Abstract
Cell fusion is fundamental to the development and physiology of multicellular organisms, such as fertilization, placentation, development of skeletal muscle and bone. Oncogenic virus-mediated cell fusion, however, may lead to chromosomal instability (CIN) by various mechanisms when tumor suppressor p53 is deregulated and produce oncogenic aneuploid cells. It is worth noting that all human oncogenic viruses, including human papillomavirus (HPV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), human herpesviruses-8/Kaposi sarcoma herpesvirus (HHV-8/KSHV) and human T-cell lymphotropic virus type 1 (HTLV-1), are capable of both inducing cell fusion and inhibiting the functions of p53 as well as pRb. Although it is now not clear whether a link between virus-mediated cell fusion and cancer established in experimental systems also exists in humans, the fact that the observation of tetraploid cells is more frequent in virus-positive than virus-negative premalignant lesions supports this link. Additionally, there are now no available vaccines against most oncogenic viruses except for HBV and HPV. Given these, developing fusion inhibitors is beneficial to cancer prevention and therapy of virus-associated cancers via inhibiting virus entry, spread and oncogenic role.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
