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Review
. 2021 May 27;13(11):2625.
doi: 10.3390/cancers13112625.

Virus-Driven Carcinogenesis

Yuichiro Hatano  1 , Takayasu Ideta  2   3 , Akihiro Hirata  4 , Kayoko Hatano  5 , Hiroyuki Tomita  1 , Hideshi Okada  6 , Masahito Shimizu  2 , Takuji Tanaka  7 , Akira Hara  1
Affiliations
Review

Virus-Driven Carcinogenesis

Yuichiro Hatano et al. Cancers (Basel). .

Abstract

Cancer arises from the accumulation of genetic and epigenetic alterations. Even in the era of precision oncology, carcinogens contributing to neoplastic process are still an important focus of research. Comprehensive genomic analyses have revealed various combinations of base substitutions, referred to as the mutational signatures, in cancer. Each mutational signature is believed to arise from specific DNA damage and repair processes, including carcinogens. However, as a type of carcinogen, tumor viruses increase the cancer risk by alternative mechanisms, including insertional mutagenesis, viral oncogenes, and immunosuppression. In this review, we summarize virus-driven carcinogenesis to provide a framework for the control of malignant cell proliferation. We first provide a brief overview of oncogenic viruses and describe their implication in virus-related tumors. Next, we describe tumor viruses (HPV, Human papilloma virus; HBV, Hepatitis B virus; HCV, Hepatitis C virus; EBV, Epstein-Barr virus; Kaposi sarcoma herpesvirus; MCV, Merkel cell polyoma virus; HTLV-1, Human T-cell lymphotropic virus, type-1) and tumor virus-related cancers. Lastly, we introduce emerging tumor virus candidates, human cytomegalovirus (CMV), human herpesvirus-6 (HHV-6) and adeno-associated virus-2 (AAV-2). We expect this review to be a hub in a complex network of data for virus-associated carcinogenesis.

Keywords: EBV; HBV; HCV; HIV-1; HPV; HTLV-1; KSHV; MCV; tumor virus.

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Conflict of interest statement

The authors declare no conflict of interest.

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