The L83L ORF of African swine fever virus strain Georgia encodes for a non-essential gene that interacts with the host protein IL-1β

•L83L is an early expressed protein in ASFV.•L83L is a binding partner for host protein Il-1β.•Deletion of L83L in ASFV does not decrease virus virulence in swine. African swine fever virus (ASFV) causes a contagious and frequently lethal disease of pigs causing significant economic consequences to...

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Published in:Virus research Vol. 249; pp. 116 - 123
Main Authors: Borca, Manuel V., O’Donnell, Vivian, Holinka, Lauren G., Ramírez-Medina, Elizabeth, Clark, Benjamin A., Vuono, Elizabeth A., Berggren, Keith, Alfano, Marialexia, Carey, Lucas B., Richt, Juergen A., Risatti, Guillermo R., Gladue, Douglas P.
Format: Journal Article
Language:English
Published: Netherlands Elsevier B.V 02-04-2018
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Summary:•L83L is an early expressed protein in ASFV.•L83L is a binding partner for host protein Il-1β.•Deletion of L83L in ASFV does not decrease virus virulence in swine. African swine fever virus (ASFV) causes a contagious and frequently lethal disease of pigs causing significant economic consequences to the swine industry. The ASFV genome encodes for more than 150 genes, but only a few of them have been studied in detail. Here we report the characterization of open reading frame L83L which encodes a highly conserved protein across all ASFV isolates. A recombinant ASFV harboring a HA tagged L83L protein was developed (ASFV-G-L83L-HA) and used to demonstrate that L83L is a transiently expressed early virus protein. A recombinant ASFV lacking the L83L gene (ASFV-G-ΔL83L) was developed from the highly virulent field isolate Georgia2007 (ASFV-G) and was used to show that L83L is a non-essential gene. ASFV-G-ΔL83L had similar replication in primary swine macrophage cells when compared to its parental virus ASFV-G. Analysis of host-protein interactions for L83L identified IL-1β as its host ligand. Experimental infection of domestic pigs showed that ASFV-G-ΔL83L is as virulent as the parental virus ASFV-G.
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ISSN:0168-1702
1872-7492
DOI:10.1016/j.virusres.2018.03.017