Abstract

Infectious Bursal Disease Virus (IBDV) has haunted the poultry industry with severe, prolonged immunosuppression of chickens when infected at an early age and can easily lead to other secondary infections. Understanding the pathogenic mechanisms could lead to effective prevention and control of Infectious Bursal Disease (IBD). Evidence suggests that the N-terminal domain of polymerase in segment B plays an important role, but it is not clear which part or residual is crucial for the pathogenicity. Using a reverse genetics technique, a molecular clone (rNN1172) of the parental vvIBDV strain NN1172 was generated, and its pathogenicity was found to be the same as the parental virus. Then, three recombinant chimeric viruses were rescued based on the rNN1172 and substituted with the counterparts in the N-terminal domain of the attenuated vaccine strain B87: the rNN1172-B87VP1a (substituting the full region of the 1–167 aa residuals), the rNN1172-B87VP1a∆4 (substituting the region of the 5–167 aa residuals), and the rNN1172-VP1∆4 (one single aa residual substitution V4I), to better explore the role of the N-terminal domain of polymerase on the viral pathogenicity. Interestingly, all these substitutions played different roles in the viral pathogenicity: the mortality of the rNN1172-B87VP1a-challenged chickens was significantly reduced from 30% to 0%. No obvious lesion was found in the histopathological examination, and the lowest viral genome copy number was also detected in the bursa when compared to the parental and two other recombinant viruses. The mortalities caused by rNN1172-B87VP1a∆4 and rNN1172-B87VP1∆4, respectively, were all reduced to 10% and had a delayed onset of death. Our results also revealed that the pathogenicity of the IBDV was consistent with the viral replication efficiency in vivo (bursae). This study demonstrated that the full region of the N-terminal of polymerase plays an important role in viral replication and pathogenicity, but the substitutions of its partial region or a single residual do not completely lead to the virus attenuation to Three-Yellow chickens, although that significantly reduces its pathogenicity.

Highlights

  • Infectious Bursal Disease Virus (IBDV), a member of the genus Avibirnavirus of the family Birnaviridae, is a major pathogen causing immunosuppressive disease in chickens and is economically significant to the poultry industry worldwide [1]

  • Our results indicate that the N-terminus with substitution of the attenuated vaccine strain B87 in the RNA polymerase of very virulent IBDV” (vvIBDV) can significantly reduce the viral pathogenicity in Three-Yellow chickens

  • Some efforts have been made to understand the molecular biology of IBDV, the molecular basis for the pathogenicity of IBDV is not fully understood

Read more

Summary

Introduction

Infectious Bursal Disease Virus (IBDV), a member of the genus Avibirnavirus of the family Birnaviridae, is a major pathogen causing immunosuppressive disease in chickens and is economically significant to the poultry industry worldwide [1]. Since 2017, more and more novel variant strains with great immunosuppressive effects in chickens emerged in most parts of China [23]. These were isolated from vaccinated chicken flocks in which the classical vaccines had been proven ineffective at controlling novel variant strains [25,26]. The mechanisms of these changes are not fully understood. All these studies failed to fully elucidate the pathogenesis of the virus

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call