The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
PML Contributes to a Cellular Mechanism of Repression of Herpes Simplex Virus Type 1 Infection That Is Inactivated by ICP0
Abstract
Promyelocytic leukemia (PML) nuclear bodies (also known as ND10) are nuclear substructures that contain several proteins, including PML itself, Sp100, and hDaxx. PML has been implicated in many cellular processes, and ND10 are frequently associated with the replicating genomes of DNA viruses. During herpes simplex virus type 1 (HSV-1) infection, the viral regulatory protein ICP0 localizes to ND10 and induces the degradation of PML, thereby disrupting ND10 and dispersing their constituent proteins. ICP0-null mutant viruses are defective in PML degradation and ND10 disruption, and concomitantly they initiate productive infection very inefficiently. Although these data are consistent with a repressive role for PML and/or ND10 during HSV-1 infection, evidence in support of this hypothesis has been inconclusive. By use of short interfering RNA technology, we demonstrate that depletion of PML increases both gene expression and plaque formation by an ICP0-negative HSV-1 mutant, while having no effect on wild-type HSV-1. We conclude that PML contributes to a cellular antiviral repression mechanism that is countered by the activity of ICP0.
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Cites
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The transcriptional role of PML and the nuclear body
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PML protein isoforms and the RBCC/TRIM motif
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Cited by
TRIM family proteins and their emerging roles in innate immunity
Ozato, K., Shin, D.-M., Chang, T.-H., & Morse, H. C. (2008) · Nature Reviews Immunology · doi:10.1038/nri2413 · Cited by 1,120
Chromatin control of herpes simplex virus lytic and latent infection
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The molecular basis of herpes simplex virus latency
Nicoll, M. P., Proença, J. T., & Efstathiou, S. (2012) · FEMS Microbiology Reviews · doi:10.1111/j.1574-6976.2011.00320.x · Cited by 286
Rapid induction of alternative lengthening of telomeres by depletion of the histone chaperone ASF1
O'Sullivan, R. J., Arnoult, N., Lackner, D. H., Oganesian, L., Haggblom, C., Corpet, A., Almouzni, G., & Karlseder, J. (2014) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.2754 · Cited by 259
Inhibition of HSV-1 Replication by Gene Editing Strategy
Roehm, P. C., Shekarabi, M., Wollebo, H. S., Bellizzi, A., He, L., Salkind, J., & Khalili, K. (2016) · Scientific Reports · doi:10.1038/srep23146 · Cited by 128
Metadata
- Authors
- Everett, R. D., Rechter, S., Papior, P., Tavalai, N., Stamminger, T., & Orr, A.
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2006-08-15
- Volume
- 80
- Issue
- 16
- Pages
- 7995-8005
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- OpenAlex
- W1968697793
- Cited by
- 327
- References
- 41
- FWCI
- 17.26
- Type
- journal article
- Language
- en
- Open access
- closed
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- Everett, R. D., Rechter, S., Papior, P., Tavalai, N., Stamminger, T., & Orr, A. (2006). PML Contributes to a Cellular Mechanism of Repression of Herpes Simplex Virus Type 1 Infection That Is Inactivated by ICP0. Journal of Virology. https://doi.org/10.1128/jvi.00734-06
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