A 15-year analysis of molecular epidemiology of avian infectious bronchitis coronavirus in China

Abstract

A comprehensive study of the epidemiology and pathogenicity of infectious bronchitis virus (IBV) in China was carried out by molecular characterization of the S1 gene from 46 isolates obtained for this study and 174 reference strains isolated over a 15-year period. Nine types were found according to sequence analysis and phylogenetic study of the S1 gene. The co-circulation of multiple IBV types and the ongoing emergence of IBV variants are the epidemiological challenges in China. Factors contributing to the continual emergence include mutations, insertions and deletions in the S1 protein genes; recombination between local IBV strains circulating in chicken flocks in China; and recombination between local strains and vaccine strains. Vaccination-challenge analysis between circulating field strains and Mass-type H120 vaccine indicated the need to develop new vaccines from local IBV strains. These results also emphasize the importance of continued IBV surveillance in China.

Fig. 1

Geographical locations of Chinese provinces or cities from where IBV strains were obtained over 15 years. The light grey indicated isolates found in the GenBank. The dark grey reflected the virus isolated both in the study and isolates found in the GenBank.

Fig. 2

Phylogenetic tree constructed based on the S1 subunit of the spike protein using neighbour-joining. The tree was rooted with the first 1572 nucleotides, starting with the ATG encoding the translation initiation codon (a). Each type of IBVs was grouped in one circle or box and the representative strains were boxed. The percentage of each type of IBV isolate is indicated (b).

Fig. 3

Sequence alignment of the HVRs of S1 amino acid sequences from IBV variants. Deleted amino acids are represented as dashes. Variants with the same pattern of insertions and deletions are listed with only one representative. The positions of deduced amino acids start with the methionine encoded by the ATG start codon of the S1 gene.

Fig. 4

Sequence and alignment of the S1 genes from the W118 and the pathogenic 4/91 strains. Nucleotides that are different between the two sequences are indicated in red. The positions of nucleotides begin with the ATG that encodes the start codon of S1. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)

Fig. 5

Sequence alignment of S1 genes from the CK/CH/LGD/04III and the 4/91 vaccine strains. Deleted nucleotides are represented as dots. Nucleotide identities are in parentheses. The positions of nucleotides are given from the ATG that encodes the start codon of S1.