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Infectious bursal disease (IBD) is an acute, highly contagious, immunosuppressive, and fatal infectious disease of young chickens caused by infectious bursal disease virus (IBDV). Since 2017, a new trend has been discovered in the IBDV epidemic, with very virulent IBDV (vvIBDV) and novel variant IBDV (nVarIBDV) becoming the two current dominant strains in East Asia including China. In this study, we compared the biological characteristics of the vvIBDV (HLJ0504 strain), nVarIBDV (SHG19 strain), and attenuated IBDV (attIBDV, Gt strain) using specific-pathogen-free (SPF) chicken infection model. The results showed that vvIBDV distributed in multiple tissues, replicated the fastest in lymphoid organs such as bursa of Fabricius, induced significant viremia and virus excretion, and is the most pathogenic virus with a mortality of more than 80%. The nVarIBDV had a weaker replication capability and did not kill the chickens but caused severe damage to the central immune organ bursa of Fabricius and B lymphocytes and induced significant viremia and virus excretion. The attIBDV strain was found not to be pathogenic. Further studies preliminarily suggested that the expression level of inflammatory factors triggered by HLJ0504 was the highest, followed by the SHG19 group. This study is the first to systematically compare the pathogenic characteristics of three IBDVs closely related to poultry industry from the perspectives of clinical signs, micro-pathology, virus replication, and distribution. It is of great importance to obtain an extensive knowledge of epidemiology, pathogenicity, and comprehensive prevention, and control of various IBDV strains. [ABSTRACT FROM AUTHOR]

Infectious bursal disease is an acute, immunosuppressive infectious disease in chickens caused by the infectious bursal disease virus (IBDV), which causes huge economic losses to the global poultry industry. Persistently circulating very virulent IBDV (vvIBDV) and newly emerging novel variant IBDV (nVarIBDV) are the two dominant epidemic strains of IBDV in East Asian countries such as China. Compared to lethal vvIBDV, nonlethal nVarIBDV has more insidious pathogenicity and can partially escape the immune protection of the existing vvIBDV vaccine, suggesting its potential adaptive survival strategy. However, the underlying molecular mechanism remains unknown. The viral capsid protein VP2 is closely related to cell tropism, virulence, and antigenic variation of IBDV. In this study, for the first time, we demonstrated that residue 279 of VP2 is responsible for the difference in pathogenicity between nVarIBDV and vvIBDV and that the D279N substitution reduces the lethality of vvIBDV from 70% to 0%. Moreover, a significant reduction in the viral load and inflammatory factor levels in the immune organs and blood of infected chickens may be important mechanisms for reducing the lethality of IBDV. Additionally, residue 279 was an important molecular basis for the antigenic differences between nVarIBDV and vvIBDV. D279N substitution reduced the neutralizing ability of vvIBDV antiserum against nVarIBDV by affecting the binding ability of antibodies and antigens. Our results indicate that nVarIBDV has an infection transmission strategy that facilitates its survival by hiding viral pathogenicity and escaping antiserum neutralization, which not only has significant implications for the systemic cognition of viral genetic evolution and pathogenesis but also provides new ideas for the comprehensive prevention and control of IBDV. [ABSTRACT FROM AUTHOR]