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Nat Med. 2019 Dec;25(12):1865-1872. doi: 10.1038/s41591-019-0667-0. Epub 2019 Dec 2.

Prospective virome analyses in young children at increased genetic risk for type 1 diabetes.

Author information

Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Alkek Center for Metagenomics and Microbiome Research, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA.
Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX, USA.
Barbara Davis Center for Diabetes, University of Colorado, Aurora, CO, USA.
Department of Pediatrics, Turku University Hospital, Turku, Finland.
Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland.
Institute of Diabetes Research, Helmholtz Zentrum München, Munich, Germany.
Forschergruppe Diabetes, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany.
Forschergruppe Diabetes e.V, Munich, Germany.
Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Department of Clinical Sciences, Lund University/CRC, Skane University Hospital, Malmö, Sweden.
National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, USA.
Pacific Northwest Research Institute, Seattle, WA, USA.
Department of Pediatrics, University of Florida Diabetes Institute, Gainesville, FL, USA.
Department of Virology, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.


Viruses are implicated in autoimmune destruction of pancreatic islet β cells, which results in insulin deficiency and type 1 diabetes (T1D)1-4. Certain enteroviruses can infect β cells in vitro5, have been detected in the pancreatic islets of patients with T1D6 and have shown an association with T1D in meta-analyses4. However, establishing consistency in findings across studies has proven difficult. Obstacles to convincingly linking RNA viruses to islet autoimmunity may be attributed to rapid viral mutation rates, the cyclical periodicity of viruses7 and the selection of variants with altered pathogenicity and ability to spread in populations. β cells strongly express cell-surface coxsackie and adenovirus receptor (CXADR) genes, which can facilitate enterovirus infection8. Studies of human pancreata and cultured islets have shown significant variation in enteroviral virulence to β cells between serotypes and within the same serotype9,10. In this large-scale study of known eukaryotic DNA and RNA viruses in stools from children, we evaluated fecally shed viruses in relation to islet autoimmunity and T1D. This study showed that prolonged enterovirus B rather than independent, short-duration enterovirus B infections may be involved in the development of islet autoimmunity, but not T1D, in some young children. Furthermore, we found that fewer early-life human mastadenovirus C infections, as well as CXADR rs6517774, independently correlated with islet autoimmunity.


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