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Characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/CH/LJL/140901-like backbone and an S2 fragment from a 4/91-like virus

In this study, we isolated an infectious bronchitis virus, designated I1101/16, from broiler breeders in China. Analysis of the S1 gene showed that isolate I1101/16 was genetically close to strain ck/CH/LJL/140901, which belongs to the TW I genotype (also known as lineage GI-7 based on the recent IB...

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Autores principales: Jiang, Lei, Han, Zongxi, Chen, Yuqiu, Zhao, Wenjun, Sun, Junfeng, Zhao, Yan, Liu, Shengwang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier B.V. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7114561/
https://www.ncbi.nlm.nih.gov/pubmed/29141204
http://dx.doi.org/10.1016/j.virusres.2017.11.007
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author Jiang, Lei
Han, Zongxi
Chen, Yuqiu
Zhao, Wenjun
Sun, Junfeng
Zhao, Yan
Liu, Shengwang
author_facet Jiang, Lei
Han, Zongxi
Chen, Yuqiu
Zhao, Wenjun
Sun, Junfeng
Zhao, Yan
Liu, Shengwang
author_sort Jiang, Lei
collection PubMed
description In this study, we isolated an infectious bronchitis virus, designated I1101/16, from broiler breeders in China. Analysis of the S1 gene showed that isolate I1101/16 was genetically close to strain ck/CH/LJL/140901, which belongs to the TW I genotype (also known as lineage GI-7 based on the recent IBV classification), however the S2 gene showed genetic diversity comparing to that of S1 gene. Comparison of the genomic sequences showed that the genome of isolate I1101/16 was similar to that of strain ck/CH/LJL/140901 from the 5′ end of the genome to the 5′ end of the S2 gene and from the 5′ end of the 3a gene to the end of the genome, whereas the remaining parts of the genome sequences were more closely related to those of strain 4/91 than those of ck/CH/LJL/140901, thereby suggesting that recombination might have occurred during the origin of the virus. SimPlot and Bootscan analysis of the complete genomic sequence confirmed this hypothesis, where it showed that isolate I1101/16 arose through recombination events between ck/CH/LJL/140901- and 4/91-like viruses. Isolate I1101/16 and strain ck/CH/LJL/140901 shared identical amino acids in almost all five of their B cell epitopes, but the two viruses had a serotype relatedness value of 65, which is well below 80, i.e., the lower cutoff value for viruses of the same serotype. In addition, pathogenicity tests demonstrated that isolate I1101/16 was more pathogenic to 1-day-old specific-pathogen-free chickens than strain ck/CH/LJL/140901, according to analysis of the clinical signs, whereas strain ck/CH/LJL/140901 exhibited prolonged replication and shedding after challenge compared with isolate I1101/16. This study did not provide evidence that recombination can directly alter the antigenicity, virulence, replication, shedding, and tissue tropism of a virus, but it did show that recombination events are likely to be major determinants of viral evolution.
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spelling pubmed-71145612020-04-02 Characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/CH/LJL/140901-like backbone and an S2 fragment from a 4/91-like virus Jiang, Lei Han, Zongxi Chen, Yuqiu Zhao, Wenjun Sun, Junfeng Zhao, Yan Liu, Shengwang Virus Res Article In this study, we isolated an infectious bronchitis virus, designated I1101/16, from broiler breeders in China. Analysis of the S1 gene showed that isolate I1101/16 was genetically close to strain ck/CH/LJL/140901, which belongs to the TW I genotype (also known as lineage GI-7 based on the recent IBV classification), however the S2 gene showed genetic diversity comparing to that of S1 gene. Comparison of the genomic sequences showed that the genome of isolate I1101/16 was similar to that of strain ck/CH/LJL/140901 from the 5′ end of the genome to the 5′ end of the S2 gene and from the 5′ end of the 3a gene to the end of the genome, whereas the remaining parts of the genome sequences were more closely related to those of strain 4/91 than those of ck/CH/LJL/140901, thereby suggesting that recombination might have occurred during the origin of the virus. SimPlot and Bootscan analysis of the complete genomic sequence confirmed this hypothesis, where it showed that isolate I1101/16 arose through recombination events between ck/CH/LJL/140901- and 4/91-like viruses. Isolate I1101/16 and strain ck/CH/LJL/140901 shared identical amino acids in almost all five of their B cell epitopes, but the two viruses had a serotype relatedness value of 65, which is well below 80, i.e., the lower cutoff value for viruses of the same serotype. In addition, pathogenicity tests demonstrated that isolate I1101/16 was more pathogenic to 1-day-old specific-pathogen-free chickens than strain ck/CH/LJL/140901, according to analysis of the clinical signs, whereas strain ck/CH/LJL/140901 exhibited prolonged replication and shedding after challenge compared with isolate I1101/16. This study did not provide evidence that recombination can directly alter the antigenicity, virulence, replication, shedding, and tissue tropism of a virus, but it did show that recombination events are likely to be major determinants of viral evolution. Elsevier B.V. 2018-01-15 2017-11-12 /pmc/articles/PMC7114561/ /pubmed/29141204 http://dx.doi.org/10.1016/j.virusres.2017.11.007 Text en © 2017 Elsevier B.V. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Article
Jiang, Lei
Han, Zongxi
Chen, Yuqiu
Zhao, Wenjun
Sun, Junfeng
Zhao, Yan
Liu, Shengwang
Characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/CH/LJL/140901-like backbone and an S2 fragment from a 4/91-like virus
title Characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/CH/LJL/140901-like backbone and an S2 fragment from a 4/91-like virus
title_full Characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/CH/LJL/140901-like backbone and an S2 fragment from a 4/91-like virus
title_fullStr Characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/CH/LJL/140901-like backbone and an S2 fragment from a 4/91-like virus
title_full_unstemmed Characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/CH/LJL/140901-like backbone and an S2 fragment from a 4/91-like virus
title_short Characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/CH/LJL/140901-like backbone and an S2 fragment from a 4/91-like virus
title_sort characterization of the complete genome, antigenicity, pathogenicity, tissue tropism, and shedding of a recombinant avian infectious bronchitis virus with a ck/ch/ljl/140901-like backbone and an s2 fragment from a 4/91-like virus
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7114561/
https://www.ncbi.nlm.nih.gov/pubmed/29141204
http://dx.doi.org/10.1016/j.virusres.2017.11.007
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