CMV is an opportunistic pathogenic microorganism. In vivo it can proliferate in epitheliums, white blood cells and sperm cells, and it is prone to cause latent infection of salivary gland, mammary gland, kidney and white blood cells. In IBD patients, immunosuppressive therapy, impaired absorption of nutrients, dysfunction of the immune system, render them susceptible to CMV infection
, which is consistent with the high infective rate of CMV in immunosuppressed individuals, such as acquired immunodeficiency syndrome (AIDS), transplant recipients, cancer, chemotherapy, but rare in immunocompetent individuals.
The detection methods of CMV infection in IBD patients included DNA detection, serological tests (serum anti-CMV IgM, IgG), histopathology (inclusion bodies detection) in this study. Body fluids or tissue sample was feasible to CMV culture, but it was time-consuming and also had low sensitivity, which limited clinical application
. The detection of CMV-DNA was considered as the most sensitive method
, but it was associated with false positive results, thereby decreasing its specificity. Increase in serum anti-CMV IgM level occurred in recent CMV infection and it had high sensitivity and specificity
, while anti-CMV IgG indicated past CMV infection. Sensitivity of H&E was 10% to 87%
, CMV inclusion bodies could be found in biopsy specimens from colon with inflamed and ulcerated mucosa
. We used CMV-DNA specific fragment UL93, anti-CMV IgG and IgM to detect CMV infection in IBD patients and healthy controls. Positive rates in IBD patients were 84.07%, 76.11%, 1.77% for CMV DNA, anti-CMV IgG and IgM respectively, and 59.66%, 50.69%, 0.34% for healthy controls. CMV-UL93 and anti-CMV IgG were significantly higher in IBD patients as compared to controls, thereby indicating the association between IBD and CMV.
The positive rate of CMV UL-93 or anti-CMV IgG in the healthy controls was about 50–60%, whereas in IBD patients it was around 70–80%. A research conducted in India showed the CMV DNA positive rate was just 12.70% in IBD patients
, which was remarkably lower than in our country. The small number of subjects enrolled (63 IBD patients) could account for the low positive rate in the Indian study. Another research done in France showed 60% positive rate in IBD patients
, which was consistent with our research. In developed countries, the anti-CMV IgG positive rate was found to be above 70%
Anti-CMV IgM positive rate is only 1.77% in our research, which was lower as compared to an Indian study, including IBD patients with both active disease and in remission
, where the rate was 9.52%. Anti-CMV IgM positive rate in healthy controls (0.34%) was no different with IBD patients (P = 0.235), which was related with small amount of people included.
Presence of anti-CMV IgM indicated recent infection of CMV. However in biopsies taken from the pathological sites of intestinal mucosa of anti-CMV IgM positive IBD patients, no inclusion bodies was detected. This was probably due to the low sensitivity of histological examination. The site from where the biopsy was taken, and the amount of tissue retrieved, may also influence the sensitivity of finding inclusion bodies. Next stage we should recruit enough biopsies and screen CMV by immunohistochemistry.
In a model of multivariate analysis adjusting for multiple factors for UC. Disease location seemed to be significantly associate with CMV infection or re-activation, this may be associated with the theory that CMV was prone to proliferate in granulation tissue
. Pancolitis involved with larger areas of ulcerative mucosa, which promote proliferation of CMV. Some researches
 found that CMV was readily discovered in granulation tissue and tissue from deep ulcers, which suggested that CMV could penetrate inflamed mucosa via mononuclear cells, and then proliferate in the mucosa. A recent study
 showed that the murine CMV (MCMV) could not induce acute colitis, but the latent MCMV infection could increase the severity of the dextran sulfate sodium (DSS) induced colitis. Moreover, acute MCMV infection could significantly increase the serum and intestinal natural killer cells, interleukin (IL)-6, TNF-α, IFN-γ, indicating that CMV infection can modulate mucosal immunity, thereby increasing susceptibility to inflammation. CMV infection can also activate oncogenes, kinases, transcription factors inducing tumorigenesis, which may be one of the reasons of the higher incidence of colorectal cancer in IBD patients
. CMV played a role in the initiation and progression of inflammation in IBD. The treatment of 5-ASAs, corticosteroids and immunosupressents were no longer significant associated with CMV infection in multivariate analysis.
Currently there is no absolute indication for antiviral therapy in CMV-positive IBD patients. However Eddleston recommends antiviral therapy in immunocompetent
 found out that ganciclovir could reduce mortality rate and surgical intervention rate, while de Saussure P
 showed that antiviral therapy had no effect on the disease course.
In summary, as compared to healthy individuals, IBD patients have a predisposition to CMV infection. No risk factor was found to be significantly correlated with CMV infection in risk factors analysis.