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Scientific paper - Original scientific paper
The Cytomegalovirus Tegument Protein UL35 Antagonizes Pattern Recognition Receptor- Mediated Type I IFN Transcription
Microorganisms, 8 (2020), 6; 1-26. https://doi.org/10.3390/microorganisms8060790
Fabits, Markus; Gonçalves Magalhães, Vladimir; Chan, Baca; Girault, Virginie; Elbasani, Endrit; Rossetti, Elisa; Saeland, Eirikur; Messerle, Martin; Pichlmair, Andreas; Lisnić, Vanda Juranić; Brinkmann, Melanie M.

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Fabits, M., Gonçalves Magalhães, V., Chan, B., Girault, V., Elbasani, E., Rossetti, E. ... Brinkmann, M. M. (2020). The Cytomegalovirus Tegument Protein UL35 Antagonizes Pattern Recognition Receptor- Mediated Type I IFN Transcription. Microorganisms, 8. (6), 1-26. doi: 10.3390/microorganisms8060790

Fabits, Markus, et al. "The Cytomegalovirus Tegument Protein UL35 Antagonizes Pattern Recognition Receptor- Mediated Type I IFN Transcription." Microorganisms, vol. 8, no. 6, 2020, pp. 1-26. https://doi.org/10.3390/microorganisms8060790

Fabits, Markus, Vladimir Gonçalves Magalhães, Baca Chan, Virginie Girault, Endrit Elbasani, Elisa Rossetti, Eirikur Saeland, et al. "The Cytomegalovirus Tegument Protein UL35 Antagonizes Pattern Recognition Receptor- Mediated Type I IFN Transcription." Microorganisms 8, no. 6 (2020): 1-26. https://doi.org/10.3390/microorganisms8060790

Fabits, M., et al. (2020) 'The Cytomegalovirus Tegument Protein UL35 Antagonizes Pattern Recognition Receptor- Mediated Type I IFN Transcription', Microorganisms, 8(6), pp. 1-26. doi: 10.3390/microorganisms8060790

Fabits M, Gonçalves Magalhães V, Chan B, Girault V, Elbasani E, Rossetti E, and sur.. The Cytomegalovirus Tegument Protein UL35 Antagonizes Pattern Recognition Receptor- Mediated Type I IFN Transcription. Microorganisms [Internet]. 2020 [cited 2024 November 12];8(6):1-26. doi: 10.3390/microorganisms8060790

M. Fabits, et al., "The Cytomegalovirus Tegument Protein UL35 Antagonizes Pattern Recognition Receptor- Mediated Type I IFN Transcription", Microorganisms, vol. 8, no. 6, pp. 1-26, 2020. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:809461. [Accessed: 12 November 2024]

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Metadata
Title (english)The Cytomegalovirus Tegument Protein UL35 Antagonizes Pattern Recognition Receptor- Mediated Type I IFN Transcription
AuthorMarkus Fabits
AuthorVladimir Gonçalves Magalhães
AuthorBaca Chan
AuthorVirginie Girault
AuthorEndrit Elbasani
AuthorElisa Rossetti
AuthorEirikur Saeland
AuthorMartin Messerle
AuthorAndreas Pichlmair
AuthorVanda Juranić Lisnić
AuthorMelanie M. Brinkmann
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Histology and Embryology)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
Abstract: The rapid activation of pattern recognition receptor (PRR)-mediated type I interferon (IFN) signaling is crucial for the host response to infection. In turn, human cytomegalovirus (HCMV) must evade this potent response to establish life- long infection. Here, we reveal that the HCMV tegument protein UL35 antagonizes the activation of type I IFN transcription downstream of the DNA and RNA sensors cGAS and RIG-I, respectively. We show that ectopic expression of UL35 diminishes the type I IFN response, while infection with a recombinant HCMV lacking UL35 induces an elevated type I IFN response compared to wildtype HCMV. With a series of luciferase reporter assays and the analysis of signaling kinetics upon HCMV infection, we observed that UL35 downmodulates PRR signaling at the level of the key signaling factor TANK- binding kinase 1 (TBK1). Finally, we demonstrate that UL35 and TBK1 co-immunoprecipitate when co-expressed in HEK293T cells. In addition, we show that a previously reported cellular binding partner of UL35, O-GlcNAc transferase (OGT), post-translationally GlcNAcylates UL35, but that this modification is not required for the antagonizing effect of UL35 on PRR signaling. In summary, we have identified UL35 as the first HCMV protein to antagonize the type I IFN response at the level of TBK1, thereby enriching our understanding of how this important herpesvirus escapes host immune responses.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleMicroorganisms
Numberingvol. 8, no. 6, pp. 1-26
p-ISSN2076-2607
DOIhttps://doi.org/10.3390/microorganisms8060790
URN:NBNurn:nbn:hr:184:809461
Publication2020
Document URLhttp://bib.irb.hr/1107363
Type of resourceText
Access conditionsOpen access
Terms of useLicence Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) icon
Created on2022-03-10 14:34:02