Viral competition and maternal immunity influence the clinical disease caused by very virulent infectious bursal disease virus.

The very virulent form of infectious bursal disease virus (vvIBDV) causes an immunosuppressive disease that is further characterized by the rapid onset of morbidity and high mortality in susceptible chickens. In 2009, vvIBDV was first reported in California, U. S. A., and since that time only a few cases of acute infectious bursal disease attributed to vvIBDV have been recognized in California. In other countries where vvIBDV has become established, it rapidly spreads to most poultry-producing regions. Two factors that may be involved in limiting the spread or reducing the severity of the clinical disease caused by vvIBDV in the U. S. A. are maternal immunity and competition with endemic variant strains of the virus. In this study, the ability of vvIBDV to infect and cause disease in maternally immune layer chickens was examined at weekly intervals over a 5-wk period during which their neutralizing maternal antibodies waned. Birds inoculated with vvIBDV at 2, 3, and 4 wk of age seemed healthy throughout the duration of the experiment, but macroscopic and microscopic lesions were observed in their bursa tissues. A real-time reverse transcriptase-polymerase chain reaction (RT-PCR) assay also confirmed the presence of vvIBDV RNA in their bursa tissues, indicating this virus was infecting the birds even at 2 wk of age when neutralizing maternal antibodies to infectious bursal disease virus were still relatively high (> 2000 geometric mean antibody titer). No mortality was observed in any birds when inoculated at 2, 3, or 4 wk of age; however, inoculation at 5 and 6 wk of age resulted in 10% and 20% mortality, respectively. Three experiments on the competition between vvIBDV and the two variant viruses T1 and FF6 were conducted. In all three experiments, specific-pathogen-free (SPF) birds that were inoculated with only the vvIBDV became acutely moribund, and except for Experiment 1 (62% mortality) all succumbed to the infection within 4 days of being exposed. When the variant viruses were inoculated into SPF chickens at 4 wk of age and the vvIBDV was administered 10 days later, a real-time reverse transcriptase (RT)-PCR assay was positive for the variant T1 and FF6 viral RNA but negative for vvIBDV RNA, indicating the vvIBDV isolate could not establish an infection in the bursa tissues of these birds. No clinical disease or mortality was observed in the birds, but macroscopic and microscopic lesions typical of a variant virus infection were observed. When the interval was shortened to 2 days, both variant viruses and vvIBDV were detected by RT-PCR, but the vvIBDV viral load in the bursa tissue was significantly lower compared with that of birds inoculated with vvIBDV alone. No clinical disease or mortality was observed, and macroscopic and microscopic lesions in the bursa of these birds were not typical of a vvIBDV infection but instead resembled a pathogenic classic virus infection. When the variant viruses and vvIBDV were inoculated simultaneously into 4-wk-old SPF chickens only the vvIBDV RNA was detected in the bursa tissues of the birds, and no reduction in viral load as measured by real-time RT-PCR was detected. Mortality (30%-40%) was reduced in these duel-infected birds compared with the 100% mortality observed in birds that received vvIBDV alone. The data suggest that maternal immunity and competition with variant viruses are acting to reduce the clinical signs and anticipated mortality after an vvIBDV infection, which may increase the chances that vvIBDV is not being recognized in commercial poultry operations.