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Review
.2020 Feb 15;9(2):125.
doi: 10.3390/pathogens9020125.

Herpesviral Latency-Common Themes

Affiliations
Review

Herpesviral Latency-Common Themes

Magdalena Weidner-Glunde et al. Pathogens..

Abstract

Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency.

Keywords: Alphaherpesvirinae; Betaherpesvirinae; Gammaherpesvirinae; gene expression; herpesvirus; latency; lytic cycle; lytic inducers; persistence; reactivation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Latency establishment and lytic reactivation of herpesviruses. Following an initial lytic infection, herpesviruses establish latency mostly in dividing cells (except alphaherpesviruses), during which the viral genome is maintained as an episome and is tethered to cellular chromatin; lytic reactivation of gammaherpesviruses and betaherpesviruses may be cell differentiation dependent and occurs upon receiving the stimulus for terminal differentiation. EBV, a gammaherpesvirus, infects naïve B cells and remains latent throughout their differentiation until memory B cells carrying latent virus become activated and differentiate into plasma cells, which induces lytic reactivation. HCMV, a betaherpesvirus, establishes latency in cells of the myeloid lineage, its lytic cycle is activated upon differentiation into macrophages and dendritic cells. Additionally, HCMV can also establish latency in neural lineage and undergo lytic cycle in neurons, although the details of HCMV neural infection need to be studied further to resolve observed contradictions. In contrast HSV-1, an alphaherpesvirus establishes latency in sensory neurons and the lytic reactivation is induced upon receiving a specific stimulus. Viral genomes are symbolized by a black circle in the nucleus.
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References

    1. Pellett P.E., Roizman B. Herpesviridae. In: Knipe D.M., Howley P.M., editors. Fields Virology. 6th ed. Volume 2 Lippincott Williams & Wilkins; Philadelphia, PA, USA: 2013.
    1. Speck S.H., Ganem D. Viral latency and its regulation: Lessons from the gamma-herpesviruses. Cell Host Microbe. 2010;8:100–115. doi: 10.1016/j.chom.2010.06.014. - DOI - PMC - PubMed
    1. Roizman B., Knipe D.M., Whitley R.J. Herpes Simplex Viruses. In: Knipe D.M., Howley P.M., editors. Fields Virology. 6th ed. Volume 2 Lippincott Williams & Wilkins; Philadelphia, PA, USA: 2013.
    1. Spear P.G., Longnecker R. Herpesvirus entry: An update. J. Virol. 2003;77:10179–10185. doi: 10.1128/JVI.77.19.10179-10185.2003. - DOI - PMC - PubMed
    1. Whitley R.J. Herpesviruses. In: Baron S., editor. Medical Microbiology. 4th ed. University of Texas Medical Branch at Galveston; Galveston, TX, USA: 1996.

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