Abstract
The development of islet autoimmunity and type 1 diabetes has long been linked with enteroviral infection but a causal relationship has proven hard to establish. This is partly because much of the epidemiological evidence derives from studies of neutralising antibody generation in blood samples while less attention has been paid to the pancreatic beta cell as a site of infection. Nevertheless, recent studies have revealed that beta cells express specific enteroviral receptors and that they can sustain a productive enteroviral infection. Importantly, they can also mount antiviral responses which attenuate viral replication and may favour the establishment of a persistent enteroviral infection. Together, these responses combine to create the Trojan horse by which enteroviruses might precipitate islet autoimmunity.
Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Antiviral Agents / adverse effects
-
Antiviral Agents / therapeutic use*
-
Biomarkers / blood
-
Blood Glucose / drug effects*
-
Blood Glucose / metabolism
-
Diabetes Mellitus, Type 1 / blood
-
Diabetes Mellitus, Type 1 / drug therapy*
-
Diabetes Mellitus, Type 1 / immunology
-
Diabetes Mellitus, Type 1 / virology
-
Drug Design
-
Enterovirus / drug effects*
-
Enterovirus / pathogenicity
-
Enterovirus Infections / blood
-
Enterovirus Infections / drug therapy*
-
Enterovirus Infections / immunology
-
Enterovirus Infections / virology
-
Host-Pathogen Interactions
-
Humans
-
Hypoglycemic Agents / adverse effects
-
Hypoglycemic Agents / therapeutic use*
-
Insulin-Secreting Cells / drug effects*
-
Insulin-Secreting Cells / immunology
-
Insulin-Secreting Cells / metabolism
-
Insulin-Secreting Cells / virology
-
Risk Factors
Substances
-
Antiviral Agents
-
Biomarkers
-
Blood Glucose
-
Hypoglycemic Agents