AccessCommunication Genomic Alterations of the Infectious Bronchitis Virus (IBV) Strain of the GI-23 Lineage Induced by Passages in Chickens and Quails
International Journal of Molecular Sciences
Data
2025Autor
Domanska-Blicharz, Katarzyna
Sajewicz-Krukowska, Joanna
Lisowska, Anna
Opolska, Justyna
Tarasiuk, Karolina
Dziadek, Kamila
Metadane
Pokaż pełny rekordStreszczenie
Infectious bronchitis virus (IBV) of the GI-23 lineage, which first emerged in the
Middle East in the late 1990s, has since spread worldwide. The factors driving its expansion,
whether human involvement, wild bird migration, or the virus’s biological traits, are still
unclear. This study aimed to trace the genome evolution of GI-23 IBV in chickens and its
adaptability to quails, which are susceptible to both gamma- and deltacoronaviruses. Thirty
specific-pathogen-free (SPF) birds, aged between two and three weeks, were used. Initially,
three birds were inoculated with the G052/2016 IBV via the oculo-nasal route. On the
third day post-infection (dpi), oropharyngeal swabs were collected from the whole group,
pooled, and subsequently used to infect three next birds. This process was repeated nine
more times during consecutive IBV passages (P-I–P-X), and eventually, virus sequencing
was performed using Next-Generation Sequencing (NGS). The obtained results showed
that quails were not susceptible to the IBV GI-23 lineage, as the virus RNA was detected in
low amounts only during the first passage (QP-I) with no further detections in later rounds
of IBV passaging. In chickens, only mild diarrhea symptoms appeared in a few individuals.
The NGS analysis identified sixty-two single nucleotide variants (SNVs), thirty of which
caused amino acid changes, twenty-eight were synonymous, and one SNV introduced a
stop codon. Three SNVs were found in untranslated regions. However, none of these SNVs
lasted beyond seven passages, with forty-four being unique SNVs. The Shannon entropy
values measured during passages varied for pol1a, pol1b, S, 5a, 5b, and N genes, with overall
genome complexity peaking at CP-VI and CP-X. The highest complexity was observed in
the pol1a (CP-X) and S genes (CP-IV, CP-VI, CP-VIII, and CP-X). Along with the S gene
that was under positive selection, eight codons in pol1a were also positively selected. These
findings suggest that even in an adapted host, IBV variability does not stabilize without
immune pressure, indicating continuous molecular changes within its genome.
Zbiory
- Publikacje [640]