scholarly journals A Multi-Omics Study of Chicken Infected by Nephropathogenic Infectious Bronchitis Virus

Viruses ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 1070 ◽  
Author(s):  
Puzhi Xu ◽  
Ping Liu ◽  
Changming Zhou ◽  
Yan Shi ◽  
Qingpeng Wu ◽  
...  

Chicken gout resulting from nephropathogenic infectious bronchitis virus (NIBV) has become a serious kidney disease problem in chicken worldwide with alterations of the metabolic phenotypes in multiple metabolic pathways. To investigate the mechanisms in chicken responding to NIBV infection, we examined the global transcriptomic and metabolomic profiles of the chicken’s kidney using RNA-seq and GC–TOF/MS, respectively. Furthermore, we analyzed the alterations in cecal microorganism composition in chickens using 16S rRNA-seq. Integrated analysis of these three phenotypic datasets further managed to create correlations between the altered kidney transcriptomes and metabolome, and between kidney metabolome and gut microbiome. We found that 2868 genes and 160 metabolites were deferentially expressed or accumulated in the kidney during NIBV infection processes. These genes and metabolites were linked to NIBV-infection related processes, including immune response, signal transduction, peroxisome, purine, and amino acid metabolism. In addition, the comprehensive correlations between the kidney metabolome and cecal microbial community showed contributions of gut microbiota in the progression of NIBV-infection. Taken together, our research comprehensively describes the host responses during NIBV infection and provides new clues for further dissection of specific gene functions, metabolite affections, and the role of gut microbiota during chicken gout.

2019 ◽  
Vol 50 (1) ◽  
Author(s):  
Giovanni Franzo ◽  
Matteo Legnardi ◽  
Claudia Maria Tucciarone ◽  
Michele Drigo ◽  
Marco Martini ◽  
...  

Abstract Despite the fact that vaccine resistance has been typically considered a rare phenomenon, some episodes of vaccine failure have been reported with increasing frequency in intensively-raised livestock. Infectious bronchitis virus (IBV) is a widespread avian coronavirus, whose control relies mainly on extensive vaccine administration. Unfortunately, the continuous emergence of new vaccine-immunity escaping variants prompts the development of new vaccines. In the present work, a molecular epidemiology study was performed to evaluate the potential role of homologous vaccination in driving IBV evolution. This was undertaken by assessing IBV viral RNA sequences from the ORF encoding the S1 portion of viral surface glycoprotein (S) before and after the introduction of a new live vaccine on broiler farms in northern-Italy. The results of several biostatistics analyses consistently demonstrate the presence of a higher pressure in the post-vaccination period. Natural selection was detected essentially on sites located on the protein surface, within or nearby domains involved in viral attachment or related functions. This evidence strongly supports the action of vaccine-induced immunity in conditioning viral evolution, potentially leading to the emergence of new vaccine-escape variants. The great plasticity of rapidly-evolving RNA-viruses in response to human intervention, which extends beyond the poultry industry, is demonstrated, claiming further attention due to their relevance for animal and especially human health.


2020 ◽  
Vol 101 (6) ◽  
pp. 599-608
Author(s):  
K. M. Bouwman ◽  
N. Habraeken ◽  
A. Laconi ◽  
A. J. Berends ◽  
L. Groenewoud ◽  
...  

Infection of chicken coronavirus infectious bronchitis virus (IBV) is initiated by binding of the viral heavily N-glycosylated attachment protein spike to the alpha-2,3-linked sialic acid receptor Neu5Ac. Previously, we have shown that N-glycosylation of recombinantly expressed receptor binding domain (RBD) of the spike of IBV-M41 is of critical importance for binding to chicken trachea tissue. Here we investigated the role of N-glycosylation of the RBD on receptor specificity and virus replication in the context of the virus particle. Using our reverse genetics system we were able to generate recombinant IBVs for nine-out-of-ten individual N-glycosylation mutants. In vitro growth kinetics of these viruses were comparable to the virus containing the wild-type M41-S1. Furthermore, Neu5Ac binding by the recombinant viruses containing single N-glycosylation site knock-out mutations matched the Neu5Ac binding observed with the recombinant RBDs. Five N-glycosylation mutants lost the ability to bind Neu5Ac and gained binding to a different, yet unknown, sialylated glycan receptor on host cells. These results demonstrate that N-glycosylation of IBV is a determinant for receptor specificity.


Author(s):  
Dilara Kiran ◽  
Randall J. Basaraba

Infection with Mycobacterium tuberculosis (Mtb) leading to tuberculosis (TB) disease continues to be a major global health challenge. Critical barriers, including but not limited to the development of multi-drug resistance, lack of diagnostic assays that detect patients with latent TB, an effective vaccine that prevents Mtb infection, and infectious and non-infectious comorbidities that complicate active TB, continue to hinder progress toward a TB cure. To complement the ongoing development of new antimicrobial drugs, investigators in the field are exploring the value of host-directed therapies (HDTs). This therapeutic strategy targets the host, rather than Mtb, and is intended to augment host responses to infection such that the host is better equipped to prevent or clear infection and resolve chronic inflammation. Metabolic pathways of immune cells have been identified as promising HDT targets as more metabolites and metabolic pathways have shown to play a role in TB pathogenesis and disease progression. Specifically, this review highlights the potential role of lactate as both an immunomodulatory metabolite and a potentially important signaling molecule during the host response to Mtb infection. While long thought to be an inert end product of primarily glucose metabolism, the cancer research field has discovered the importance of lactate in carcinogenesis and resistance to chemotherapeutic drug treatment. Herein, we discuss similarities between the TB granuloma and tumor microenvironments in the context of lactate metabolism and identify key metabolic and signaling pathways that have been shown to play a role in tumor progression but have yet to be explored within the context of TB. Ultimately, lactate metabolism and signaling could be viable HDT targets for TB; however, critical additional research is needed to better understand the role of lactate at the host-pathogen interface during Mtb infection before adopting this HDT strategy.


