Journal
SEMINARS IN CANCER BIOLOGY
Volume 23, Issue 5, Pages 323-328Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2013.05.005
Keywords
Autophagy; Human tumor viruses; Oncogene-induced senescence (OIS); Unfolded protein response (UPR)
Categories
Funding
- GRL
- Hastings Foundation
- Fletcher Jones Foundation
- Peter A. Jones T32 Training Grant in Viral and Chemical Carcinogenesis
- [CA082057]
- [CA31363]
- [CA115284]
- [AI073099]
- [AI083025]
- [HL110609]
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Autophagy is a highly conserved and regulated process in eukaryotic cells by which components of the cytoplasm, such as damaged organelles and foreign pathogens, become enveloped into double-membrane autophagosome vesicles that fuse with the lysosome for degradation. Viruses are adept at subverting host cellular pathways for their replication and survival. The human tumor viruses, Epstein-Barr virus (EBV), Kaposi's Sarcoma-Associated Herpesvirus (KSHV), Hepatitis B virus (HBV), and Hepatitis C virus (HCV), have evolved novel ways of modulating autophagy during productive and latent stages of the virus life cycle. This review will discuss how the autophagy pathway becomes activated upon viral infection and the role of viral proteins in regulating the autophagy pathway. Specifically, we will examine how virus-encoded homologs of autophagy proteins evade autophagy-mediated degradation by blocking the induction, elongation, or maturation steps in the autophagy pathway. We will also discuss how certain viruses enhance autophagy induction or usurp autophagic machinery for their own replication. A comprehensive understanding of the autophagic response to tumor viruses may enable the discovery of novel antiviral and/or anticancer drug therapies. (C) 2013 Elsevier Ltd. All rights reserved.
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