Abstract:Rotavirus G (RVG) strains have been detected in a variety of avian species, but RVG genomes have been published from only a single pigeon and two chicken strains. Two turkey RVG strains were identified and characterized, one in a hatchery with no reported health issues and the other in a hatchery with high embryo/poult mortality. The two turkey RVG strains shared only an 85.3 % nucleotide sequence identity in the VP7 gene while the other genes possessed high nucleotide identity among them (96.3–99.9 %). Low nu… Show more
“…Segment 7, encoding the NSP3 protein, was most closely related to the MK204407.1 Grey teal partial NSP3 protein (only 152 amino acids given) from Australia in the year 2017 5 with 64.9% identity. The complete NSP3 protein of the PBDRVG/PBD08.18 was most identical but still distant to KY689682.1 Turkey rotavirus G from the US in the year 2016 17 with 44.3% identity only. It should also be noted that the NSP4 protein was not generated from the Grey teal sample from Australia 5 and hence was not available for comparison.…”
Section: Resultsmentioning
confidence: 93%
“…S3 of Supplementary Material 2 ), it is clear that the rotavirus G forms two different clades. Clade A includes the rotavirus G from chicken 18 , turkey 17 , avocet 19 and pigeon while Clade B includes the rotavirus G from the Pacific black duck, Grey teal 5 and Ruddy turnstone 19 . Figure 4 Phylogenetic analysis of the amino acid sequences of the VP6 protein of Pacific black duck rotavirus G segment S6 (PBDRVG/PBD08.18).…”
Section: Resultsmentioning
confidence: 99%
“…Clade B includes the rotavirus G from the Pacific black duck, Grey teal 5 and Ruddy turnstone 19 (all three viruses from Australia). In contrast, clade A includes the rotavirus G from chicken 18 , turkey 17 , avocet 19 (from Australia) and pigeon (unpublished). The most diverse segments of PBDRVG/PBD08.18 were S3 (VP4 protein), S9 (VP7 protein) and S10 (NSP4 protein).…”
Birds, notably wild ducks, are reservoirs of pathogenic and zoonotic viruses such as influenza viruses and coronaviruses. In the current study, we used metagenomics to detect and characterise avian DNA and RNA viruses from wild Pacific black ducks, Chestnut teals and Grey teals collected at different time points from a single location. We characterised a likely new species of duck aviadenovirus and a novel duck gyrovirus. We also report what, to the best of our knowledge, is the first finding of an avian orthoreovirus from Pacific black ducks and a rotavirus F from Chestnut teals. Other viruses characterised from the samples from these wild ducks belong to the virus families Astroviridae, Caliciviridae and Coronaviridae. Some of the viruses may have potential cross-species transmissibility, while others indicated a wide genetic diversity of duck viruses within a genus. The study also showed evidence of potential transmission of viruses along the East Asian—Australasian Flyway; potentially facilitated by migrating shorebirds. The detection and characterisation of several avian viruses not previously described, and causing asymptomatic but potentially also symptomatic infections suggest the need for more virus surveillance studies for pathogenic and potential zoonotic viruses in wildlife reservoirs.
“…Segment 7, encoding the NSP3 protein, was most closely related to the MK204407.1 Grey teal partial NSP3 protein (only 152 amino acids given) from Australia in the year 2017 5 with 64.9% identity. The complete NSP3 protein of the PBDRVG/PBD08.18 was most identical but still distant to KY689682.1 Turkey rotavirus G from the US in the year 2016 17 with 44.3% identity only. It should also be noted that the NSP4 protein was not generated from the Grey teal sample from Australia 5 and hence was not available for comparison.…”
Section: Resultsmentioning
confidence: 93%
“…S3 of Supplementary Material 2 ), it is clear that the rotavirus G forms two different clades. Clade A includes the rotavirus G from chicken 18 , turkey 17 , avocet 19 and pigeon while Clade B includes the rotavirus G from the Pacific black duck, Grey teal 5 and Ruddy turnstone 19 . Figure 4 Phylogenetic analysis of the amino acid sequences of the VP6 protein of Pacific black duck rotavirus G segment S6 (PBDRVG/PBD08.18).…”
Section: Resultsmentioning
confidence: 99%
“…Clade B includes the rotavirus G from the Pacific black duck, Grey teal 5 and Ruddy turnstone 19 (all three viruses from Australia). In contrast, clade A includes the rotavirus G from chicken 18 , turkey 17 , avocet 19 (from Australia) and pigeon (unpublished). The most diverse segments of PBDRVG/PBD08.18 were S3 (VP4 protein), S9 (VP7 protein) and S10 (NSP4 protein).…”
Birds, notably wild ducks, are reservoirs of pathogenic and zoonotic viruses such as influenza viruses and coronaviruses. In the current study, we used metagenomics to detect and characterise avian DNA and RNA viruses from wild Pacific black ducks, Chestnut teals and Grey teals collected at different time points from a single location. We characterised a likely new species of duck aviadenovirus and a novel duck gyrovirus. We also report what, to the best of our knowledge, is the first finding of an avian orthoreovirus from Pacific black ducks and a rotavirus F from Chestnut teals. Other viruses characterised from the samples from these wild ducks belong to the virus families Astroviridae, Caliciviridae and Coronaviridae. Some of the viruses may have potential cross-species transmissibility, while others indicated a wide genetic diversity of duck viruses within a genus. The study also showed evidence of potential transmission of viruses along the East Asian—Australasian Flyway; potentially facilitated by migrating shorebirds. The detection and characterisation of several avian viruses not previously described, and causing asymptomatic but potentially also symptomatic infections suggest the need for more virus surveillance studies for pathogenic and potential zoonotic viruses in wildlife reservoirs.