2020 ◽  
Author(s):  
Hao Li ◽  
Pengfei Cui ◽  
Xue Fu ◽  
Lan Zhang ◽  
Wenjun Yan ◽  
...  

Abstract Background: Avian infectious bronchitis virus (IBV) is a gammacoronavirus that seriously affects the world's poultry industry Long non coding RNAs (lncRNAs), a subset of non coding RNAs greater than 200 nucleotides in length, have been recently recognized as pivotal factors during the pathogenesis of viral infection. However, how lncRNAs in host cul tured cells respond to IBV infection was little known. Herein, we detected the expression profiles of the mRNAs and lncRNAs in IBV infected HD11 cells. Results: By RNA seq, 2640 novel lncRNAs were identified, and 181 lncRNAs (59 up regulated lncRNAs , 122 down regulated lncRNAs) exhibited significant difference in expression levels in IBV infected HD11 cells compared with the uninfected. Based on the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) data bases, the significant diff erentially expressed (DE) lncRNAs, such as MSTRG.25416.43, MSTRG.6458.31, MSTRG.14220.1 and MSTRG.21445.2, were mainly involved in the regulation of cellular innate immunity and amino acid, nucleic acid metabolism. In addition, 30 DE lncRNAs were screened out, and these lncRNAs may interact with gga miR 30d to regulate IBV replication. Conclusions:Our results provided novel insights into the functions of lncRNAs and the possible pathogenic mechanism following IBV infection.


PLoS ONE ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. e0170123 ◽  
Author(s):  
Huichen Guo ◽  
Mei Huang ◽  
Quan Yuan ◽  
Yanquan Wei ◽  
Yuan Gao ◽  
...  

Virology ◽  
2021 ◽  
Author(s):  
Shahnas M. Najimudeen ◽  
Catalina Barboza-Solis ◽  
Ahmed Ali ◽  
Sabrina M. Buharideen ◽  
Ishara M. Isham ◽  
...  

2019 ◽  
Vol 20 (2) ◽  
pp. 438 ◽  
Author(s):  
Alejandra Chávez-Carbajal ◽  
Khemlal Nirmalkar ◽  
Ana Pérez-Lizaur ◽  
Fernando Hernández-Quiroz ◽  
Silvia Ramírez-del-Alto ◽  
...  

Obesity is an excessive fat accumulation that could lead to complications like metabolic syndrome. There are reports on gut microbiota and metabolic syndrome in relation to dietary, host genetics, and other environmental factors; however, it is necessary to explore the role of the gut microbiota metabolic pathways in populations like Mexicans, where the prevalence of obesity and metabolic syndrome is high. This study identify alterations of the gut microbiota in a sample of healthy Mexican women (CO), women with obesity (OB), and women with obesity plus metabolic syndrome (OMS). We studied 67 women, characterizing their anthropometric and biochemical parameters along with their gut bacterial diversity by high-throughput DNA sequencing. Our results indicate that in OB or OMS women, Firmicutes was the most abundant bacterial phylum. We observed significant changes in abundances of bacteria belonging to the Ruminococcaceae, Lachnospiraceae, and Erysipelotrichaceae families and significant enrichment of gut bacteria from 16 different taxa that might explain the observed metabolic alterations between the groups. Finally, the predicted functional metagenome of the gut microbiota found in each category shows differences in metabolic pathways related to lipid metabolism. We demonstrate that Mexican women have a particular bacterial gut microbiota characteristic of each phenotype. There are bacteria that potentially explain the observed metabolic differences between the groups, and gut bacteria in OMS and OB conditions carry more genes of metabolic pathways implicated in lipid metabolism.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Xiaolin Zhang ◽  
Xiuli Shao ◽  
Ruijia Zhang ◽  
Rongli Zhu ◽  
Rui Feng

Abstract Background Dilated cardiomyopathy (DCM) is a serious cardiac heterogeneous pathological disease, which may be caused by mutations in the LMNA gene. Lamins interact with not only lamina-associated domains (LADs) but also euchromatin by alone or associates with the lamina-associated polypeptide 2 alpha (LAP2α). Numerous studies have documented that LMNA regulates gene expression by interacting with LADs in heterochromatin. However, the role of LMNA in regulating euchromatin in DCM is poorly understood. Here, we determine the differential binding genes on euchromatin in DCM induced by LMNA mutation by performing an integrated analysis of bioinformatics and explore the possible molecular pathogenesis mechanism. Results Six hundred twenty-three and 4484 differential binding genes were identified by ChIP-seq technology. The ChIP-seq analysis results and matched RNA-Seq transcriptome data were integrated to further validate the differential binding genes of ChIP-seq. Five and 60 candidate genes involved in a series of downstream analysis were identified. Finally, 4 key genes (CREBBP, PPP2R2B, BMP4, and BMP7) were harvested, and these genes may regulate LMNA mutation-induced DCM through WNT/β-catenin or TGFβ-BMP pathways. Conclusions We identified four key genes that may serve as potential biomarkers and novel therapeutic targets. Our study also illuminates the possible molecular pathogenesis mechanism that the abnormal binding between LMNA or LAP2α-lamin A/C complexes and euchromatin DNA in LMNA mutations, which may cause DCM through the changes of CREBBP, PPP2R2B, BMP4, BMP7 expressions, and the dysregulation of WNT/β-catenin or TGFβ-BMP pathways, providing valuable insights to improve the occurrence and development of DCM. Graphic abstract


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