Role of MicroRNAs in Host Defense against Infectious Bursal Disease Virus (IBDV) Infection: A Hidden Front Line

Abstract

Infectious bursal disease (IBD) is an acute, highly contagious and immunosuppressive avian disease caused by infectious bursal disease virus (IBDV). In recent years, remarkable progress has been made in the understanding of the pathogenesis of IBDV infection and the host response, including apoptosis, autophagy and the inhibition of innate immunity. Not only a number of host proteins interacting with or targeted by viral proteins participate in these processes, but microRNAs (miRNAs) are also involved in the host response to IBDV infection. If an IBDV–host interaction at the protein level is taken imaginatively as the front line of the battle between invaders (pathogens) and defenders (host cells), their fight at the RNA level resembles the hidden front line. miRNAs are a class of non-coding single-stranded endogenous RNA molecules with a length of approximately 22 nucleotides (nt) that play important roles in regulating gene expression at the post-transcriptional level. Insights into the roles of viral proteins and miRNAs in host response will add to the understanding of the pathogenesis of IBDV infection. The interaction of viral proteins with cellular targets during IBDV infection were previously well-reviewed. This review focuses mainly on the current knowledge of the host response to IBDV infection at the RNA level, in particular, of the nine well-characterized miRNAs that affect cell apoptosis, the innate immune response and viral replication.

Genome-wide identification of chicken bursae of Fabricius miRNAs in response to very virulent infectious bursal disease virus

“…For instance, gga-miR-1723, gga-miR-222b-3p, gga-miR-1782, gga-miR-449a, and gga-miR-1563 exhibited significantly varied expression levels following IBV infection in chicken kidneys [45]. Interestingly, we also found that gga-miR-130b-3p, gga-miR-142-5p, gga-miR-454-3p, gga-miR-27b-3p, gga-miR-1635, and gga-miR-155 were DE in vvIBDV-infected cells [21,29]. However, previously reported highly expressed miRNAs were not significantly DE in vvIBDV-infected BF.…”

“…Moreover, aberrantly expressed miRNAs in cells or tissues play a crucial role in virus-host interactions [20]. It has been reported that classical IBDV infection affects miRNA expression in DF-1 cells [21]. The discovery of miRNAs provides new insights into the mechanisms of gene regulation [22][23][24][25][26][27][28][29][30][31].…”

A Timely Review of Cross-Kingdom Regulation of Plant-Derived MicroRNAs

“…Some miRNAs could target viral genomes and proteins to suppress virus replication ( Wen et al, 2013 ). While, other miRNAs, like gga-miR-142-5p ( Ouyang et al, 2018 ), miRNA-16-5p ( Duan et al, 2020 ), may inhibit host defense and enhance virus replication and infection ( Li and Zheng, 2020 ). There is evidence that miRNAs exert antiviral effects on virus infection by modulation of certain immune and antiviral pathways, such as the janus kinase-signal transducer and activator of transcription (JAK-STAT), toll-like receptor, and mitogen-activated protein kinase signaling pathways ( Lin et al, 2016 ; Fu et al, 2018 ).…”

Pathological Changes and Pathogenic Mechanisms of Infectious Bursal Disease (IBD) in Chickens Infected with IBD Viruses of Different Pathogenicities

“…JARQ 56 (1) 2022 N. Tanimura on various aspects of IBD, including the acute form of IBD caused by very virulent IBDV (vvIBDV) (van den Berg 2000), host-pathogen interactions (Ingrao et al 2013, Li & Zheng 2020, Qin & Zheng 2017, pathogenesis and immunosuppression (Sharma et al 2000), the current status of vaccines against IBD (Müller et al 2012), and management strategies (Dey et al 2019). However, the molecular basis for the pathogenicity of the virus has not been fully determined (Qi et al 2013, Eterradossi & Saif 2020, and the pathogenesis of IBD remains to be elucidated.…”