scholarly journals Molecular Biology and Pathological Process of an Infectious Bronchitis Virus with Enteric Tropism in Commercial Broilers

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1477
Author(s):  
Ana P. da Silva ◽  
Ruediger Hauck ◽  
Sabrina R. C. Nociti ◽  
Colin Kern ◽  
H. L. Shivaprasad ◽  
...  
Keyword(s):  
Infectious Bronchitis Virus ◽  
Molecular Mechanisms ◽  
Phylogenetic Analyses ◽  
Nucleotide Composition ◽  
Pathological Process ◽  
Tissue Tropism ◽  
Full Genome ◽  
Infectious Bronchitis ◽  
Viral Shedding ◽  
Intestinal Lesions

Infectious bronchitis virus (IBV) induces respiratory and urogenital disease in chickens. Although IBV replicates in the gastrointestinal tract, enteric lesions are uncommon. We have reported a case of runting-stunting syndrome in commercial broilers from which an IBV variant was isolated from the intestines. The isolate, CalEnt, demonstrated an enteric tissue tropism in chicken embryos and SPF chickens experimentally. Here, we determined the full genome of CalEnt and compared it to other IBV strains, in addition to comparing the pathobiology of CalEnt and M41 in commercial broilers. Despite the high whole-genome identity to other IBV strains, CalEnt is rather unique in its nucleotide composition. The S gene phylogenetic analyses showed great similarity between CalEnt and Cal 99. Clinically, vent staining was slightly more frequent in CalEnt-infected birds than those challenged with M41. Furthermore, IBV IHC detection was more evident and the viral shedding in feces was overall higher with the CalEnt challenge compared with M41. Despite underlying intestinal lesions caused by coccidiosis and salmonellosis vaccination, microscopic lesions in CalEnt-infected chickens were more severe than in M41-infected chickens or controls, supporting the enteric tropism of CalEnt. Further studies in SPF chickens are needed to determine the pathogenesis of the virus, its molecular mechanisms for the enteric tropism, and its influence in intestinal health.

scholarly journals Infectious bronchitis virus attaches to lipid rafts and enters cells via clathrin mediated endocytosis

2018 ◽  
Author(s):  
Huan Wang ◽  
Yingjie Sun ◽  
Xiang Mao ◽  
Chunchun Meng ◽  
Lei Tan ◽  
...  
Keyword(s):  
Lipid Rafts ◽  
Infectious Bronchitis Virus ◽  
Time Course ◽  
Molecular Mechanisms ◽  
Low Ph ◽  
Infection Process ◽  
Late Endosome ◽  
Poultry Industry ◽  
Infectious Bronchitis ◽  
Late Endosomes

ABSTRACTDue to its economic importance to in poultry industry, the biology and pathogenesis of infectious bronchitis virus (IBV) have been investigated extensively. However, the molecular mechanisms involved in IBV entry are not well characterized. In this study, systematic approaches were used to dissect IBV entry process in various susceptible cells. First, we observed that lipid rafts were involved in IBV attachment. Second, low pH in intracyplasmic vesicles was required for virus entry. By using the specific clathrin mediated endocytosis (CME) inhibitor or knock down of clathrin heavy chain (CHC), we demonstrated that IBV mainly utilized the CME for its entry. Furthermore, GTPase dynamin1 was involved in virus containing vesicle scission and internalization. Surprisingly, CME adaptor Eps15 had no effect on IBV internalization. Third, the penetration of IBV into cells led to active cytoskeleton rearrangement. After internalization, virus particles moved along with the classical endosome/lysosome track, as evidenced by co-localization of R18 labeled IBV with vehicle markers Rab5/Rab7/LAMP1 along with the infection time course. Functional inactivation of Rab5 and Rab7 significantly inhibited IBV infection. VCP, a protein helps early endosome maturation, was involved virus trafficking. Finally, by using the dual R18/DiOC labeled IBV, we observed that membrane fusion with late endosome/lysosome membranes was induced between 2-3 h.p.i.. Taken together, our findings demonstrate that IBV virions attach to lipid rafts and are internalized into cells via CME, move along with early/late endosomes-lysosomes, finally fuse with late endosome-lysosome membranes, release virus genome into cytoplasm. This study provides comprehensive images of IBV attachment-internalization-trafficking-fusion steps.IMPORTANCEIBV, the avian coronavirus isolated in 1937, infects chicken and causes economic loss in poultry industry. It has been reported that the entry of IBV requires low pH. However, the molecular mechanisms underlying IBV internalization and trafficking remain to be clarified. Therefore, we employed multiple chemical and molecular approaches to dissect the entry mechanisms of IBV in susceptible cells. Our results showed IBV entry was significantly inhibited when clathrin-mediated endocytosis (CME) was blocked by chemical inhibitor or depletion of clathrin protein. Moreover, by using R18-labeled IBV, we found that IBV particles attached to lipid rafts, led to actin rearrangement, and moved along with the entire endosomal system. R18/DiOC labeling method showed that IBV fused with late endosomes or lysosomes. This is the first report to describe the entire entry process of IBV, allowing for a better understanding of the infection process of group III avian coronavirus.

