Immune evasion strategy involving propionylation by the KSHV interferon regulatory factor 1 (vIRF1).
Journal
PLoS pathogens
ISSN: 1553-7374
Titre abrégé: PLoS Pathog
Pays: United States
ID NLM: 101238921
Informations de publication
Date de publication:
04 2023
04 2023
Historique:
received:
04
12
2022
accepted:
28
03
2023
revised:
18
04
2023
medline:
20
4
2023
pubmed:
7
4
2023
entrez:
6
4
2023
Statut:
epublish
Résumé
Post-translational modifications (PTMs) are essential for host antiviral immune response and viral immune evasion. Among a set of novel acylations, lysine propionylation (Kpr) has been detected in both histone and non-histone proteins. However, whether protein propionylation occurs in any viral proteins and whether such modifications regulate viral immune evasion remain elusive. Here, we show that Kaposi's sarcoma-associated herpesvirus (KSHV)-encoded viral interferon regulatory factor 1 (vIRF1) can be propionylated in lysine residues, which is required for effective inhibition of IFN-β production and antiviral signaling. Mechanistically, vIRF1 promotes its own propionylation by blocking SIRT6's interaction with ubiquitin-specific peptidase 10 (USP10) leading to its degradation via a ubiquitin-proteasome pathway. Furthermore, vIRF1 propionylation is required for its function to block IRF3-CBP/p300 recruitment and repress the STING DNA sensing pathway. A SIRT6-specific activator, UBCS039, rescues propionylated vIRF1-mediated repression of IFN-β signaling. These results reveal a novel mechanism of viral evasion of innate immunity through propionylation of a viral protein. The findings suggest that enzymes involved in viral propionylation could be potential targets for preventing viral infections.
Identifiants
pubmed: 37023208
doi: 10.1371/journal.ppat.1011324
pii: PPATHOGENS-D-22-02106
pmc: PMC10112802
doi:
Substances chimiques
Antiviral Agents
0
Interferon Regulatory Factor-1
0
Interferon Regulatory Factor-3
0
Lysine
K3Z4F929H6
Sirtuins
EC 3.5.1.-
viral interferon regulatory factors
0
Viral Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1011324Informations de copyright
Copyright: © 2023 Shi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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