Abstract
Besides its well-described impact in immunosuppressed patients, the role of human cytomegalovirus (HCMV) in the pathogenesis of cancer has been more recently investigated. In cancer, HCMV could favor the progression and the spread of the tumor, a paradigm named oncomodulation. Although oncomodulation could account for part of the protumoral effect of HCMV, it might not explain the whole impact of HCMV infection on the tumor and the tumoral microenvironment. On the contrary cases have been reported where HCMV infection slows down the progression and the spread of the tumor. In addition, HCMV proteins have oncogenic properties per se, HCMV activates pro-oncogenic pathways in infected cells, and recently the direct transformation of cells following HCMV infection has been described, which gave rise to tumors when injected in mice. Thus, beyond the oncomodulation model, this review will assess the direct transforming role of HMCV-infected cells and the potential classification of HCMV as an oncovirus.
Highlights
The human cytomegalovirus belongs to the Herpesviridae family with a double stranded DNA genome of 236 kbp in size [1]
These results indicate that apoptosis induction occurs both at the site of human cytomegalovirus (HCMV)
Among the 15–20% of human cancers caused by infections, several viruses have been named as human oncoviruses, including Epstein–Barr virus (EBV), hepatitis B virus (HBV), human T-lymphotropic virus-1 (HTLV-1), human papillomavirus (HPV), hepatitis C virus (HCV), Kaposi’s sarcoma associated herpesvirus (KSHV or HHV8), and Merkel cell polyomavirus [64]
Summary
The human cytomegalovirus belongs to the Herpesviridae family with a double stranded DNA genome of 236 kbp in size [1]. Several cellular functions involved in tumor development are targeted by HCMV gene products including cell cycle dysregulation, cellular immortalization, mutation and instability of the viral genome, enhanced cell survival, and immune escape with tumor spread [5,6,7,8]. Human mammary epithelial cells (HMECs) are productively infected by HCMV clinical isolates with low levels of replication [15,16]. The ULb’ sequence is critical for the viral tropism and favors the replication of HCMV in several primary cell types including epithelial cells, endothelial cells, and myeloid cells [13,20]. Besides epithelial cells and fibroblasts, HCMV infects persistently monocytes/macrophages, which behave like a viral reservoir and favor the viral spread through the body [21,22]. HCMV-induced oncomodulation has been extensively studied so far, the direct involvement of HCMV in cell transformation and identifying viral genes favoring such a transformation could define HCMV as an oncovirus
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