Comparison of fiber gene sequences of inclusion body hepatitis (IBH) and non-IBH strains of serotype 8 and 11 fowl adenoviruses.

Grgić H, Krell PJ, Nagy E
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Fowl adenoviruses (FAdVs) are common in broiler operations, and the most frequently isolated FAdVs belong to serotypes 1, 8, and 11. Serotype 1 viruses are considered nonpathogenic. While some serotype 8 and 11 viruses cause inclusion body hepatitis (IBH), these virus serotypes can also be isolated from non-IBH cases. The fiber protein is one of the major constituents of the adenoviral capsid, involved in virus entry, and it has been implicated in the variation of virulence of FAdVs. The fiber gene sequences of four FAdV-8 and four FAdV-11 isolates from both IBH and non-IBH cases were determined and analyzed for a possible association of the fiber gene sequence in virulence. The fiber protein can be divided into tail, shaft, and head domains comprising some specific features. The conserved “RKRP” sequence motif (aa 17-aa 20) fit the consensus sequence predicted for the nuclear localization signal, while the “VYPF” motif (aa 53-aa 56), involved in the penton base interaction, was also found. Similar to mammalian adenoviruses, 17 pseudo-repeats with an average length of 16 aa were detected in the FAdV-8 fiber shaft region, while 20 pseudo-repeats with an average length of 18 aa were found in FAdV-11 fibers. There was a 144-147 nt difference between the fiber genes of the two FAdV serotypes. In the shaft region, the TLWT motif that marks the beginning of the fiber head domain of the mastadenovirus was not evident among examined FAdVs. The FAdV-11 isolates had 99.1 % aa sequence identity and 99.3 % similarity to each other, and there was no conserved aa substitution within the fibers. The FAdV-8 fiber proteins showed an overall lower, 89 % aa sequence identity and 93.4 % similarity, to each other and 22 nonsynonymous mutations were detected. Virulence markers were not detected in the analyzed fiber gene sequences of the different pathotypes of the two FAdV serotypes.

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Posted in 2014 Publications, Publication Nagy, Publications.