Amino acids contributing to antigenic drift in the infectious bursal disease Birnavirus (IBDV)

Abstract

We examined the effect of amino acids 222 and 254 on antigenicity of the variant Del-E strain of infectious bursal disease virus (IBDV). Using molecular epidemiology, we identified a virus designated as Del-E-222 that was identical to Del-E except for alanine at position 222. A second virus was generated using reverse genetics of the Del-E backbone to create Del-E-254 that contained an asparagine at amino acid 254. The Del-E-222 and Del-E-254 viruses were tested for their ability to escape neutralizing immunity provided by parenteral vaccination. The bursas from birds vaccinated with parental Del-E and challenged with Del-E-222 or Del-E-254 had macroscopic lesions typical of an IBDV infection, and their B-BW ratios were significantly smaller than the controls. Microscopic lesions included lymphocyte depletion and confirmed the ability of Del-E-222 and Del-E-254 to break through the immunity induced by the parental Del-E virus vaccination. Both mutations appear to be contributing to antigenic drift.

Genetic Characterization of Infectious Bursal Disease Viruses Associated with Gumboro Outbreaks in Commercial Broilers from Asyut Province, Egypt

“…Glutamic acid is characterized by negatively charged (acidic) R group, whereas the R group in alanine is nonpolar (hydrophobic). It is probable that this change from negative charge to nonpolar may modify the protein folding or the interaction with other molecules that may change the topography of the neutralizing epitopes that may lead to vaccination failure [19]. …”

Phylogeographic distribution of very virulent infectious bursal disease virus isolates in the Iberian Peninsula

“…Despite the regions under purifying selection being wider than the hydrophilic peaks, this is most probably a consequence of a hitchhiking effect commonly observed in regions under strong functional constraint (Barton, 2000). Considering that any change within these hydrophilic regions may potentially cause a change in the antigenic features of an isolate (Letzel et al, 2007;Jackwood & Sommer-Wagner, 2011), a strong purifying selection pattern as observed in this study could indicate a lack of a selection-driven immune escape in the evolutive pathway of the virus. Partial VP2 sequences have been widely used in routine diagnosis and epidemiological studies worldwide (Jackwood & Sommer-Wagner, 2011).…”

“…Considering that any change within these hydrophilic regions may potentially cause a change in the antigenic features of an isolate (Letzel et al, 2007;Jackwood & Sommer-Wagner, 2011), a strong purifying selection pattern as observed in this study could indicate a lack of a selection-driven immune escape in the evolutive pathway of the virus. Partial VP2 sequences have been widely used in routine diagnosis and epidemiological studies worldwide (Jackwood & Sommer-Wagner, 2011). Nonetheless, in order to accurately infer an IBDV phenotype, genome fragments including segments A and B need to be analysed.…”

A single mutation in the PBC loop of VP2 is involved in the in vitro replication of infectious bursal disease virus

“…Sometimes, T residue at position 222 of VP2 has also been observed in a few variant strains, including DEL-E, GLS, and GA988 (Jackwood and Sommer-Wagner, 2011;Letzel et al, 2007). Recently, a new occurring mutation P222S was observed in Belg strain (Letzel et al, 2007).…”

“…A single substitution at position 222 (P222S or A222T) was able to alter the antigenic pattern of IBDV because an S or T residue at position 222 is the essential part of the epitope that reacts with MAb 67 (Letzel et al, 2007). Recently, a natural mutation T222A was shown to allow the Del-E strain to break through the maternal immunity induced by parenteral vaccination (Jackwood and Sommer-Wagner, 2011).…”