Host Combats IBDV Infection at Both Protein and RNA Levels

Abstract

Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by infectious bursal disease virus (IBDV). In recent years, with the emergence of IBDV variants and recombinant strains, IBDV still threatens the poultry industry worldwide. It seems that the battle between host and IBDV will never end. Thus, it is urgent to develop a more comprehensive and effective strategy for the control of this disease. A better understanding of the mechanisms underlying virus–host interactions would be of help in the development of novel vaccines. Recently, much progress has been made in the understanding of the host response against IBDV infection. If the battle between host and IBDV at the protein level is considered the front line, at the RNA level, it can be taken as a hidden line. The host combats IBDV infection at both the front and hidden lines. Therefore, this review focuses on our current understanding of the host response to IBDV infection at both the protein and RNA levels.

Infectious bursal disease virus VP5 triggers host shutoff in a transcription-dependent manner

“…Innate immune responses, including IFNs signaling and inflammatory responses, play essential roles in combating IBDV infection ( 2 ). To investigate the impact of impaired host protein synthesis on the innate immune responses to IBDV infection, we also examined the transcriptional activation of IFN-β, Mx dynamin-like GTPase 1 (Mx1), inducible nitric oxide synthase (iNOS), and interleukin-1β (IL-1β) induced by HT or KO strains at the same final titer in DF1 cells ( Fig.…”

“…Additionally, the expression of pro-inflammatory factors, IL-1β and iNOS, in the infection group with the parental strain was also notably restricted. Prior research indicates that uncontrolled acute inflammatory response caused by IBDV infection may trigger a “cytokine storm,” leading to severe consequences like sepsis and host death ( 2 ). In contrast, within normal limits, the inflammatory response promotes phagocytosis and clearance of IBDV.…”

“…Viral infections trigger the host’s integrated stress response, activating antiviral immune responses upon recognizing viral nucleic acids and proteins ( 1 ). As part of this interaction, viruses manipulate host processes at various levels to regulate or evade both innate and adaptive immune responses, promoting self-survival and efficient transmission ( 2 ). In response to this host-virus arms race, viruses have evolved multiple strategies to suppress antiviral responses ( 3 – 5 ).…”

“…Infectious bursal disease (IBD), caused by the IBD virus (IBDV), is a major immunosuppressive infectious disease that poses a serious threat to the global poultry industry ( 2 , 18 , 19 ). IBDV infection induces host immunosuppression by directly attacking and damaging the bursa of Fabricius, a central immune organ in chickens, resulting in increased susceptibility to other pathogenic infections and reduced vaccination efficacy ( 20 , 21 ).…”

“…Among the viral proteins encoded by IBDV, VP5 is the only non-essential protein for viral replication. Previous studies have demonstrated that the IFNs and pro-inflammatory mediators, such as cytokines, chemokines, and antimicrobial peptides, effectively limits and clears IBDV viral infection ( 2 , 29 ). Recently, single-cell sequencing studies have shown that intranasal inoculation with IBDV allows the virus to quickly traverse the immune barrier, accessing the target organ, bursa, and establishing infection ( 30 ).…”