Abstract
JCV infection occurs early in childhood and last throughout life. JCV has been associated to colorectal cancer and might contribute to the cancer phenotype by several mechanisms. Among JCV proteins, particularly two of them, large T-antigen and agnoprotein, can interfere with cell cycle control and genomic instability mechanisms, but other viral proteins might also contribute to the process. Part of viral DNA sequences are detected in carcinoma lesions, but less frequently in adenomas, and not in the normal surrounding tissue, suggesting they are integrated in the host cell genome and these integrations have been selected; in addition viral integration can cause a gene, or chromosomal damage. The inflammatory infiltration caused by a local chronic viral infection in the intestine can contribute to the selection and expansion of a tumor prone cell in a cytokine rich microenvironment. JCV may not be the cause of colorectal cancer, but it can be a relevant risk factor and able to facilitate progression at one or several stages in tumor progression. JCV transient effects might lead to selective expansion of tumor cells. Since there is not a direct cause and effect relationship, JCV infection may be an alternative to low frequency cancer predisposition genes.