The Host Signaling Pathways Hijacked by Oncogenic Viruses

نویسندگان

  • Yong - Sam Jung
  • Lorne A Babiuk
  • Yingjuan Qian
چکیده

Viruses can only reproduce by infecting live cells. During their replication, some viruses manipulate the host cell machinery in such a way that may cause the host cell to reproduce out of control and become carcinogenesis. These viruses are known as oncogenic viruses, also named as “tumor viruses” or “cancer viruses”. In 1909, Francis Peyton Rous showed that cancer could be transmitted through cell-free tumor extracts and thus viruses must be responsible for transmitting the tumor [1,2]. A new epoch began after that, the first human tumor virus Epstein-Barr virus (EBV) was identified from Burkitt’s lymphoma in 1964 [3]. Currently, more than eight human tumor viruses are known. Human oncogenic viruses are classified into two categories according to their genomes, DNA viruses and RNA viruses. Most human tumor viruses belong to DNA viruses, including Epstein Barr virus (EBV), Human Herpes Virus (HHV4), Hepatitis B Virus (HBV), Human Papilloma Viruses (HPV), Kaposi’s Sarcoma Herpes Virus (KSHV), and Merkel cell polyomavirus. Human T-Lymphotropic Virus-I (HTLV-I) and Hepatitis C Virus (HCV) belong to human RNA tumor viruses (Table 1). Similarly, there are also some important animal oncogenic viruses that greatly affect the development of the livestock industry. For examples, Marek’s Disease Virus (MDV) and Jaagsiekte Sheep Retrovirus (JSRV) can induce serious T cell lymphoma in chicken and lung cancer in sheep, respectively.

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تاریخ انتشار 2017