The Non-Homologous End Joining Protein PAXX Acts to Restrict HSV-1 Infection.
Fernandes Dos Santos, Paula
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Trigg, B., Lauer, K., Fernandes Dos Santos, P., Coleman, H., Balmus, G., Mansur, D. S., & Ferguson, B. (2017). The Non-Homologous End Joining Protein PAXX Acts to Restrict HSV-1 Infection.. Viruses, 9 (11)https://doi.org/10.3390/v9110342
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, 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.
Cell Line, Animals, Humans, Mice, Herpesvirus 1, Human, Virion, Herpes Simplex, DNA-Binding Proteins, Interferons, Viral Proteins, Virus Replication, Genes, Viral, Genome, Viral, DNA End-Joining Repair
Wellcome Trust (201946/Z/16/Z)
External DOI: https://doi.org/10.3390/v9110342
This record's URL: https://www.repository.cam.ac.uk/handle/1810/276812
Attribution 4.0 International
Licence URL: http://creativecommons.org/licenses/by/4.0/
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