Frontiers in Immunology · 2019 · 24 citations · 54 references
Life SciencesImmunologyInfectious DiseasesImmunology Of Infectious DiseasesInnate ImmunityMolecular VirologyAnimal VirusesAntiviral ImmunityCellular Immunity In InfectionImmune Gene RegulationRuminant Infectious DiseasesViral PathogenesisCellular Immune Response To VirusesGlobal Gene RegulationHost Antiviral ResponseHost Response MarkersT Helper CellsTranscriptome AnalysisViral Immune ResponsesWhole Transcriptome Analysis
In this study, transcriptome analysis of PPRV infected PBMC subsets-T helper cells, T cytotoxic cells, monocytes, and B lymphocytes was done to delineate their role in host response. PPRV was found to infect lymphocytes and not monocytes. The established receptor for PPRV-SLAM was found downregulated in lymphocytes and non-differentially expressed in monocytes. A profound deviation in the global gene expression profile with a large number of unique upregulated genes (851) and downregulated genes (605) was observed in monocytes in comparison to lymphocytes. ISGs-ISG15, Mx1, Mx2, RSAD2, IFIT3, and IFIT5 that play a role in antiviral response and the genes for viral sensors-MDA5, LGP2, and RIG1, were found to be upregulated in lymphocytes and downregulated in monocytes. The transcription factors-IRF-7 and STAT-1 that regulate expression of most of the ISGs were found activated in lymphocytes and not in monocytes. Interferon signaling pathway and RIG1 like receptor signaling pathway were found activated in lymphocytes and not in monocytes. This contrast in gene expression profiles and signaling pathways indicated the predominant role of lymphocytes in generating the antiviral response against PPRV in goats, thus, giving us new insights into host response to PPRV.
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