TIM22 and TIM29 inhibit HBV replication by up-regulating SRSF1 expression.
J Med Virol
; 96(2): e29439, 2024 Feb.
Article
en En
| MEDLINE
| ID: mdl-38294104
ABSTRACT
Hepatitis B virus (HBV) infection is a serious global health problem. After the viruses infect the human body, the host can respond to the virus infection by coordinating various cellular responses, in which mitochondria play an important role. Evidence has shown that mitochondrial proteins are involved in host antiviral responses. In this study, we found that the overexpression of TIM22 and TIM29, the members of the inner membrane translocase TIM22 complex, significantly reduced the level of intracellular HBV DNA and RNA and secreted HBV surface antigens and E antigen. The effects of TIM22 and TIM29 on HBV replication and transcription is attributed to the reduction of core promoter activity mediated by the increased expression of SRSF1 which acts as a suppressor of HBV replication. This study provides new evidence for the critical role of mitochondria in the resistance of HBV infection and new targets for the development of treatment against HBV infection.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Contexto en salud:
2_ODS3
Problema de salud:
2_cobertura_universal
/
2_enfermedades_transmissibles
Asunto principal:
Virus de la Hepatitis B
/
Factores de Empalme Serina-Arginina
/
Proteínas del Complejo de Importación de Proteínas Precursoras Mitocondriales
/
Hepatitis B
Límite:
Humans
Idioma:
En
Revista:
J Med Virol
Año:
2024
Tipo del documento:
Article
País de afiliación:
China