“…The detailed luxS gene sequences of the reference strains were listed in Supplementary Data . Multiple sequence alignments were performed by the maximum likelihood algorithm method (bootstrap analysis with 1,000 replicates) with MEGA Version 6.06 (Chen et al, 2017 ).…”
Haemophilus parasuis (H. parasuis) is a kind of opportunistic pathogen of the upper respiratory tract of piglets. Under certain circumstances, virulent strains can breach the mucosal barrier and enter the bloodstream, causing severe Glässer's disease. Many virulence factors are found to be related to the pathogenicity of H. parasuis strain, but the pathogenic mechanism remains unclear. LuxS/AI-2, as a kind of very important quorum sensing system, affects the growth characteristics, biofilm formation, antibiotic production, virulence, and metabolism of different strains. In order to investigate the effect of luxS/AI-2 quorum sensing system on the virulence of H. parasuis, a deletion mutant strain (ΔluxS) and complemented strain (C-luxS) were constructed and characterized. The results showed that the luxS gene participated in regulating and controlling stress resistance, biofilm formation and virulence. Compared with wild-type strain, ΔluxS strain decreased the production of AI-2 molecules and the tolerance toward oxidative stress and heat shock, and it reduced the abilities of autoagglutination, hemagglutination, and adherence, whereas it increased the abilities to form biofilm in vitro. In vivo experiments showed that ΔluxS strain attenuated its virulence about 10-folds and significantly decreased its tissue burden of bacteria in mice, compared with the wild-type strain. Taken together, the luxS/AI-2 quorum sensing system in H. parasuis not only plays an important role in growth and biofilm formation, but also affects the pathogenicity of H. parasuis.
“…RVs are nonenveloped double-strand RNA (dsRNA) viruses. RVs are classified into ten antigentically and genetically distinct groups from A-J, designed as RVA, RVB, RVC, RVD, RVE, RVF, RVG, RVH, RVI and RVJ respectively [5][6][7]. RVAs were thought to be the most prevalent and pathogenic among the ten groups [8]; however, recent data has demonstrated increased prevalence and pathogenicity of RVB, RVC and RVH in humans and pigs [9][10][11].…”
Rotaviruses (RVs) are a leading cause of acute viral gastroenteritis in young children and livestock worldwide. Growing evidence suggests that host cellular glycans, such as histo-blood group antigens (HBGAs) and sialic acids (SA), are recognized by the RV surface protein VP4. However, a mechanistic understanding of these interactions and their effects on RV infection and pathogenesis is lacking. Here, we established a porcine crypt-derived 3D intestinal enteroids (PIEs) culture system which contains all intestinal epithelial cells identified in vivo and represents a unique physiologically functional model to study RV-glycan interactions in vitro. PIEs expressing different HBGAs (A+, H+, and A+/H+) were established and isolation, propagation, differentiation and RV infection conditions were optimized. Differentiated PIEs were infected with human RV (HRV) G1P[8] Wa, porcine RV (PRV) G9P[13], PRV Gottfried G4P[6] or PRV OSU G5P[7] virulent and attenuated strains and virus replication was measured by qRT-PCR. Our results indicated that virulent HRV G1P[8] Wa replicated to the highest titers in A+ PIEs, while a distinct trend was observed for PRV G9P[13] or G5P[7] with highest titers in H+ PIEs. Attenuated Wa and Gottfried strains replicated poorly in PIEs while the replication of attenuated G9P[13] and OSU strains in PIEs was relatively efficient. However, the replication of all 4 attenuate strains was less affected by the PIE HBGA phenotypes. HBGA synthesis inhibitor 2-F-Peracetyl-Fucose (2F) treatment demonstrated that HBGAs are essential for G1P[8] Wa replication; however, they may only serve as a cofactor for PRVs G9P[13] and OSU G5P[7]. Interestingly, contrasting outcomes were observed following sialidase treatment which significantly enhanced G9P[13] replication, but inhibited the growth of G5P[7]. These observations suggest that some additional receptors recognized by G9P[13] become unmasked after removal of terminal SA. Overall, our results confirm that differential HBGAs-RV and SA-RV interactions determine replication efficacy of virulent group A RVs in PIEs. Consequently, targeting individual glycans for development of therapeutics may not yield uniform results for various RV strains.
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