Next Article in Journal / Special Issue
Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle
Previous Article in Journal
Vaccinia Virus Natural Infections in Brazil: The Good, the Bad, and the Ugly
Previous Article in Special Issue
Hepatitis B Virus and DNA Damage Response: Interactions and Consequences for the Infection
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessArticle
Viruses 2017, 9(11), 342; doi:10.3390/v9110342

The Non-Homologous End Joining Protein PAXX Acts to Restrict HSV-1 Infection

Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK
Laboratory of Immunobiology, Department of Microbiology, Immunology and Parasitology, Universidade Federal de Santa Catarina, Santa Catarina 88040-900, Brazil
Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK
Wellcome Trust Sanger Institute, Cambridge CB10 1HH, UK
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Received: 11 September 2017 / Revised: 2 November 2017 / Accepted: 6 November 2017 / Published: 16 November 2017
(This article belongs to the Special Issue Viruses and the DNA Damage Response)
View Full-Text   |   Download PDF [3245 KB, uploaded 16 November 2017]   |  


Herpes simplex virus 1 (HSV-1) has extensive interactions with the host DNA damage response (DDR) machinery that can be either detrimental or beneficial to the virus. Proteins in the homologous recombination pathway are known to be required for efficient replication of the viral genome, while different members of the classical non-homologous end-joining (c-NHEJ) pathway have opposing effects on HSV-1 infection. Here, we have investigated the role of the recently-discovered c-NHEJ component, PAXX (Paralogue of XRCC4 and XLF), which we found to be excluded from the nucleus during HSV-1 infection. We have established that cells lacking PAXX have an intact innate immune response to HSV-1 but show a defect in viral genome replication efficiency. Counterintuitively, PAXX−/− cells were able to produce greater numbers of infectious virions, indicating that PAXX acts to restrict HSV-1 infection in a manner that is different from other c-NHEJ factors. View Full-Text
Keywords: herpes simplex virus 1; HSV-1; DNA damage response; DDR; PAXX; c-NHEJ; classical non-homologous end joining herpes simplex virus 1; HSV-1; DNA damage response; DDR; PAXX; c-NHEJ; classical non-homologous end joining

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Supplementary material

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Trigg, B.J.; Lauer, K.B.; Fernandes dos Santos, P.; Coleman, H.; Balmus, G.; Mansur, D.S.; Ferguson, B.J. The Non-Homologous End Joining Protein PAXX Acts to Restrict HSV-1 Infection. Viruses 2017, 9, 342.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top