Related Experiment Video

Updated: May 18, 2026

Lentiviral Mediated Gene Silencing in Human Pseudoislet Prepared in Low Attachment Plates
11:24

Lentiviral Mediated Gene Silencing in Human Pseudoislet Prepared in Low Attachment Plates

Published on: May 14, 2019

Enterovirus-induced gene expression profile is critical for human pancreatic islet destruction

P Ylipaasto1, T Smura, P Gopalacharyulu

  • 1Intestinal Viruses Unit, National Institute for Health and Welfare (THL), Helsinki, Finland.

Diabetologia
|September 18, 2012
PubMed
Abstract

Insights

Enterovirus infection triggers specific gene expression patterns in pancreatic islets, leading to inflammation and cell death. These patterns vary by virus strain, influencing the risk of type 1 diabetes development.

Area of Science:

  • Virology
  • Immunology
  • Endocrinology

Background:

  • Viral infections, particularly enteroviruses, are implicated in the pathogenesis of type 1 diabetes.
  • Beta cell destruction and autoantigen release can initiate autoimmune responses leading to diabetes.
  • Understanding virus-induced immune responses and beta cell damage is crucial for identifying diabetogenic viruses.

Purpose of the Study:

  • To investigate the specific gene expression patterns induced by enterovirus infections in human pancreatic islets.
  • To determine if these patterns differ between lytic and benign enterovirus strains.
  • To correlate viral characteristics with the induction of islet destruction and inflammatory responses.

Main Methods:

  • Global gene expression and cytokine profiles were analyzed in primary human pancreatic islets.
  • DNA microarrays were used to assess changes in gene expression.
  • Enterovirus strains, isolated from type 1 diabetes cases or known to cause diabetes-like conditions in mice, were employed.

Main Results:

  • Lytic enterovirus infections correlated with the expression of pro-inflammatory cytokine genes (IL-1α, IL-1β, TNF-α), which impair beta cell function.
  • All tested enterovirus strains induced increased expression of genes related to double-stranded RNA recognition, antiviral responses, cytokines, and chemokines.
  • Lytic Coxsackievirus B5 (CBV-5)-DS infection downregulated genes involved in glycolysis and insulin secretion.

Conclusions:

  • Enterovirus infection elicits distinct, virus-strain-specific gene expression patterns that promote pancreatic islet destruction and inflammation.
  • Neither viral replication nor cytotoxic cytokine production alone fully explains necrotic cell death.
  • Enterovirus-induced islet necrosis likely results from a combination of factors, including viral replication, cytokine production, and cellular energy depletion.

More Related Videos

Single-cell RNA Sequencing and Analysis of Human Pancreatic Islets11:34

Single-cell RNA Sequencing and Analysis of Human Pancreatic Islets

Published on: July 18, 2019

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets09:31

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets

Published on: June 25, 2012

Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...