read more at BMJ.comScience 07 Apr 2017: Vol. 36, Issue 6333, pp. 44-50.; and SCILOG

    Edited by Jefferson Adams

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    “An enterovirus infection”. Enterovirus is not the name of the virus strain, it’s a category of viruses, like a reovirus or a rotavirus. 

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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Jefferson Adams
    Celiac.com 03/22/2010 - The main cause for gluten intolerance continues to puzzle scientists, but pathogenesis theories include both genetic susceptibility and environmental triggers, like a virus or infection.
    For the first time, scientists working with the Academy of Finland’s Research Program on Nutrition, Food, and Health have found genes in the body that are associated both with the immune system and with the body's ability to properly digest gluten in the intestinal tract.
    Gluten intolerance arises from an autoimmune reaction in the small intestine to the gluten protein found in wheat, barley and rye. Academy Research Fellow Paivi Saavalainen, a veteran researcher in hereditary risk factors for gluten intolerance, says that "some of the genes we have identified are linked with human immune defense against viruses. This may indicate that virus infections may be connected in some way with the onset of gluten intolerance.”
    Data shows that rates of celiac disease in America have increased more than 400% since World War II. Meanwhile, a Finnish scientist internationally known for his gluten research says that the number of people in Finland who suffer from gluten intolerance has doubled over the last two decades.
    Since the early 1980s, the percentage of Finns with gluten intolerance has risen from about 1 percent of adults to about 2 percent, according to Professor Markku Mäki, head of a research project in the Academy of Finland's Research Program on Nutrition, Food and Health.
    "We've already seen a similar trend emerge earlier on where allergies and certain autoimmune disorders are concerned. Screening has shown that gluten intolerance occurs in 1.5 per cent of Finnish children and 2.7 per cent of the elderly. The higher figure for older people is explained by the fact that the condition becomes more frequent with age," says Mäki.
    For the immune study, when researchers scanned the genetic maps of more than 9400 celiac patients, they found areas of immune system disturbance. Their evidence also indicated that genes connected with the inability to digest gluten were also connected with other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis.
    Saavalainen and his team have succeeded in localizing risk genes in both individual patients and entire families, which adds weight to the notion that gluten intolerance is inherited.
    The researchers are hoping to use the genetic information to craft better screening tests for gluten intolerance, as up to 75% of people with gluten intolerance remain undiagnosed due to mild or atypical symptoms, and many with condition may unwittingly suffer damage to their intestinal villi. Professor Maki points out that many present first with iron deficient, or folic acid deficient, anemia.
    Source:
    Academy of Finland
     

    Jefferson Adams
    Celiac.com 07/27/2016 - Celiac disease is an immune-based disorder triggered by an adverse immune reaction to gluten proteins in genetically susceptible people. A new study shows that certain viral diseases may increase celiac risk, and confirms a link between intestinal viral infections and celiac disease.
    Reinhard Hinterleitner earned his PhD from the Medical University of Innsbruck in molecular cell biology and oncology at the group of Gottfried Baier at the Department of Medical Genetics, Molecular and Clinical Pharmacology. He is currently doing postdoctoral research at the University of Chicago as part of an Erwin Schrödinger Fellowship.
    Dr. Hinterleitner looked at blood samples and 150 small-intestine biopsies from celiac patients and compared them with those of a healthy control group. He found that intestinal viruses can trigger a sort of long-term false alarm in celiac patients by upsetting the small intestine and transforming regulatory T lymphocytes into pro-inflammatory T lymphocytes.
    "The dendritic cells are also alerted by the infection. If gluten...is consumed at the same time as a viral infection occurs, the already alerted dendritic cells also present gluten antigens to the T lymphocytes," said Dr. Hinterleitner.
    This can result in the transmission of incorrect information, and can trigger an inflammatory response in T lymphocytes that attacks both the virus and the gluten. They have seen as much in genetically engineered celiac mouse models, wherein a reoviral infection of the small intestine of mice triggers clinical symptoms similar to those experienced by celiac patients who consume gluten.
    This might also explain why infants who have already had a rotavirus infection are more likely to develop celiac disease. Because if an infant is suffering from a viral infection at the same time, the first intake of gluten, which is supposed to establish oral tolerance to gluten, might in fact have the opposite effect.
    If this is true, early vaccination against intestinal viruses such as rota- and reovirus in early childhood might reduce the incidence of celiac disease.
    They estimate that introducing gluten at the same time as intestinal virus infection results in a long-term loss of oral tolerance to gluten in the 20 percent of the population with the genetic predisposition for celiac disease, especially in patients who respond more strongly to virus infections.
    Source:
    SCILOG

