Abstract
Human oncogenic viruses include Epstein–Barr virus, hepatitis B virus, hepatitis C virus, human papilloma virus, human T-cell lymphotropic virus, Kaposi’s associated sarcoma virus, and Merkel cell polyomavirus. It would be expected that during virus–host interaction, the immune system would recognize these pathogens and eliminate them. However, through evolution, these viruses have developed a number of strategies to avoid such an outcome and successfully establish chronic infections. The persistent nature of the infection caused by these viruses is associated with their oncogenic potential. In this article, we will review the latest information on the interaction between oncogenic viruses and the innate immune system of the host. In particular, we will summarize the available knowledge on the recognition by host pattern-recognition receptors of pathogen-associated molecular patterns present in the incoming viral particle or generated during the virus’ life cycle. We will also review the data on the recognition of cell-derived danger associated molecular patterns generated during the virus infection that may impact the outcome of the host–pathogen interaction and the development cancer.
Highlights
INTRODUCTIONSeven human viruses have been found so far to cause approximately 10–20% of human cancers worldwide [1]
Seven human viruses have been found so far to cause approximately 10–20% of human cancers worldwide [1]. They include the herpesviruses, Epstein–Barr virus (EBV) and Kaposi’s associated sarcoma virus (KSHV), the hepatitis B (HBV) and hepatitis C (HCV) viruses, high-risk human papillomaviruses (HPV), the human T-cell lymphotropic virus-1 (HTLV-1), and the recently discovered Merkel cell polyomavirus (MCPyV) [1]
EBV and KSHV are the two members of this virus family that have been identified as having growth transforming potential, and we focus on these here
Summary
Seven human viruses have been found so far to cause approximately 10–20% of human cancers worldwide [1]. Exact numbers are not available for every region in the world, the number of humans that suffer a disease associated with each oncogenic virus, as compared to the number of people infected with each virus is low. It appears that during evolution these viruses have found a balance of “live and let live” with their host. There are two families of transmembrane PRRs, namely tolllike receptors (TLRs) [16] and C-type lectin receptors (CLRs) [17]. A nuclear DNA sensor was identified, IFI-16, a PYHIN protein that, together with the cytoplasmic AIM-2 DNA sensor, was proposed to form a new family of innate DNA sensors (“AIM2-like receptors” or “ALRs”)
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