CINECA IRIS Institutional Research Information System
IRIS è la soluzione IT che facilita la raccolta e la gestione dei dati relativi alle attività e ai prodotti della ricerca. Fornisce a ricercatori, amministratori e valutatori gli strumenti per monitorare i risultati della ricerca, aumentarne la visibilità e allocare in modo efficace le risorse disponibili.
EnglishMany studies reported that HSV-1 is able to regulate autophagy through mechanisms that are not well understood. Literature data also reported that HSV-1 is recognized by TLRs and it is known that their stimulation is responsible of autophagy activation via MyD88. In this work we want to elucidate the involvement of MyD88 in the regulation of autophagy in monocytic THP-1 cells during the early phases of HSV-1 replication. To this aim, MyD88 deficient cells were also used. The data obtained showed that MyD88 protein expression was up regulated during the early times of HSV-1 infection, as well as MyD88 transcripts. The up regulation was correlated with the increase of autophagosome formation, since its forced expression increases the number of GFP-LC3 dots in infected cells. Conversely, the impairing of MyD88 in MyD88 deficient THP-1 cells prevented the occurrence of autophagy upon HSV-1 infection. These results confirm that HSV-1 mediated autophagy is triggered by signalling events initiated by the binding of the virus to cell surface receptors through the MyD88 adaptor protein
| Titolo: | Recruitment of MyD88 in the early phases of HSV-1 infection |
| Autori: | |
| Data di pubblicazione: | 2014 |
| Abstract: | Many studies reported that HSV-1 is able to regulate autophagy through mechanisms that are not well understood. Literature data also reported that HSV-1 is recognized by TLRs and it is known that their stimulation is responsible of autophagy activation via MyD88. In this work we want to elucidate the involvement of MyD88 in the regulation of autophagy in monocytic THP-1 cells during the early phases of HSV-1 replication. To this aim, MyD88 deficient cells were also used. The data obtained showed that MyD88 protein expression was up regulated during the early times of HSV-1 infection, as well as MyD88 transcripts. The up regulation was correlated with the increase of autophagosome formation, since its forced expression increases the number of GFP-LC3 dots in infected cells. Conversely, the impairing of MyD88 in MyD88 deficient THP-1 cells prevented the occurrence of autophagy upon HSV-1 infection. These results confirm that HSV-1 mediated autophagy is triggered by signalling events initiated by the binding of the virus to cell surface receptors through the MyD88 adaptor protein |
| Handle: | http://hdl.handle.net/11570/3022375 |
| Appare nelle tipologie: | 14.d.1 Abstract in Atti di convegno |
File in questo prodotto:
Copyright © 2020