Genetic and biological characteristics of four novel recombinant avian infectious bronchitis viruses isolated in China

Infectious bronchitis viruses (IBVs) of GI-13 (793/B) and GI-19 (QX/LX4) lineages have been frequently detected in China in recent years. Naturally recombinant IBVs originating from the GI-13 and GI-19 lineages have also been isolated from chicken flocks with respiratory and renal problems in China. Thorough genetic and biological investigations of these recombinant viruses have led to speculation regarding their origin, evolution, and control. In order to confirm the previous results and further extend our understanding about the characteristics of the four recombinant IBV strains we had previously identified (I0718/17, I0722/17, I0724/17, and I0737/17), we conducted phylogenetic analysis by comparing their complete S1 gene sequences with those of 71 reference strains of different genotypes and lineages. We identified a close relationship between the S1 sequences of the four strains and those of GI-13 strains. The results of complete genome sequence analysis confirmed the previously identified recombination events in the four IBV strains and revealed additional recombination events in different genomic regions of strains I0718/17 and I0724/17, suggesting that the two strains originated from multiple recombination events between 4/91-like and YX10-like viruses. We comparatively evaluated the antigenicity, pathogenicity, and affinity of the four recombinant viruses and their deduced parental strains in the trachea and kidneys. Some of the strains showed comparable antigenic relatedness, pathogenicity, and affinity for the trachea and kidneys among each other and with their parental viruses; however, some of them showed varying biological characteristics. Point mutations observed in the receptor-binding domain and hypervariable region of the S1 subunit of the spike protein likely have an effect on these differences in biological characteristics, although the influence of other factors—such as host innate-immune responses and changes in genomic regions beyond the S1 protein—might also be responsible for such changes.