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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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Article information
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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References
[1.]
A.B. Rickinson, E. Kieff.
Fields Virology: Philadelphia.
Lippincott Williams & Wilkins, (2001),
[2.]
H. Sousa, A.L. Pinto-Correia, R. Medeiros, et al.
Epstein-Barr virus is associated with gastric carcinoma: the question is what is the significance?.
World J Gastroenterol, 14 (2008), pp. 4347-4351
[3.]
D. Shibata, L.M. Weiss.
Epstein-Barr virus-associated gastric adenocarcinoma.
Am J Pathol, 140 (1992), pp. 769-774
[4.]
A. Szkaradkiewicz, W. Majewski, M. Wal, et al.
Epstein-Barr virus (EBV) infection and p53 protein expression in gastric carcinoma.
Virus Res, 118 (2006), pp. 115-119
[5.]
R. Durmaz, A. Aydin, M. Koroglu, et al.
Investigation of the relationship between Epstein-Barr virus and ordinary gastric carcinoma using the nested polymerase chain reaction.
Acta Virol, 42 (1998), pp. 359-363
[6.]
G. Murphy, R. Pfeiffer, M.C. Camargo, et al.
Meta-analysis shows that prevalence of Epstein-Barr virus-positive gastric cancer differs based on sex and anatomic location.
Gastroenterology, 137 (2009), pp. 824-833
[7.]
M.L. Gulley, W. Tang.
Laboratory assays for Epstein-Barr virusrelated disease.
J Mol Diagn, 10 (2008), pp. 279-292
[8.]
J.L. Ryan, H. Fan, S.L. Glaser, et al.
Epstein-Barr virus quantitation by real-time PCR targeting multiple gene segments: a novel approach to screen for the virus in paraffin-embedded tissue and plasma.
J Mol Diagn, 6 (2004), pp. 378-385
[9.]
M.S. Wu, C.T. Shun, C.C. Wu, et al.
Epstein-Barr virus-associated gastric carcinomas: relation to H. pylori infection and genetic alterations.
Gastroenterology, 118 (2000), pp. 1031-1038
[10.]
A. Saxena, K. Nath Prasad, U. Chand Ghoshal, et al.
Association of Helicobacter pylori and Epstein-Barr virus with gastric cancer and peptic ulcer disease.
Scand J Gastroenterol, 43 (2008), pp. 669-674
[11.]
J.L. Ryan, D.R. Morgan, R.L. Dominguez, et al.
High levels of Epstein-Barr virus DNA in latently infected gastric adenocarcinoma.
Lab Invest, 89 (2009), pp. 80-90
[12.]
A. Hirano, H. Yanai, N. Shimizu, et al.
Evaluation of Epstein- Barr virus DNA load in gastric mucosa with chronic atrophic gastritis using a real-time quantitative PCR assay.
Int J Gastrointest Cancer, 34 (2003), pp. 87-94
[13.]
Y. Kaizaki, S. Sakurai, J.M. Chong, et al.
Atrophic gastritis. Epstein-Barr virus infection, and Epstein-Barr virus-associated gastric carcinoma.
Gastric Cancer, 2 (1999), pp. 101-108
[14.]
H. Yanai, K. Takada, N. Shimizu, et al.
Epstein-Barr virus infection in non-carcinomatous gastric epithelium.
[15.]
L.S. Young, A.B. Rickinson.
Epstein-Barr virus: 40 years on.
Nat Rev Cancer, 4 (2004), pp. 757-768
[16.]
J. Minoura-Etoh, K. Gotoh, R. Sato, et al.
Helicobacter pyloriassociated oxidant monochloramine induces reactivation of Epstein-Barr virus (EBV) in gastric epithelial cells latently infected with EBV.
J Med Microbiol, 55 (2006), pp. 905-911
[17.]
M. Singh, K.N. Prasad, S.K. Yachha, et al.
Genotypes of Helicobacter pylori in children with upper abdominal pain.
J Gastroenterol Hepatol, 18 (2003), pp. 1018-1023
[18.]
C. Schabereiter-Gurtner, A.M. Hirschl, B. Dragosics, et al.
Novel real-time PCR assay for detection of Helicobacter pylori infection and simultaneous clarithromycin susceptibility testing of stool and biopsy specimens.
J Clin Microbiol, 42 (2004), pp. 4512-4518
[19.]
P. Lauren.
the two histological main types of gastric carcinoma: diffuse and so-called intestinal-type carcinoma. An attempt at a histo-clinical classification.
Acta Pathol Microbiol Scand, 64 (1965), pp. 31-49
[20.]
