Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Feb 4;12(2):358.
doi: 10.3390/cancers12020358.

Viral miRNAs as Active Players and Participants in Tumorigenesis

Alessia Gallo  1 , Vitale Miceli  1 , Matteo Bulati  1 , Gioacchin Iannolo  1 , Flavia Contino  1   2 , Pier Giulio Conaldi  1
Affiliations
Review

Viral miRNAs as Active Players and Participants in Tumorigenesis

Alessia Gallo et al. Cancers (Basel). .

Abstract

The theory that viruses play a role in human cancers is now supported by scientific evidence. In fact, around 12% of human cancers, a leading cause of morbidity and mortality in some regions, are attributed to viral infections. However, the molecular mechanism remains complex to decipher. In recent decades, the uncovering of cellular miRNAs, with their invaluable potential as diagnostic and prognostic biomarkers, has increased the number of studies being conducted regarding human cancer diagnosis. Viruses develop clever mechanisms to succeed in the maintenance of the viral life cycle, and some viruses, especially herpesviruses, encode for miRNA, v-miRNAs. Through this viral miRNA, the viruses are able to manipulate cellular and viral gene expression, driving carcinogenesis and escaping the host innate or adaptive immune system. In this review, we have discussed the main viral miRNAs and virally influenced cellular pathways, and their capability to drive carcinogenesis.

Keywords: EBV; HBV; HCV; HHV-8; HPV; MCPyV; viral miRNAs.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Graphical representation of the relative abundance of viral miRNA production by Epstein–Barr virus (EBV), Kaposi’s Sarcoma Herpesvirus/Human Herpesvirus-8 (KSHV/HHV8), Human Papillomavirus (HPV), Hepatitis C Virus (HCV), Hepatitis B Virus (HBV) and Merkel Cell Polyomavirus (MCPyV) viruses.
Figure 2
Figure 2
Immunoevasive functions of viral miRNAs. Target cellular components of EBV, KSHV, and HPV miRNAs and the relavant antiviral responses of innate and adaptive immunity.
Figure 3
Figure 3
Viral miRNAs affect the pathways involved in the carcinogenesis of host cells. The picture depicts changes to cellular fate because of viral miRNAs. Genomic instability due to viral infection can induce activation of the p53 pathway, which in turn supports both DNA damage responses and cell cycle arrest. In relation to viral infection context, viral miRNAs can affect abortive cell fates such as programmed cell death with consequent cancer transformation. Arrows signify that the factor or process promotes the effect it points to, while blocking arrows signify inhibition. Orange ellipses represent viral proteins, grey ellipses represent host cell proteins, green boxes represent stages of the lytic phase of viral life cycle and blue boxes represent cellular processes affected by viral miRNAs during the viral latent phase.
See this image and copyright information in PMC

References

    1. De Martel C., Georges D., Bray F., Ferlay J., Clifford G.M. Global burden of cancer attributable to infections in 2018: A worldwide incidence analysis. Lancet Glob. Health. 2019 doi: 10.1016/S2214-109X(19)30488-7. - DOI - PubMed
    1. Moore P.S., Chang Y. Why do viruses cause cancer? Highlights of the first century of human tumour virology. Nat. Rev. Cancer. 2010;10:878–889. doi: 10.1038/nrc2961. - DOI - PMC - PubMed
    1. Grulich A.E., van Leeuwen M.T., Falster M.O., Vajdic C.M. Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: A meta-analysis. Lancet. 2007;370:59–67. doi: 10.1016/S0140-6736(07)61050-2. - DOI - PubMed
    1. Chin Y.E., Kitagawa M., Su W.C., You Z.H., Iwamoto Y., Fu X.Y. Cell growth arrest and induction of cyclin-dependent kinase inhibitor p21 WAF1/CIP1 mediated by STAT1. Science. 1996;272:719–722. doi: 10.1126/science.272.5262.719. - DOI - PubMed
    1. Takaoka A., Hayakawa S., Yanai H., Stoiber D., Negishi H., Kikuchi H., Sasaki S., Imai K., Shibue T., Honda K., et al. Integration of interferon-alpha/beta signalling to p53 responses in tumour suppression and antiviral defence. Nature. 2003;424:516–523. doi: 10.1038/nature01850. - DOI - PubMed

LinkOut - more resources