Norwegian
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
PLoS ONE 2017

The Ebola virus VP35 protein binds viral immunostimulatory and host RNAs identified through deep sequencing.

Bare registrerte brukere kan oversette artikler
Logg inn Registrer deg
Koblingen er lagret på utklippstavlen
Kari A Dilley
Alexander A Voorhies
Priya Luthra
Vinita Puri
Timothy B Stockwell
Hernan Lorenzi
Christopher F Basler
Reed S Shabman

Nøkkelord

Abstrakt

Ebola virus and Marburg virus are members of the Filovirdae family and causative agents of hemorrhagic fever with high fatality rates in humans. Filovirus virulence is partially attributed to the VP35 protein, a well-characterized inhibitor of the RIG-I-like receptor pathway that triggers the antiviral interferon (IFN) response. Prior work demonstrates the ability of VP35 to block potent RIG-I activators, such as Sendai virus (SeV), and this IFN-antagonist activity is directly correlated with its ability to bind RNA. Several structural studies demonstrate that VP35 binds short synthetic dsRNAs; yet, there are no data that identify viral immunostimulatory RNAs (isRNA) or host RNAs bound to VP35 in cells. Utilizing a SeV infection model, we demonstrate that both viral isRNA and host RNAs are bound to Ebola and Marburg VP35s in cells. By deep sequencing the purified VP35-bound RNA, we identified the SeV copy-back defective interfering (DI) RNA, previously identified as a robust RIG-I activator, as the isRNA bound by multiple filovirus VP35 proteins, including the VP35 protein from the West African outbreak strain (Makona EBOV). Moreover, RNAs isolated from a VP35 RNA-binding mutant were not immunostimulatory and did not include the SeV DI RNA. Strikingly, an analysis of host RNAs bound by wild-type, but not mutant, VP35 revealed that select host RNAs are preferentially bound by VP35 in cell culture. Taken together, these data support a model in which VP35 sequesters isRNA in virus-infected cells to avert RIG-I like receptor (RLR) activation.

Bli med på
facebooksiden vår

Den mest komplette databasen med medisinske urter støttet av vitenskap

  • Fungerer på 55 språk
  • Urtekurer støttet av vitenskap
  • Urtegjenkjenning etter bilde
  • Interaktivt GPS-kart - merk urter på stedet (kommer snart)
  • Les vitenskapelige publikasjoner relatert til søket ditt
  • Søk medisinske urter etter deres effekter
  • Organiser dine interesser og hold deg oppdatert med nyheter, kliniske studier og patenter

Skriv inn et symptom eller en sykdom og les om urter som kan hjelpe, skriv en urt og se sykdommer og symptomer den brukes mot.
* All informasjon er basert på publisert vitenskapelig forskning

Google Play badgeApp Store badge