The objective of this report is to give an overall view of the epidemiological, clinical, diagnostic and therapeutic features of Cytomegalovirus (CMV) infection in inflammatory bowel disease (IBD). A review of published reports on this topic was carried out, with particular attention paid to the selection of patients included in studies and the diagnostic methods employed. CMV is frequently associated with IBD. In some cases, CMV infection is associated with a poor outcome but it is not clear which patients are more likely to be affected and in which stage of the disease. The use of anti-viral therapy in IBD is controversial and an empirical study with controls is needed. The natural history of CMV infection related to the development and treatment of IBD has not been clarified but it is important to take it in consideration because of the possibility of viral persistence in the immunocompromised host and viral interaction with the immune system. family, which includes Epstein -Barr virus (EBV), Herpes Simplex virus tipes1 and 2 (HSV-1,2), Varicella-Zoster virus, and Human Herpes virus types 6 and 7 (HHV-6,7). Similar to infection with other viruses in the family, primary infection with CMV results in the establishment of a persistent or latent infection, due to the ability of the virus to remain integrated in the DNA of host cells. The sign of a viral infection is a cytopathic effect shown by the presence of large nuclear and cytoplasmic inclusions, represented by aggregates of replicating CMV nucleoprotein cores. To avoid recognition and destruction by CD8+T lymphocytes, the virus develops the ability to evade the immune system by several mechanisms. CMV produces some proteins, such as US2, US3 and US11, that inhibit the presentation of viral antigens to T cells, blocking the class I MHC in the endoplasmic reticulum or in the cytosol. It also produces homologues to class I MHC proteins and may compete for binding and presentation of viral antigens. Once the viral DNA remains undisturbed in the infected cells, subsequent reactivation can occur in response to several stimuli, such as immunosuppressant therapy or chemotherapy [1] . The down-regulation of the cell surface markers acts on interferon-alpha/beta dependent responses by affecting several levels of IFN signal transduction and a transcription activation pathway. CMV infection leads to the activation of Nuclear Factor kappa B (NF-kB) and its translocation to the nucleus, promoting the expression of cytokines, chemokines and cellular adhesion molecules. These mechanisms are also present in inflammatory bowel disease (IBD) where there is activation of several pro-inflammatory cytokines (such as IFN-gamma), the transcription of which is regulated through nuclear transcription factors (such as Nuclear Factor kappa B) and through a signal transducer and activator of transcription (STAT family). CMV aND IBDThe role of CMV in IBD is reviewed considering the following issues: diagnostic methods to detect the virus, prevalence of CMV in IBD according to pa...

No abstract

Our preliminary results suggest that HCMV may remain in the colon after an acute colitis flare-up despite remission; it seems that the virus is not responsible for the disease relapse.

The objective of this report is to give an overall view of the epidemiological, clinical, diagnostic and therapeutic features of Cytomegalovirus (CMV) infection in inflammatory bowel disease (IBD). A review of published reports on this topic was carried out, with particular attention paid to the selection of patients included in studies and the diagnostic methods employed. CMV is frequently associated with IBD. In some cases, CMV infection is associated with a poor outcome but it is not clear which patients are more likely to be affected and in which stage of the disease. The use of anti-viral therapy in IBD is controversial and an empirical study with controls is needed. The natural history of CMV infection related to the development and treatment of IBD has not been clarified but it is important to take it in consideration because of the possibility of viral persistence in the immunocompromised host and viral interaction with the immune system.

No abstract