These results are consistent with these genes and their associated processes having important roles in H PRRSV replication and http://www.selleckchem.com/products/kpt-330.html pathogenesis. The most prominently over represented GO terms of significant cluster profile 1 included epithelial cell differentiation, sterol, steroid, cholesterol, lipid biosynthetic and meta bolic process, actin cytoskeleton reorganization, regula tion of transport, cell proliferation and adhesion, and cellular biosynthetic process. These results suggest that H PRRSV infection could inhibit epithelial cell differentiation. Impaired regulation asso ciated with the biosynthesis and metabolism of steroids, cholesterol and lipids indicated that they could be involved in H PRRSV pathogenesis.
Innate immunity The antiviral response is triggered when host pathogen recognition receptors are engaged by pathogen associated molecular GSK-3 patterns in viral proteins and nucleic acids. Transcriptome analysis suggests that apparent reactive changes after H PRRSV infection include activation of complement pathways, PRRs and other receptors potentially responsible for H PRRSV recognition and uptake. As demonstrated in Figure 5, transcripts of the Toll like PRRs TLR2, TLR4, TLR6, TLR7, TLR9 and TLR adaptor molecule 1 were signifi cantly induced in H PRRSV infected pigs 4 7 d pi, no change was detected in expression of TLR3, which spe cializes in the recognition of viral dsRNA. Cytoplasmic PRRs DDX58 and melanoma differentiation associated gene 5, the two most important PRRs for defense against viruses, were expressed at high levels after H PRRSV infection.
Cell surface PRRs such as CD14 and CD163 were likewise up regulated after H PRRSV infection. Moreover, three categories of Fc receptors, mannose receptor C1 and c type lectin were significantly induced in H PRRSV infected lungs. After binding to H PRRSV viral PAMPs, PRRs figure 1 initiated intracellular sig naling cascades that activate transcription factors includ ing IRF1, IRF5, IRF7, IRF9, and signal transducer and activator of transcription and JAK2 kinases, IRF3 was not activated. These transcrip tion factors induced the expression of IFN g, IFN stimu lated genes including protein kinase R, 2,5 oligoadenylate synthetase and MX, and pro inflammatory cytokines and chemokines, SPIIFNs were not induced.
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