scholarly journals Pathogenicity of the Canadian Delmarva (DMV/1639) Infectious Bronchitis Virus (IBV) on Female Reproductive Tract of Chickens

Viruses ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2488
Author(s):  
Mohamed S. H. Hassan ◽  
Ahmed Ali ◽  
Sabrina M. Buharideen ◽  
Dayna Goldsmith ◽  
Carla S. Coffin ◽  
...  
Keyword(s):  
Infectious Bronchitis Virus ◽  
Reproductive Tract ◽  
Female Reproductive Tract ◽  
Economic Losses ◽  
Poultry Production ◽  
Highly Pathogenic ◽  
Production Sector ◽  
Infectious Bronchitis ◽  
Viral Shedding ◽  
Specific Pathogen

Infectious bronchitis virus (IBV) infection causes significant economic losses to various sectors of the poultry industry worldwide. Over the past few years, the incidence of false layer syndrome in Eastern Canadian layer flocks has been associated with the increased prevalence of the IBV Delmarva (DMV)/1639 strain. In this study, 1-day-old specific-pathogen-free (SPF) hens were infected with the Canadian DMV/1639 strain and observed until 16 weeks of age in order to determine if the IBV DMV/1639 strain is causing false layer syndrome. Early after infection, the virus showed a wide tissue distribution with characteristic gross and histopathological lesions in the respiratory tract and kidney. Around 60–70% of the infected hens demonstrated continuous cloacal viral shedding until the end of the experiment (at 16 weeks) which was associated with high IBV genome loads detected in the cecal tonsils. The experiment confirmed the field observations that the Canadian DMV/1639 strain is highly pathogenic to the female reproductive tract causing marked cystic lesions in the oviduct. Moreover, significant histopathological damage was observed in the ovary. Our study provides a detailed description of the pathological consequences of the IBV DMV/1639 strain circulating in an important poultry production sector.

REDUCED CHICKEN EMBRYO DWARFING EFFECT IS RELATED TO INFECTIOUS BRONCHITIS VIRUS TW2575/98 REPLICATION EFFICIENCY

2020 ◽  
Vol 46 (02n03) ◽  
pp. 85-93
Author(s):  
Cheng-Ta Tsai ◽  
Ming-Chang Lee ◽  
Ching-Ho Wang
Keyword(s):  
Vaccine Strain ◽  
Infectious Bronchitis Virus ◽  
Tissue Tropism ◽  
Renal Tubules ◽  
Pathological Changes ◽  
In Ovo ◽  
Chicken Embryos ◽  
Infectious Bronchitis ◽  
Attenuated Vaccine ◽  
Embryonic Death

An attenuated infectious bronchitis virus (TW2575/98) vaccine strain was successfully developed after 75 serial passages in embryonated chicken eggs. However, the in ovo vaccination for disease control was not applied in practice because this vaccine strain is highly pathogenic to chicken embryos (CEs) causing early death, dwarfing and other harmful effects. We compared the differences in virus replication, pathological changes, and tissue tropism between the wild virus and attenuated vaccine strain in CEs inoculated with different viral titer levels, i.e. 0.1, 1 and 10 EID[Formula: see text]/egg. The wild virus caused dwarfing effect at high titer inoculation, whereas the attenuated vaccine strain caused the dwarfing effect only at a lower viral inoculation accompanied by the earlier infection establishment and embryonic death at high and medium titers. There were no significant differences in the pathological changes in CEs infected by both wild and attenuated strains. Detected by immunohistochemistry, the viral antigens of both strains could be found mainly at the epithelium of the chorioallantoic membrane, lung parabronchus, renal tubules and some in the spleen and heart serosa. These findings indicated that the early embryonic death and dwarfing is not related to the change in cell/tissue tropism of the vaccine strain, rather on the early infection establishment and viral load. We suggest that the vaccine strain inoculated titer could be adjusted to an optimal low level for in ovo vaccination to overcome the poor hatching rate for its higher virulence to chicken embryos.

Sign in / Sign up

Export Citation Format

Share Document