FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2895736089> ?p ?o ?g. }

• W2895736089 abstract "ABSTRACT Schlafen 11 (Slfn11) is a ubiquitously expressed interferon stimulating gene (ISG) that controls synthesis of proteins by regulating tRNA abundance. Likely through this mechanism, Slfn11 has previously been shown to impair human immunodeficiency virus 1 (HIV-1) infection and the expression of codon-biased open reading frames. Because replication of positive-sense single-stranded RNA [(+)ssRNA viruses] requires the immediate translation of the incoming viral genome whereas negative sense, single stranded [(−)ssRNA] viruses carry at infection an RNA replicase that makes multiple translation competent copies of the incoming viral genome, we reasoned that (+)ssRNA viruses will be more sensitive to the effect of Slfn11 on protein synthesis than (−)ssRNA viruses. To evaluate this hypothesis, we tested the effects of Slfn11 on the replication of a panel of ssRNA viruses in the human glioblastoma cell line A172, which naturally expresses Slfn11. Depletion of Slfn11 in this cell line significantly increased the replication of (+)ssRNA viruses from the Flavivirus family , including West Nile (WNV), dengue (DENV), and Zika virus (ZIKV) but had no significant effect on the replication of the (−)ssRNA viruses vesicular stomatitis (VSV, Rhabdoviridae family ) and Rift Valley fever (RVFV, Phenuiviridae family ). Despite that WNV titers in Slfn11-deficient cells were almost 100-fold higher than in cells expressing this protein; they produced approximately two-fold less viral particles, as determined by PCR-based quantification of virion-associated WNV RNA in the cell culture supernatant. These data indicated that Slfn11 impairs WNV fitness but does not affect other steps of the viral life cycle including entry, viral RNA replication and translation, and budding. Similarly to the proposed anti-HIV-1 mechanism of Slfn11, this protein prevented WNV-induced down-regulation of a subset of tRNAs implicated in the translation of 19% of the viral polyprotein. Importantly, we provided evidence suggesting that the broad anti-viral activity of Slfn11 requires other cellular proteins, since overexpression of Slfn11 in cells that naturally lack the expression of this protein, did not impair WNV or HIV-1 infection. In summary, this study demonstrates that Slfn11 restricts flaviviruses replication by impairing viral fitness. AUTHOR SUMMARY The host targets mechanisms that viruses have evolved to optimize replication. We provide evidence that the cellular protein Schlafen 11 (Slf11) impairs replication of flaviviruses, including West Nile (WNV), dengue (DENV), and Zika virus (ZIKV). However, replication of single-stranded, negative RNA viruses was not affected. Specifically, Slf11 decreases the fitness of WNV potentially by preventing virus-induced modifications of the host tRNA repertoire that could lead to enhanced viral protein folding. Furthermore, we demonstrated that Slf11 is not the limiting factor of this novel broad anti-viral pathway." @default.
• W2895736089 created "2018-10-12" @default.
• W2895736089 creator A5009761712 @default.
• W2895736089 creator A5018339357 @default.
• W2895736089 creator A5031948181 @default.
• W2895736089 creator A5043085403 @default.
• W2895736089 creator A5062932913 @default.
• W2895736089 creator A5064875932 @default.
• W2895736089 creator A5082639332 @default.
• W2895736089 date "2018-10-03" @default.
• W2895736089 modified "2023-10-17" @default.
• W2895736089 title "Schlafen 11 Restricts Flavivirus Replication" @default.
• W2895736089 cites W1539868719 @default.
• W2895736089 cites W1593377767 @default.
• W2895736089 cites W1834855708 @default.
• W2895736089 cites W1966778471 @default.
• W2895736089 cites W1974786493 @default.
• W2895736089 cites W1990137452 @default.
• W2895736089 cites W1993985216 @default.
• W2895736089 cites W2010753155 @default.
• W2895736089 cites W2025569664 @default.
• W2895736089 cites W2032856030 @default.
• W2895736089 cites W2035475950 @default.
• W2895736089 cites W2043398720 @default.
• W2895736089 cites W2048957676 @default.
• W2895736089 cites W2055639102 @default.
• W2895736089 cites W2058277625 @default.
• W2895736089 cites W2058628249 @default.
