Your browser doesn't support javascript.
loading
The African Swine Fever Virus Virulence Determinant DP96R Suppresses Type I IFN Production Targeting IRF3.
Dodantenna, Niranjan; Cha, Ji-Won; Chathuranga, Kiramage; Chathuranga, W A Gayan; Weerawardhana, Asela; Ranathunga, Lakmal; Kim, Yongkwan; Jheong, Weonhwa; Lee, Jong-Soo.
Afiliación
  • Dodantenna N; College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
  • Cha JW; College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
  • Chathuranga K; College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
  • Chathuranga WAG; College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
  • Weerawardhana A; College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
  • Ranathunga L; College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
  • Kim Y; Wildlife Disease Response Team, National Institute of Wildlife Disease Control and Prevention, Gwangju 62407, Republic of Korea.
  • Jheong W; Wildlife Disease Response Team, National Institute of Wildlife Disease Control and Prevention, Gwangju 62407, Republic of Korea.
  • Lee JS; College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
Int J Mol Sci ; 25(4)2024 Feb 08.
Article en En | MEDLINE | ID: mdl-38396775
ABSTRACT
DP96R of African swine fever virus (ASFV), also known as uridine kinase (UK), encodes a virulence-associated protein. Previous studies have examined DP96R along with other genes in an effort to create live attenuated vaccines. While experiments in pigs have explored the impact of DP96R on the pathogenicity of ASFV, the precise molecular mechanism underlying this phenomenon remains unknown. Here, we describe a novel molecular mechanism by which DP96R suppresses interferon regulator factor-3 (IRF3)-mediated antiviral immune responses. DP96R interacts with a crucial karyopherin (KPNA) binding site within IRF3, disrupting the KPNA-IRF3 interaction and consequently impeding the translocation of IRF3 to the nucleus. Under this mechanistic basis, the ectopic expression of DP96R enhances the replication of DNA and RNA viruses by inhibiting the production of IFNs, whereas DP96R knock-down resulted in higher IFNs and IFN-stimulated gene (ISG) transcription during ASFV infection. Collectively, these findings underscore the pivotal role of DP96R in inhibiting IFN responses and increase our understanding of the relationship between DP96R and the virulence of ASFV.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Virus de la Fiebre Porcina Africana / Factor 3 Regulador del Interferón Límite: Animals / Humans Idioma: En Revista: Int J Mol Sci Año: 2024 Tipo del documento: Article Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Virus de la Fiebre Porcina Africana / Factor 3 Regulador del Interferón Límite: Animals / Humans Idioma: En Revista: Int J Mol Sci Año: 2024 Tipo del documento: Article Pais de publicación: Suiza