    Jefferson Adams
    Celiac.com 04/17/2017 - A team of researchers recently set out to test this hypothesis and to gain insights into mechanisms underlying virus-induced loss of tolerance to dietary antigens. To do so, they developed a viral infection model that makes use of two reovirus strains that infect the intestine, but which differ in their immunopathological outcomes.
    The research team included Romain Bouziat, Reinhard Hinterleitner, Judy J. Brown, Jennifer E. Stencel-Baerenwald, Mine Ikizler, Toufic Mayassi, Marlies Meisel, Sangman M. Kim, Valentina Discepolo, Andrea J. Pruijssers, Jordan D. Ernest, Jason A. Iskarpatyoti, Léa M. M. Costes, Ian Lawrence, Brad A. Palanski, Mukund Varma, Matthew A. Zurenski, Solomiia Khomandiak, Nicole McAllister, Pavithra Aravamudhan, Karl W. Boehme, Fengling Hu, Janneke N. Samsom, Hans-Christian Reinecker, Sonia S. Kupfer, Stefano Guandalini, Carol E. Semrad, Valérie Abadie, Chaitan Khosla, Luis B. Barreiro, Ramnik J. Xavier, Aylwin Ng, Terence S. Dermody, and Bana Jabri.
    Reoviruses usually infect humans and mice without overt physical symptoms. Prior research by Bouziat et al., has shown that immune responses to two gut-infecting reoviruses take different paths in mice, as noted in the Perspective by Verdu and Caminero.
    Both reoviruses triggered protective immune responses. However, when one of the reoviruses occurred in the presence of a dietary antigen, such as gluten or ovalbumin, tolerance to the dietary antigen disappeared. This was because this strain blocked the formation of tolerogenic T cells. Instead, it promoted T helper 1 immunity to the dietary antigen through interferon regulatory factor 1 signaling. Moreover, celiac disease patients also showed elevated levels of antibodies against reovirus.
    Reovirus is an avirulent pathogen that elicits protective immunity, but these researcher have shown that it can also cause a disruption of intestinal immune homeostasis at inductive and effector sites of oral tolerance by suppressing peripheral regulatory T cell (pTreg) conversion, and promoting TH1 immunity to dietary antigen. TH1 immunity to dietary antigen depended on interferon regulatory factor 1, and was unconnected to suppression of pTreg conversion, which was mediated by type-1 interferon.
    This study provides important scientific support for the idea that this seemingly mild reovirus plays a major role in the development of celiac disease.
    Clearly further study is needed to determine the exact nature of the role of reovirus in celiac disease, and to determine if these connections might prompt any changes in celiac diagnosis and treatment.
    Source:
    Science 07 Apr 2017: Vol. 36, Issue 6333, pp. 44-50. DOI: 10.1126/science.aah5298  
     
    The researchers are variously affiliated with the Department of Medicine, the Department of Pathology, and the Committee on Immunology at the University of Chicago in Chicago, IL, USA; the Department of Pathology, Microbiology, and Immunology, the Department of Pediatrics, and the Elizabeth B. Lamb Center for Pediatric Research at Vanderbilt University Medical Center in Nashville, TN, USA; the Department of Translational Medical Sciences, Section of Pediatrics, University of Naples Federico II, and CeInGe–Biotecnologie Avanzate, Naples, Italy; the Laboratory of Pediatrics, Division of Gastroenterology and Nutrition, Erasmus University Medical Center Rotterdam-Sophia Children’s Hospital, Rotterdam, Netherlands; the Department of Chemistry, Stanford University, Stanford, CA, USA; the Division of Gastroenterology, Department of Medicine, Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; the Broad Institute of MIT and Harvard University, Cambridge, MA, USA; the University of Chicago Celiac Disease Center at the University of Chicago, Chicago, IL, USA; the Section of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Chicago, Chicago, IL, USA; the Department of Microbiology, Infectiology, and Immunology, University of Montreal, and the Centre Hospitalier Universitaire (CHU) Sainte-Justine Research Center, Montreal, Quebec, Canada; the Department of Chemical Engineering, Stanford University, Stanford, CA, USA; the Stanford ChEM-H, Stanford University, Stanford, California, USA; the Department of Genetics, CHU Sainte-Justine Research Center, Montreal, Quebec, Canada; the Center for Computational and Integrative Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; the Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; and the Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

    Jefferson Adams
    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.

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