• W2895736089 cites W2060197446 @default.
• W2895736089 cites W2075606650 @default.
• W2895736089 cites W2085489729 @default.
• W2895736089 cites W2091528429 @default.
• W2895736089 cites W2101054047 @default.
• W2895736089 cites W2117312105 @default.
• W2895736089 cites W2120253101 @default.
• W2895736089 cites W2121155221 @default.
• W2895736089 cites W2127168227 @default.
• W2895736089 cites W2150701651 @default.
• W2895736089 cites W2161286669 @default.
• W2895736089 cites W2199045960 @default.
• W2895736089 cites W2396592079 @default.
• W2895736089 cites W2524063359 @default.
• W2895736089 cites W2540278950 @default.
• W2895736089 cites W2556980854 @default.
• W2895736089 cites W2565214472 @default.
• W2895736089 cites W2588648082 @default.
• W2895736089 cites W2620912806 @default.
• W2895736089 cites W2735574967 @default.
• W2895736089 cites W2793350125 @default.
• W2895736089 cites W2803056412 @default.
• W2895736089 cites W32715603 @default.
• W2895736089 doi "https://doi.org/10.1101/434563" @default.
• W2895736089 hasPublicationYear "2018" @default.
• W2895736089 type Work @default.
• W2895736089 sameAs 2895736089 @default.
• W2895736089 citedByCount "2" @default.
• W2895736089 countsByYear W28957360892019 @default.
• W2895736089 countsByYear W28957360892023 @default.
• W2895736089 crossrefType "posted-content" @default.
• W2895736089 hasAuthorship W2895736089A5009761712 @default.
• W2895736089 hasAuthorship W2895736089A5018339357 @default.
• W2895736089 hasAuthorship W2895736089A5031948181 @default.
• W2895736089 hasAuthorship W2895736089A5043085403 @default.
• W2895736089 hasAuthorship W2895736089A5062932913 @default.
• W2895736089 hasAuthorship W2895736089A5064875932 @default.
• W2895736089 hasAuthorship W2895736089A5082639332 @default.
• W2895736089 hasBestOaLocation W28957360891 @default.
• W2895736089 hasConcept C104317684 @default.
• W2895736089 hasConcept C140704245 @default.
• W2895736089 hasConcept C159047783 @default.
• W2895736089 hasConcept C2522874641 @default.
• W2895736089 hasConcept C2776178377 @default.
• W2895736089 hasConcept C2776408679 @default.
• W2895736089 hasConcept C2777510210 @default.
• W2895736089 hasConcept C2778960357 @default.
• W2895736089 hasConcept C2779057330 @default.
• W2895736089 hasConcept C2780568436 @default.
• W2895736089 hasConcept C533803919 @default.
• W2895736089 hasConcept C54355233 @default.
• W2895736089 hasConcept C67705224 @default.
• W2895736089 hasConcept C86803240 @default.
• W2895736089 hasConceptScore W2895736089C104317684 @default.
• W2895736089 hasConceptScore W2895736089C140704245 @default.
• W2895736089 hasConceptScore W2895736089C159047783 @default.
• W2895736089 hasConceptScore W2895736089C2522874641 @default.
• W2895736089 hasConceptScore W2895736089C2776178377 @default.
• W2895736089 hasConceptScore W2895736089C2776408679 @default.
• W2895736089 hasConceptScore W2895736089C2777510210 @default.
• W2895736089 hasConceptScore W2895736089C2778960357 @default.
• W2895736089 hasConceptScore W2895736089C2779057330 @default.
• W2895736089 hasConceptScore W2895736089C2780568436 @default.
• W2895736089 hasConceptScore W2895736089C533803919 @default.
• W2895736089 hasConceptScore W2895736089C54355233 @default.
• W2895736089 hasConceptScore W2895736089C67705224 @default.
• W2895736089 hasConceptScore W2895736089C86803240 @default.
• W2895736089 hasLocation W28957360891 @default.
• W2895736089 hasOpenAccess W2895736089 @default.
• W2895736089 hasPrimaryLocation W28957360891 @default.
• W2895736089 hasRelatedWork W2090996633 @default.
• W2895736089 hasRelatedWork W2100364502 @default.

• next