Related Experiment Video
Updated: Apr 6, 2026
Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
Published on: September 28, 2022
Epstein-Barr virus association with peptic ulcer disease
María G Cárdenas-Mondragón1, Javier Torres1, Lourdes Flores-Luna2
1Unidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias (UIMEIP), Hospital de Pediatría, CMN Siglo-XXI, Instituto Mexicano del Seguro Social (IMSS), Avenida Cuauhtémoc 330, Colonia Doctores, Delegación Cuauhtémoc, 06720 Ciudad de México, DF, Mexico.
Epstein-Barr virus (EBV) reactivation is linked to peptic ulcer disease (PUD). This study suggests EBV reactivation may increase the risk of developing both duodenal and gastric ulcers.
Area of Science:
- Gastroenterology
- Virology
- Immunology
Background:
- Peptic ulcer disease (PUD) is commonly associated with Helicobacter pylori (HP) infection and NSAID use.
- However, PUD can occur independently of these known risk factors.
- Epstein-Barr virus (EBV) reactivation has recently been implicated in gastric pre-malignant and malignant lesions.
Purpose of the Study:
- To investigate a potential association between EBV reactivation and the development of PUD.
- To explore if EBV plays a role in PUD pathogenesis beyond established risk factors.
Main Methods:
- Sera from 207 Mexican subjects (129 controls, 78 PUD patients) were analyzed.
- Antibodies against EBV reactivation antigen, HP, and the HP virulence factor CagA were measured.
- Statistical analyses were performed to determine associations between EBV, HP, CagA, and PUD.
Main Results:
- Duodenal PUD showed a significant association with high anti-EBV IgG titers (OR = 2.5, p = 0.022).
- Gastric PUD was positively associated with anti-EBV IgA (OR = 10.1, p = 0.002).
- These findings suggest a specific role for EBV reactivation in different types of PUD.
Conclusions:
- EBV reactivation in gastric and duodenal epithelium is suggested to increase the risk of developing PUD.
- The study highlights EBV as a potential contributing factor in PUD development.
- Further research is warranted to elucidate the mechanisms of EBV in PUD pathogenesis.
More Related Videos
09:43An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection
Published on: March 30, 2018
08:44Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis
Published on: September 7, 2022
Related Concept Videos
01:30Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
01:28Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
01:27Peptic Ulcer
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.