RIP3 Regulates Autophagy and Promotes Coxsackievirus B3 Infection of Intestinal Epithelial Cells.
Cell Host Microbe
; 18(2): 221-32, 2015 Aug 12.
Article
en En
| MEDLINE
| ID: mdl-26269957
ABSTRACT
Receptor interacting protein kinase-3 (RIP3) is an essential kinase for necroptotic cell death signaling and has been implicated in antiviral cell death signaling upon DNA virus infection. Here, we performed high-throughput RNAi screening and identified RIP3 as a positive regulator of coxsackievirus B3 (CVB) replication in intestinal epithelial cells (IECs). RIP3 regulates autophagy, a process utilized by CVB for viral replication factory assembly, and depletion of RIP3 inhibits autophagic flux and leads to the accumulation of autophagosomes and amphisomes. Additionally, later in infection, RIP3 is cleaved by the CVB-encoded cysteine protease 3C(pro), which serves to abrogate RIP3-mediated necrotic signaling and induce a nonnecrotic form of cell death. Taken together, our results show that temporal targeting of RIP3 allows CVB to benefit from its roles in regulating autophagy while inhibiting the induction of necroptotic cell death.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Autofagia
/
Proteínas Virales
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Replicación Viral
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Cisteína Endopeptidasas
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Enterovirus Humano B
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Células Epiteliales
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Proteína Serina-Treonina Quinasas de Interacción con Receptores
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Interacciones Huésped-Patógeno
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
Cell Host Microbe
Asunto de la revista:
MICROBIOLOGIA
Año:
2015
Tipo del documento:
Article
País de afiliación:
Estados Unidos