OAS1 suppresses African swine fever virus replication by recruiting TRIM21 to degrade viral major capsid protein.
J Virol
; 97(10): e0121723, 2023 10 31.
Article
em En
| MEDLINE
| ID: mdl-37815352
ABSTRACT
IMPORTANCE African swine fever virus (ASFV) completes the replication process by resisting host antiviral response via inhibiting interferon (IFN) secretion and interferon-stimulated genes (ISGs) function. 2', 5'-Oligoadenylate synthetase gene 1 (OAS1) has been reported to inhibit the replication of various RNA and some DNA viruses. However, the regulatory mechanisms involved in the ASFV-induced IFN-related pathway still need to be fully elucidated. Here, we found that OAS1, as a critical host factor, inhibits ASFV replication in an RNaseL-dependent manner. Furthermore, overexpression of OAS1 can promote the activation of the JAK-STAT pathway promoting innate immune responses. In addition, OAS1 plays a new function, which could interact with ASFV P72 protein to suppress ASFV infection. Mechanistically, OAS1 enhances the proteasomal degradation of P72 by promoting TRIM21-mediated ubiquitination. Meanwhile, P72 inhibits the production of avSG and affects the interaction between OAS1 and DDX6. Our findings demonstrated OAS1 as an important target against ASFV replication and revealed the mechanisms and intrinsic regulatory relationships during ASFV infection.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Replicação Viral
/
2',5'-Oligoadenilato Sintetase
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Febre Suína Africana
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Vírus da Febre Suína Africana
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Proteínas com Motivo Tripartido
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
J Virol
Ano de publicação:
2023
Tipo de documento:
Article
País de afiliação:
China