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©2013 Baishideng. All rights reserved.
World J Virol. May 12, 2013; 2(2): 102-109
Published online May 12, 2013. doi: 10.5501/wjv.v2.i2.102
Published online May 12, 2013. doi: 10.5501/wjv.v2.i2.102
How virus persistence can initiate the tumorigenesis process
Simone Avanzi, Alessandro Ripalti, Department of Oncology, Hematology and Laboratory Medicine, Operative Unit of Microbiology, A.O-U. di Bologna Policlinico S. Orsola-Malpighi, 40138 Bologna, Italy
Gualtiero Alvisi, Department of Molecular Medicine, Microbiology Section University of Padua, 35100 Padua, Italy
Author contributions: Ripalti A formulated the hypothesis; Avanzi S and Alvisi G criticized and revised the hypothesis; Avanzi S, Alvisi G and Ripalti A wrote the article.
Correspondence to: Dr. Alessandro Ripalti, Department of Oncology, Hematology and Laboratory Medicine, Operative Unit of Microbiology, A.O-U. di Bologna Policlinico S. Orsola-Malpighi, via Massarenti 9, 40138 Bologna, Italy. alessandro.ripalti@unibo.it
Telephone: +39-51-4290921 Fax: +39-51-307397
Received: December 5, 2012
Revised: April 4, 2013
Accepted: April 10, 2013
Published online: May 12, 2013
Revised: April 4, 2013
Accepted: April 10, 2013
Published online: May 12, 2013
Core Tip
Core tip: Current models for viral driven oncogenesis cannot explain why tumor development in carriers of tumorigenic viruses is a very rare event, occurring decades after virus infection. Considering that viruses are mutagenic agents per se and human oncogenic viruses additionally establish latent and persistent infections, we attempt here to provide a general mechanism of tumor initiation both for RNA and DNA viruses, suggesting viruses could be both necessary and sufficient in triggering human tumorigenesis initiation.