Viral Carcinogenesis: Factors Inducing DNA Damage and Virus Integration

Cancers

Yan Chen¹  Vonetta Williams¹  Maria Filippova¹  Valery Filippov¹ 

[1] Department of Basic Science, Loma Linda University, Loma Linda, CA 92354, USA;

关键词: virus;    DNA damage;    ROS;    carcinogenesis;    HBV;    HPV;    MCV;    EBV;    integration;   

DOI  :  10.3390/cancers6042155

来源: mdpi

【 摘 要 】

Viruses are the causative agents of 10%–15% of human cancers worldwide. The most common outcome for virus-induced reprogramming is genomic instability, including accumulation of mutations, aberrations and DNA damage. Although each virus has its own specific mechanism for promoting carcinogenesis, the majority of DNA oncogenic viruses encode oncogenes that transform infected cells, frequently by targeting p53 and pRB. In addition, integration of viral DNA into the human genome can also play an important role in promoting tumor development for several viruses, including HBV and HPV. Because viral integration requires the breakage of both the viral and the host DNA, the integration rate is believed to be linked to the levels of DNA damage. DNA damage can be caused by both endogenous and exogenous factors, including inflammation induced by either the virus itself or by co-infections with other agents, environmental agents and other factors. Typically, cancer develops years to decades following the initial infection. A better understanding of virus-mediated carcinogenesis, the networking of pathways involved in transformation and the relevant risk factors, particularly in those cases where tumorigenesis proceeds by way of virus integration, will help to suggest prophylactic and therapeutic strategies to reduce the risk of virus-mediated cancer.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.