Impact of Cytomegalovirus infection on immune signatures in cancer patients

Excerpt

Human Cytomegalovirus (CMV) is a wide-spread persistent beta-herpes virus, infection with which has a substantial effect on the distribution of different T-cell subsets, especially CD8+ T-cells, driving them towards a late-differentiated, more “elderly” phenotype [1‐3]. In an infected host, a significant fraction of the immune system (even up to 30% of CD4+ and CD8+ memory responses in some individuals) is committed to controlling the virus [4]. Our unpublished results in hormone-resistant non-metastatic prostate cancer show that CMV-seropositive patients have significantly lower levels of naïve CD8+ T-cells and a higher frequency of late-differentiated CD27− and TEMRA (CCR7−, CD45RA+) CD8+ T-cells compared to CMV-seronegative patients. Such an “old” CD8 compartment has also been observed in healthy CMV-seropositive individuals [3, 5] and is rapidly induced after primary infection with the virus [6‐8], suggesting CMV (and not only chronological age) as a driving force for human immunosenescence. …