Section of Infections - Infections and Cancer Biology Group
Approximately 20% of cancers worldwide are induced by infectious agents. This proportion is even higher in low-resource countries, as the socio-economic context makes infectious conditions more widespread. Based on evidence from epidemiological and biological studies, the IARC has classified as Group 1 carcinogens six viruses associated with the origin of certain types of human cancers: Epstein-Barr virus (EBV); Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV/HHV8); human papillomavirus (HPV); hepatitis B virus (HBV); hepatitis C virus (HCV); and human T-lymphotropic virus type 1 (HTLV-1), as well as the bacterium Helicobacter pylori (H. pylori). The mucosal high-risk HPV types are the etiological agents of cervical cancer as well as a sub-set of ano-genital and head and neck carcinomas. They are responsible for about 5% of all virus-induced cancers.
In addition to these infectious agents, emerging lines of evidence support the involvement of other infectious agents in human carcinogenesis. The cutaneous HPV types that belong to the genus beta of the HPV phylogenetic tree are associated with the development of non-melanoma skin cancer (NMSC) in patients affected by a rare autosomal recessive genetic disorder called Epidermodysplasia verruciformis (EV). However, several findings also support their carcinogenic role in normal populations. A novel human polyomavirus, MCV, has recently been discovered and appears to be associated with a rare tumour, Merkel Cell sarcoma, in immunosuppressed individuals.
The development of cancers induced by infectious agents is intimately linked to their persistence in the host. In fact, pathological abnormalities are not usually observed when infections are rapidly cleared by the immune system, while cancer development risk dramatically increases after the establishment of a chronic infection. Studies on specific cancer-associated viruses, e.g. mucosal high-risk HPV types, have clearly shown that the persistence of the infection promotes the accumulation of DNA damage that may lead to the inactivation of tumour suppressors or activation of cellular oncogenes, facilitating the neoplastic transformation of the infected cells. Therefore, understanding the viral mechanisms of evasion of the immune surveillance is of paramount importance to develop preventive strategies against HPV-associated diseases.