P187 Differential distribution of Epstein-Barr virus and Cytomegalovirus in colonic mucosa in patients with active ulcerative colitis

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Background: Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) are members of the herpesvirus family. CMV reactivation is often complicated with ulcerative colitis (UC), and is known as the one of exacerbation factors in its pathophysiology. On the other hand, EBV is indicated on the association with oncogenesis including several cancer or lymphoproliferative disorder. However, the association between EBV reactivation and colonic inflammation is still unclear.

Methods: Sixty-four active UC patients who received colonoscopy between January 2005 and January 2015 in Kyoto University Hospital were enrolled in this study. We assessed EBV and CMV reactivation in inflamed and non-inflamed colonic mucosa of active UC patients. Biopsy specimens were obtained from both inflamed and non-inflamed colonic mucosa in each patient. Viral load of EBV and CMV was measured by real-time PCR cdetection of each DNA quantity more than 10 copies/μgDNA. Moreover, we examined the correlation between positivity of each viruses and patients' backgrounds.

Results: (1) Of 64 UC patients, 20 patients (31.3%) and 31 patients (48.4%) were positive for CMV and EBV, respectively. No significant correlation between EBV and CMV reactivation was observed (p=0.33). CMV-DNA was detected in both inflamed and non-inflamed colonic mucosa only in 5 of 20 patients (25.0%) with CMV reactivation. In contrast, 21 of 31 EBV-positive patients (67.7%) had EBV reactivation in not only inflamed but also non-inflamed colonic mucosa.

(2) There was no significant difference in patients' backgrounds between CMV-positive and CMV-negative group.

(3) Mayo endoscopic score was significantly higher in EBV-positive group than EBV-negative group (2.5 vs 2.0, p=0.04). Moreover, the proportion of patients treated with anti TNF-α antibody was significantly higher in EBV-positive group compared to EBV-negative group (16.1% vs 0.0%, p=0.02).

Conclusions: Our data suggests that a mechanism of EBV reactivation would be different from that of CMV reactivation, and might include blockade of TNF-α. Further studies are required to clarify a role of EBV reactivation on colonic inflammation in UC patients.

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