Isolation of a variant infectious bronchitis virus in Australia that further illustrates diversity among emerging strains

Abstract

Australian infectious bronchitis viruses (IBV) have undergone a separate evolution due to geographic isolation. Consequently, changes occurring in Australian IBV illustrate, independently from other countries, types of variability that could occur in emerging IBV strains. Previously, we have identified two distinct genetic groups of IBV, designated subgroups 1 and 2. IBV strains of subgroup 1 have S1 and N proteins that share a high degree of amino acid identity, 81 to 98% in S1 and 91 to 99% in N. Subgroup 2 strains possess S1 and N proteins that share a low level of identity with subgroup 1 strains: 54 to 62% in S1 and 60 to 62% in N. This paper describes the isolation and characterisation of a third, previously undetected genetic group of IBV in Australia. The subgroup 3 strains, represented by isolate chicken/Australia/N2/04, had an S1 protein that shared a low level of identity with both subgroups 1 and 2: 61 to 63% and 56 to 59%, respectively. However, the N protein and the 3' untranslated region were similar to subgroup 1: 90 to 97% identical with the N protein of subgroup 1 strains. This N4/02 subgroup 3 of IBV is reminiscent of two other strains, D1466 and DE072, isolated in the Netherlands and in the USA, respectively. The emergence of the subgroup 3 viruses in Australia, as well as the emergence of subgroup 2 in 1988, could not be explained by any of the mechanisms that are currently considered to be involved in generation of IBV variants.

Evaluation of a novel strain of infectious bronchitis virus emerged as a result of spike gene recombination between two highly diverged parent strains

“…Subgroup 3 strains, such as N1/03, are respiratory pathogens (Ignjatovic et al, 2006;Mardani et al, 2006a) and cause substantial lesions in the trachea associated with moderate to severe clinical signs of respiratory disease, a slightly increased rate of mortality and reduced growth rate (Ignjatovic et al, 2006). In contrast, subgroup 2 strains, such as N1/88, cause only mild lesions in the trachea and are associated with minimal signs of respiratory disease (Ignjatovic et al, 1997).…”

“…SimPlot analysis examines relationships between nucleotide sequences at a set incremental level to provide a more accurate representation of the relationship between strains than using identity scores to compare entire stretches of genomic sequence. A point of crossover between the similarity plots indicates a shift from a high identity to a low identity (or vice versa), and therefore indicates a potential point of recombination (Lole et al, 1999 (Wadey & Faragher, 1981;Sapats et al, 1996;Ignjatovic et al, 2006;Mardani et al, 2006aMardani et al, , 2008Mardani et al, , 2010. The vaccine strains included in these analyses were Armidale, VicS and S (Wadey & Faragher, 1981).…”

“…Australian subgroup 3 strains, first detected in 2002, emerged as a result of recombination and have a high sequence identity over the entire structural protein gene region, except for the S1 gene, with subgroup 1 strains. The S1 gene was determined to be of a different lineage, most closely related to subgroup 2 strains (Ignjatovic et al, 2006;Mardani et al, 2010). To date, subgroup 3 strains have only been detected in the trachea of chickens displaying respiratory disease (Ignjatovic et al, 2006).…”

“…The S1 gene was determined to be of a different lineage, most closely related to subgroup 2 strains (Ignjatovic et al, 2006;Mardani et al, 2010). To date, subgroup 3 strains have only been detected in the trachea of chickens displaying respiratory disease (Ignjatovic et al, 2006).…”

Genotipificación de variantes del virus de bronquitis infecciosa aviar en el departamento del Tolima, Colombia

“…Studies using molecular methods have shown that the new strains or serotypes have only a few changes in amino acid in the S1 portion of the viral spike protein, while most of the genome remains unchanged (4,5). These changes may occur due to an immune pressure caused by widespread use of vaccines, genetic recombination or of coexistent infections, or even a dominant serotype reduction as a result of vaccination, allowing other emerging field strains (1,4,6,7). The transmembrane domain is one of cleavage S1 region of the S virus structural protein, which is a hypervariable region, and the most antigenic and responsible for inducing protection against the virus (3).…”