Your browser has javascript turned off or blocked. This will lead to some parts of our website to not work properly or at all. Turn on javascript for best performance.

The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here:

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Default user image.

Åke Lernmark

Principal investigator

Default user image.

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


  • Kendra Vehik
  • Kristian F Lynch
  • Matthew C Wong
  • Xiangjun Tian
  • Matthew C Ross
  • Richard A Gibbs
  • Nadim J Ajami
  • Joseph F Petrosino
  • Marian Rewers
  • Jorma Toppari
  • Anette G Ziegler
  • Jin-Xiong She
  • Ake Lernmark
  • Beena Akolkar
  • William A Hagopian
  • Desmond A Schatz
  • Jeffrey P Krischer
  • Heikki Hyöty
  • Richard E Lloyd

Summary, in English

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.


  • Diabetes and Celiac Unit
  • EXODIAB: Excellence in Diabetes Research in Sweden

Publishing year







Nature Medicine





Document type

Journal article


Nature Publishing Group


  • Endocrinology and Diabetes
  • Medical Genetics



Research group

  • Diabetes and Celiac Unit


  • ISSN: 1546-170X