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      Early Nuclear Events after Herpesviral Infection

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          Abstract

          Herpesviruses are important pathogens that can cause significant morbidity and mortality in the human population. Herpesviruses have a double-stranded DNA genome, and viral genome replication takes place inside the nucleus. Upon entering the nucleus, herpesviruses have to overcome the obstacle of cellular proteins in order to enable viral gene expression and genome replication. In this review, we want to highlight cellular proteins that sense incoming viral genomes of the DNA-damage repair (DDR) pathway and of PML-nuclear bodies (PML-NBs) that all can act as antiviral restriction factors within the first hours after the viral genome is released into the nucleus. We show the function and significance of both nuclear DNA sensors, the DDR and PML-NBs, and demonstrate for three human herpesviruses of the alpha-, beta- and gamma-subfamilies, HSV-1, HCMV and KSHV respectively, how viral tegument proteins antagonize these pathways.

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          IFI16 acts as a nuclear pathogen sensor to induce the inflammasome in response to Kaposi Sarcoma-associated herpesvirus infection.

          Nagaraj Kerur, Mohanan Valiya Veettil, Neelam Sharma-Walia … (2011)
          Inflammasomes are cytoplasmic sensors of foreign molecules, including pathogens, and function to induce caspase-1 activation and IL-1β cytokine maturation. Whether such a mechanism exists in the nucleus and is effective against nuclear replicating pathogens is unknown. Nuclear replicating herpesvirus KSHV is associated with Kaposi Sarcoma, an angioproliferative tumor characterized by an inflammatory microenvironment including IL-1β. We demonstrate that during KSHV infection of endothelial cells, interferon gamma-inducible protein 16 (IFI16) interacts with the adaptor molecule ASC and procaspase-1 to form a functional inflammasome. This complex was initially detected in the nucleus and subsequently in the perinuclear area. KSHV gene expression and/or latent KSHV genome is required for inflammasome activation and IFI16 colocalizes with the KSHV genome in the infected cell nucleus. Caspase-1 activation by KSHV was reduced by IFI16 and ASC silencing. Our studies reveal IFI16 as a nuclear pathogen sensor and demonstrate that the inflammasome also functions in the nucleus. Copyright © 2011 Elsevier Inc. All rights reserved.
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            RNF168 ubiquitinates K13-15 on H2A/H2AX to drive DNA damage signaling.

            Francesca Mattiroli, Joseph H.A. Vissers, Willem J. van Dijk … (2012)
            Ubiquitin-dependent signaling during the DNA damage response (DDR) to double-strand breaks (DSBs) is initiated by two E3 ligases, RNF8 and RNF168, targeting histone H2A and H2AX. RNF8 is the first ligase recruited to the damage site, and RNF168 follows RNF8-dependent ubiquitination. This suggests that RNF8 initiates H2A/H2AX ubiquitination with K63-linked ubiquitin chains and RNF168 extends them. Here, we show that RNF8 is inactive toward nucleosomal H2A, whereas RNF168 catalyzes the monoubiquitination of the histones specifically on K13-15. Structure-based mutagenesis of RNF8 and RNF168 RING domains shows that a charged residue determines whether nucleosomal proteins are recognized. We find that K63 ubiquitin chains are conjugated to RNF168-dependent H2A/H2AX monoubiquitination at K13-15 and not on K118-119. Using a mutant of RNF168 unable to target histones but still catalyzing ubiquitin chains at DSBs, we show that ubiquitin chains per se are insufficient for signaling, but RNF168 target ubiquitination is required for DDR. Copyright © 2012 Elsevier Inc. All rights reserved.
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              Global and Regional Estimates of Prevalent and Incident Herpes Simplex Virus Type 1 Infections in 2012

              Katharine Looker, Amalia Magaret, Margaret T May … (2015)
              Background Herpes simplex virus type 1 (HSV-1) commonly causes orolabial ulcers, while HSV-2 commonly causes genital ulcers. However, HSV-1 is an increasing cause of genital infection. Previously, the World Health Organization estimated the global burden of HSV-2 for 2003 and for 2012. The global burden of HSV-1 has not been estimated. Methods We fitted a constant-incidence model to pooled HSV-1 prevalence data from literature searches for 6 World Health Organization regions and used 2012 population data to derive global numbers of 0-49-year-olds with prevalent and incident HSV-1 infection. To estimate genital HSV-1, we applied values for the proportion of incident infections that are genital. Findings We estimated that 3709 million people (range: 3440–3878 million) aged 0–49 years had prevalent HSV-1 infection in 2012 (67%), with highest prevalence in Africa, South-East Asia and Western Pacific. Assuming 50% of incident infections among 15-49-year-olds are genital, an estimated 140 million (range: 67–212 million) people had prevalent genital HSV-1 infection, most of which occurred in the Americas, Europe and Western Pacific. Conclusions The global burden of HSV-1 infection is huge. Genital HSV-1 burden can be substantial but varies widely by region. Future control efforts, including development of HSV vaccines, should consider the epidemiology of HSV-1 in addition to HSV-2, and especially the relative contribution of HSV-1 to genital infection.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Clin Med
                Journal ID (iso-abbrev): J Clin Med
                Journal ID (publisher-id): jcm
                Title: Journal of Clinical Medicine
                Publisher: MDPI
                ISSN (Electronic): 2077-0383
                Publication date (Electronic): 07 September 2019
                Publication date Collection: September 2019
                Volume: 8
                Issue: 9
                Electronic Location Identifier: 1408
                Affiliations
                Institute for Clinical and Molecular Virology, University Hospital Erlangen, Friedrich Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany
                Author notes
                Author information
                https://orcid.org/0000-0003-1900-5891
                https://orcid.org/0000-0001-8873-3863
                Article
                Publisher ID: jcm-08-01408
                DOI: 10.3390/jcm8091408
                PMC ID: 6780142
                PubMed ID: 31500286
                SO-VID: e01606e4-6508-4b9c-aada-347d4df15243
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 23 July 2019
                Date accepted : 03 September 2019
                Categories
                Subject: Review

                Keywords: herpesviruses,double-stranded dna virus,dna-damage repair,dna-damage response,nuclear dna sensors,restriction factors,hsv-1,herpes simplex virus,cmv,cytomegalovirus,kshv,kaposi’s sarcoma-associated herpesvirus,double strand break,nhej,non-homologous end joining,hr,homology repair,infection,virus,pml,pml nuclear bodies,nd10,virus-host interaction,sp100,daxx,atrx,icp-0,ie-1,orf75,hhv-6
                Data availability:
                Keywords: herpesviruses, double-stranded dna virus, dna-damage repair, dna-damage response, nuclear dna sensors, restriction factors, hsv-1, herpes simplex virus, cmv, cytomegalovirus, kshv, kaposi’s sarcoma-associated herpesvirus, double strand break, nhej, non-homologous end joining, hr, homology repair, infection, virus, pml, pml nuclear bodies, nd10, virus-host interaction, sp100, daxx, atrx, icp-0, ie-1, orf75, hhv-6

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