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Vol. 15. Issue 6.
Pages 583-590 (November - December 2011)
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Vol. 15. Issue 6.
Pages 583-590 (November - December 2011)
Original article
Open Access
Epstein-Barr virus DNA load and its association with Helicobacter pylori infection in gastroduodenal diseases
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Sanket Kumar Shukla1, K.N. Prasad2,
Corresponding author
knprasad@sgpgi.ac.in

Correspondence to.
, Aparna Tripathi1, Avinash Singh1, Ashish Saxena3, Uday Chand Ghoshal4, Narendra Krishnani5, Nuzhat Husain2
1 Department of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, India
2 Department of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences; Department of Pathology, Ram Manohar Lohia Institute of Medical Sciences, India
3 Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, USA
4 Department of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, India
5 Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, India
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Abstract

Helicobacter pylori and Epstein-Barr virus (EBV) infections are common worldwide. Although H. pylori infection is a major factor in gastroduodenal diseases, its role in association with EBV infection is unknown.

Objective

To study the association of H. pylori infection and EBV DNA load in patients with gastroduodenal diseases.

Methods

Biopsy samples were collected from 200 adult patients [non-ulcer dyspepsia (NUD) 100, peptic ulcer disease (PUD) 50, gastric carcinoma (GC) 50] undergoing upper gastrointestinal endoscopy. H. pylori infection was diagnosed by rapid urease test, culture, histopathology, PCR and Q-PCR. EBV DNA was detected by non-polymorphic Epstein- Barr nuclear antigen-1 (EBNA-1) gene based Q-PCR.

Results

In patients with GC and PUD, EBV DNA was detected more often than NUD (GC versus NUD = 90% versus 37%, p < 0.001; PUD versus NUD = 70% versus 37%, p < 0.001). The dual prevalence of H. pylori infection and EBV DNA was significantly higher in patients with GC and PUD than in those with NUD. Median copy number of EBV DNA was considerably higher in GC and PUD than NUD (p < 0.01). The copy number of EBV DNA was significantly higher in H. pylori infected patients (p = 0.015). The number of ureA gene copies was also found to be significantly higher in PUD and NUD with presence of EBV DNA. However, in GC no significant difference was seen between EBV positive and negative status.

Conclusion

There was a trend for higher EBV DNA load in H. pylori positive individuals suggesting a probable role of H. pylori in modulating the conversion of EBV to its lytic phase.

Keywords:
Epstein-Barr virus infections
stomach neoplasms
Helicobacter pylori
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