Host combats porcine reproductive and respiratory syndrome virus infection at non-coding RNAs level

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) poses a significant threat to the global swine industry. The emergence of new, highly virulent strains has precipitated recurrent outbreaks worldwide, underscoring the ongoing battle between host and virus. Thus, there is an imperative to formulate a more comprehensive and effective disease control strategy. Studies have shown that host non-coding RNA (ncRNA) is an important regulator of host - virus interactions in PRRSV infection. Hence, a thorough comprehension of the roles played by ncRNAs in PRRSV infection can augment our understanding of the pathogenic mechanisms underlying PRRSV infection. This review focuses on elucidating contemporary insights into the roles of host microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) in PRRSV infection, providing both theoretical foundations and fresh perspectives for ongoing research into the mechanisms driving PRRSV infection and its pathogenesis.

Keywords: Porcine reproductive and respiratory syndrome virus; circular RNAs; long non-coding RNAs; microRNAs; viral infection.

Figure 1.

Schematic diagram of the roles of non-coding RNAs (ncRNAs) in host response to PRRSV infection. The innate immune response serves as the first line of defence against viral infections, involving the activation of multiple antiviral signalling pathways and the activation and expression of antiviral factors. PRRSV infection can induce or suppress the expression of host ncRnas, which can, in turn, indirectly inhibit viral replication and proliferation by regulating relevant antiviral factors and affecting the expression of antiviral innate immune molecules. The target gene sites involved in regulating non-coding RNAs in the innate immune response signalling pathways are concentrated in the RLR signalling pathway, nf-κB signalling pathway, and JAK-STAT signalling pathway. IL-6: interleukin 6; SOCS1/3: suppressor of cytokine signalling 3; tnf-α: necrosis factor alpha; STAT1: signal transducer and activator of transcription 1; MYH9: myosin heavy chain 9; SRP14: signal recognition particle 14.

Figure 2.

Schematic diagram of the roles of ncRNAs in host response to PRRSV infection. PRRSV infection affects the expression of ncRNAs in host cells. (a) These miRNAs inhibit PRRSV replication by directly targeting the viral genome or viral proteins; (b) these ncRNAs promote PRRSV replication by targeting antiviral host factors or the immune signalling pathways. JAK1: janus kinase 1; IFNAR2: interferon alpha and beta receptor subunit 2; HSP60: heat shock protein 60; IRF1/7: interferon regulatory factor 1/7; TRIM22: tripartite motif-containing (TRIM) 22; HO-1: haem oxygenase-1.