B. Luo, Y. Wang, X.F. Wang, et al.
Expression of Epstein-Barr virus genes in EBV-associated gastric carcinomas.
World J Gastroenterol, 11 (2005), pp. 629-633
[21.]
P.C. Chen, C.C. Pan, A.H. Yang, et al.
Detection of Epstein-Barr virus genome within thymic epithelial tumours in Taiwanese patients by nested PCR. PCR in situ hybridization, and RNA in situ hybridization.
J Pathol, 197 (2002), pp. 684-688
[22.]
Y.J. Gan, B.I. Razzouk, T. Su, et al.
A defective, rearranged Epstein- Barr virus genome in EBER-negative and EBER-positive Hodgkins disease.
Am J Pathol, 160 (2002), pp. 781-786
[23.]
M. Korabecna, M. Ludvikova, A. Skalova.
Molecular diagnosis of Epstein-Barr virus in paraffin-embedded tissues of tumors with abundant lymphoid infiltration.
Neoplasma, 50 (2003), pp. 8-12
[24.]
J.L. Ryan, R.J. Jones, S.H. Elmore, et al.
Epstein-Barr virus WZhet DNA can induce lytic replication in epithelial cells in vitro, although WZhet is not detectable in many human tissues in vivo.
Intervirology, 52 (2009), pp. 8-16
[25.]
L.L. Hsieh, P.J. Lin, T.C. Chen, et al.
Frequency of Epstein-Barr virus-associated gastric adenocarcinoma in Taiwan.
Cancer Lett, 129 (1998), pp. 125-129
[26.]
G. Alipov, T. Nakayama, M. Nakashima, et al.
Epstein-Barr virus- associated gastric carcinoma in Kazakhstan.
World J Gastroenterol, 11 (2005), pp. 27-30
[27.]
V.P. Lima, M.A. de Lima, A.R. Andre, et al.
H. pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: correlation with p53 mutation and c-Myc Bcl-2 and Bax expression.
World J Gastroenterol, 14 (2008), pp. 884-891
[28.]
M. Rugge, R.M. Genta.
Epstein-Barr virus: a possible accomplice in gastric oncogenesis.
J Clin Gastroenterol, 29 (1999), pp. 3-5
[29.]
A. Saxena, K.N. Prasad, U.C. Ghoshal, et al.
Polymorphism of -765G > C COX-2 is a risk factor for gastric adenocarcinoma and peptic ulcer disease in addition to H pylori infection: a study from northern India.
World J Gastroenterol, 14 (2008), pp. 1498-1503
[30.]
P. Sipponen, T.U. Kosunen, J. Valle, et al.
Helicobacter pylori infection and chronic gastritis in gastric cancer.
J Clin Pathol, 45 (1992), pp. 319-323
[31.]
M.E. Craanen, P. Blok, W. Dekker, et al.
Helicobacter pylori and early gastric cancer.
Gut, 35 (1994), pp. 1372-1374
[32.]
Y.L. Tang, R.L. Gan, B.H. Dong, et al.
Detection and location of Helicobacter pylori in human gastric carcinomas.
World J Gastroenterol, 11 (2005), pp. 1387-1391
[33.]
C. Zhang, N. Yamada, Y.L. Wu, et al.
Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer.
World J Gastroenterol, 11 (2005), pp. 791-796
[34.]
V. Kate, N. Ananthakrishnan.
Helicobacter pylori and gastric carcinoma: evidence for the link.
Natl Med J India, 13 (2000), pp. 329
[35.]
A.K. Khanna, P. Seth, G. Nath, V.K. Dixit, et al.
Correlation of Helicobacter pylori and gastric carcinoma.
J Postgrad Med, 48 (2002), pp. 27-28
[36.]
R. Sivaprakash, U.A. Rao, S.P. Thyagarajan, et al.
Investigation for the prevalence of Helicobacter pylori infection in patients with gastric carcinoma in Madras.
India. Jpn J Med Sci Biol, 49 (1996), pp. 49-56
[37.]
P.C. Konturek, J. Kania, J.W. Konturek, et al.
H. pylori infection, atrophic gastritis, cytokines, gastrin, COX-2, PPAR gamma and impaired apoptosis in gastric carcinogenesis.
Med Sci Monit, 9 (2003), pp. 53-66
[38.]
C. Semino-Mora, S.Q. Doi, A. Marty, et al.
Intracellular and interstitial expression of Helicobacter pylori virulence genes in gastric precancerous intestinal metaplasia and adenocarcinoma.
J Infect Dis, 187 (2003), pp. 1165-1177
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