Funding Source

NIH-NCI, DOD, LSU-LIFT, National Natural Science Foundation of China

Grant Number

NIH/NCI 1R01CA228166-01, DOD Career Development Award (CA140437), and LSU LIFT2 funding to Z.Q., as well as the awards from the National Natural Science Foundation of China (81472547, 81672924) and the Fundamental Research Funds for the Central Universities (22120180335) to Z.Q.

Department

Department of Chemistry

Document Type

Article

Publication Date

1-2019

Abstract

Human endogenous retroviruses (HERVs), viral-associated sequences, are normal components of the human genome and account for 8–9% of our genome. These original provirus sequences can be transactivated to produce functional products. Several reactivated HERVs have been implicated in cancers and autoimmune diseases. An emerging body of literature supports a potential role of reactivated HERVs in viral diseases, in particular viral-associated neoplasms. Demystifying studies on the mechanism(s) of HERV reactivation could provide a new framework for the development of treatment and prevention strategies targeting virus-associated tumors. Although available data suggest that coinfection by other viruses, such as Kaposi’s Sarcoma-associated herpesvirus (KSHV) and Epstein–Barr virus (EBV), may be a crucial driving force to transactivate HERV boom, the mechanisms of action of viral infection-induced HERV transactivation and the contributions of HERVs to viral oncogenesis warrant further studies. Here, we review viral coinfection contributes to HERVs transactivation with focus on human viral infection associated oncogenesis and diseases, including the abilities of viral regulators involved in HERV reactivation, and physiological effects of viral infection response on HERV reactivation.

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