Abstract
Porcine circovirus type 2 (PCV2) is closely linked to postweaning multisystemic wasting syndrome (PMWS) and other PCV-associated diseases (PCVADs), which influence the global pig industry. MicroRNAs (miRNAs) are evolutionarily conserved classes of endogenous small non-coding RNA that regulate almost every cellular process. According to our previous transcription study, PCV2 infection causes up-regulation of genes related to inflammation. To reveal the function of miRNAs in PCV2 infection and PCV2-encoded miRNAs, next generation sequencing and data analysis was performed to explore miRNA expression in PCV2-infected cells and non-infected cells. Data analysis found some small RNAs matched the PCV2 genome but PCV2 does not express miRNAs in an in vitro infection (PK-15 cells). More than 297 known and 427 novel miRNAs were identified, of which 44 miRNAs were differently expressed (DE). The pathways of inflammation mediated by chemokine and cytokine signaling pathway (P00031), were more perturbed in PCV2-infected cells than in mock controls. DE miRNAs and DE mRNA interaction network clearly revealed that PCV2 regulates the cellular inflammatory response through dysregulating the cellular miRNA-mRNA network. MiRNA overexpression and down-expression results demonstrated that miRNA dysregulation could affect PCV2 infection-induced cellular inflammatory responses. Our study revealed that host miRNA can be dysregulated by PCV2 infection and play an important role in PCV2-modulated inflammation.
Highlights
PCV belongs to the genus Circovirus and family Circoviridae, and currently, three porcine circovirus genotypes have been reported [1,2,3]
We evaluated the correlation between multiplicity of infection (MOI) and the number of Porcine circovirus type 2 (PCV2)-positive cells
The most frequently represented category of pathway was inflammation mediated by chemokine and cytokine signaling pathway (P00031) (Figure 7)
Summary
PCV belongs to the genus Circovirus and family Circoviridae, and currently, three porcine circovirus genotypes have been reported [1,2,3]. Our previous studies have reported a correlation between a deregulated immune-inflammatory response and cytokine dysfunction in infected pigs and cells [6]. Understanding of the mechanisms underlying the deregulation of immune responses remains limited. The study of miRNA-mediated host-pathogen interactions has emerged in the last decade due to the increasing knowledge regarding the role that miRNAs play in antiviral defense. There is increasing evidence indicating that viruses modulate cellular miRNA expression profiles upon host infection. The altered expression of cellular miRNAs may facilitate and/or restrict viral replication by deregulating their target genes after viral infections [13]
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