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Epstein-Barr virus DNA load and its association with Helicobacter pylori infection in gastroduodenal diseases
Shukla, Sanket Kumar; Prasad, K. N; Tripathi, Aparna; Singh, Avinash; Saxena, Ashish; Ghoshal, Uday Chand; Krishnani, Narendra; Husain, Nuzhat.
  • Shukla, Sanket Kumar; Sanjay Gandhi Postgraduate Institute of Medical Sciences. Department of Microbiology. IN
  • Prasad, K. N; Sanjay Gandhi Postgraduate Institute of Medical Sciences. Department of Microbiology. IN
  • Tripathi, Aparna; Sanjay Gandhi Postgraduate Institute of Medical Sciences. Department of Microbiology. IN
  • Singh, Avinash; Sanjay Gandhi Postgraduate Institute of Medical Sciences. Department of Microbiology. IN
  • Saxena, Ashish; University of Texas Medical Branch. Department of Biochemistry and Molecular Biology. US
  • Ghoshal, Uday Chand; s.af
  • Krishnani, Narendra; Sanjay Gandhi Postgraduate Institute of Medical Sciences. Department of Pathology. IN
  • Husain, Nuzhat; Sanjay Gandhi Postgraduate Institute of Medical Sciences. Department of Microbiology. IN
Braz. j. infect. dis ; 15(6): 583-590, Nov.-Dec. 2011. ilus, tab
Article in English | LILACS | ID: lil-610531
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 percent versus 37 percent, p < 0.001; PUD versus NUD = 70 percent versus 37 percent, 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.
Subject(s)


Full text: Available Index: LILACS (Americas) Main subject: Peptic Ulcer / Stomach Neoplasms / DNA, Viral / Helicobacter pylori / Helicobacter Infections / Epstein-Barr Virus Infections Type of study: Diagnostic study / Risk factors Limits: Adult / Female / Humans / Male Language: English Journal: Braz. j. infect. dis Journal subject: Communicable Diseases Year: 2011 Type: Article / Project document Affiliation country: India / United States Institution/Affiliation country: Sanjay Gandhi Postgraduate Institute of Medical Sciences/IN / University of Texas Medical Branch/US

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Full text: Available Index: LILACS (Americas) Main subject: Peptic Ulcer / Stomach Neoplasms / DNA, Viral / Helicobacter pylori / Helicobacter Infections / Epstein-Barr Virus Infections Type of study: Diagnostic study / Risk factors Limits: Adult / Female / Humans / Male Language: English Journal: Braz. j. infect. dis Journal subject: Communicable Diseases Year: 2011 Type: Article / Project document Affiliation country: India / United States Institution/Affiliation country: Sanjay Gandhi Postgraduate Institute of Medical Sciences/IN / University of Texas Medical Branch/US