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
. 2022 Jun 2;14(6):1215.
doi: 10.3390/v14061215.

MicroRNA Regulation of Human Herpesvirus Latency

Siyu Chen  1   2 , Yue Deng  1   2 , Dongli Pan  1   2
Affiliations
Review

MicroRNA Regulation of Human Herpesvirus Latency

Siyu Chen et al. Viruses. .

Abstract

Herpesviruses are ubiquitous human pathogens. After productive (lytic) infection, all human herpesviruses are able to establish life-long latent infection and reactivate from it. Latent infection entails suppression of viral replication, maintenance of the viral genome in infected cells, and the ability to reactivate. Most human herpesviruses encode microRNAs (miRNAs) that regulate these processes during latency. Meanwhile, cellular miRNAs are hijacked by herpesviruses to participate in these processes. The viral or cellular miRNAs either directly target viral transcripts or indirectly affect viral infection through host pathways. These findings shed light on the molecular determinants that control the lytic-latent switch and may lead to novel therapeutics targeting latent infection. We discuss the multiple mechanisms by which miRNAs regulate herpesvirus latency, focusing on the patterns in these mechanisms.

Keywords: EBV; HCMV; HSV; KSHV; herpesvirus; latency; microRNA; reactivation.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Genomic locations of human herpesvirus miRNAs. The locations of miRNA precursors are denoted by red triangles. Red characters indicate the miRNAs expressed during latent infection. Thick arrows along the genomes represent selected viral genes and the directions of transcription.
Figure 2
Figure 2
Direct targeting of viral IE genes by viral and cellular miRNAs. Blue rectangles represent viral miRNAs, and yellow rectangles represent host ones.
Figure 3
Figure 3
Regulation of apoptosis pathways by viral and cellular miRNAs. The genes directly targeted by miRNAs are indicated by orange rectangles. Green patterns represent protein modification. Some graphic elements were obtained from Servier Medical Art (SMART) (https://smart.servier.com/ (accessed on 12 May 2022)).
Figure 4
Figure 4
Regulation of host immune pathways by viral and cellular miRNAs. The genes directly targeted by miRNA are indicated by orange rectangles or characters. The red and green characters represent host and viral miRNAs, respectively. Some graphic elements were obtained from Servier Medical Art (SMART) (https://smart.servier.com/ (accessed on 12 May 2022)).
See this image and copyright information in PMC

References

    1. Cohen J.I. Herpesvirus latency. J. Clin. Investig. 2020;130:3361–3369. doi: 10.1172/JCI136225. - DOI - PMC - PubMed
    1. Arbuckle J.H., Medveczky M.M., Luka J., Hadley S.H., Luegmayr A., Ablashi D., Lund T.C., Tolar J., De Meirleir K., Montoya J.G., et al. The latent human herpesvirus-6A genome specifically integrates in telomeres of human chromosomes in vivo and in vitro. Proc. Natl. Acad. Sci. USA. 2010;107:5563–5568. doi: 10.1073/pnas.0913586107. - DOI - PMC - PubMed
    1. Knipe D.M., Lieberman P.M., Jung J.U., McBride A.A., Morris K.V., Ott M., Margolis D., Nieto A., Nevels M., Parks R.J., et al. Snapshots: Chromatin control of viral infection. Virology. 2013;435:141–156. doi: 10.1016/j.virol.2012.09.023. - DOI - PMC - PubMed
    1. Bartel D.P. Metazoan MicroRNAs. Cell. 2018;173:20–51. doi: 10.1016/j.cell.2018.03.006. - DOI - PMC - PubMed
    1. Friedman R.C., Farh K.K., Burge C.B., Bartel D.P. Most mammalian mRNAs are conserved targets of microRNAs. Genome Res. 2009;19:92–105. doi: 10.1101/gr.082701.108. - DOI - PMC - PubMed

Publication types

LinkOut - more resources