Genome wide host gene expression analysis in chicken lungs infected with avian influenza viruses

Ranaware, P.B.; Mishra, Anamika; Vijayakumar, P.; Gandhale, Pradeep N.; Sudhakar, Shashi Bhushan; Kumar, Himanshu; Kulkarni, D. D.; Raut, Ashwin Ashok

doi:10.1016/j.ijid.2016.02.218

Cited by 5 publications

(6 citation statements)

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“…IL8L1 and IL8L2, CCL5 and SCYA4 vary with the subtype of AIV and infective dose. Although expression of XLC1, CCLi10 and CCL19 is upregulated in H5N1 or H9N2 infection in chickens or ducks (39)(40)(41), expression of XCL1, CCLi10 and CCL19 was not detected in DF-1 cells infected with H5N1 and H9N2 AIVs. This may be because the complexity of the organism is far greater than that of a single cell type, and the host's immune system may be involved.…”

Section: Discussionmentioning

confidence: 88%

Dynamic analysis of expression of chemokine and cytokine gene responses to H5N1 and H9N2 avian influenza viruses in DF‐1 cells

Luo

Liu

et al. 2018

Microbiology and Immunology

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H5N1 and H9N2 are the most important causes of avian influenza in China. Chemokines and cytokines play important roles in inflammatory response that clearly differ between H5N1 and H9N2 infection. To investigate whether chemokines and cytokines are differentially regulated following H5N1 and H9N2 AIVs infection, dynamic expression of chemokines and cytokines, including IL8L1, IL8L2, CX3CL1, CCL5, CCL20, K203, SCYA4, XLC1, CCLi10, CCL19, IFN-α, IFN-β, IL-1β, IL-6 and TNF-α, were analyzed by real-time quantitative RT-PCR in DF-1 cells. It was found that IL8L1, IL8L2, CX3CL1, CCL5, CCL20, K203, SCYA4, IFN-α, IFN-β, IL-1β, IL-6 and TNF-α increased significantly after induction of H5N1 or H9N2 AIV infection, whereas no expression of XCL1, CCLi10 or CCL19 was detected. H9N2 AIV infection was associated with much stronger chemokine responses than infection with H5N1, whereas the cytokines showed opposite results. It was found that K203 is a constant chemotactic factor independent of subtype of AIVs and infectious dose, CCL20 and IL-1β are constant regardless of the infectious dose but depend on the subtype of AIV, chemotactic factors IL8L1, IL8L2 and CCL5 are dependent both on subtype of AIVs and infectious dose, and K203, CX3CL1, SCYA4, CCL20, IFN-α, IL-1β and TNF-α are specific to responses to H5N1 AIV infection whereas K203, CCL20, IFN-β, IL-1β and IL-6 are specific to H9N2 infection. These results provide basic data for explaining differences in inflammation and phenotypes of histopathological changes caused by H5N1 and H9N2 and add new information on the roles of chemokines and cytokines in virulence of AIVs.

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Section: Discussionmentioning

confidence: 88%

Dynamic analysis of expression of chemokine and cytokine gene responses to H5N1 and H9N2 avian influenza viruses in DF‐1 cells

Luo

Liu

et al. 2018

Microbiology and Immunology

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“…This RNase L-dependent pathway is best characterized; however, recent studies have described OAS antiviral activity through a RNase L-independent pathway 35,36 . In chickens, OAS has been shown to be encoded by only one gene (OASL) 37 and to be upregulated after infection with different viruses 38,39 including NDV 3,4,21 . The role of OASL in the control of NDV replication was confirmed in vitro 8 , as the overexpression of OASL reduced the replication of NDV and the absence of OASL significantly enhanced viral replication.…”

Section: Discussionmentioning

confidence: 99%

Genetic responses of inbred chicken lines illustrate importance of eIF2 family and immune-related genes in resistance to Newcastle disease virus

Vesco

Kaiser

Monson

et al. 2020

Sci Rep

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newcastle disease virus (nDV) replication depends on the translation machinery of the host cell; therefore, the eukaryotic translation initiation factor 2 (eIF2) gene family is a likely candidate for control of viral replication. We hypothesized that differential expression of host genes related to translation and innate immune response could contribute to differential resistance to NDV in inbred Fayoumi and Leghorn lines. The expression of twenty-one genes related to the interferon signaling pathway and the eIF2 family was evaluated at two-and six-days post infection (dpi) in the spleen from both lines, either challenged by NDV or nonchallenged. Higher expression of OASL in nDV challenged versus nonchallenged spleen was observed in Leghorns at 2 dpi. Lower expression of EIF2B5 was found in nDV challenged than nonchallenged Fayoumis and Leghorns at 2 dpi. At 2 dpi, NDV challenged Fayoumis had lower expression of EIF2B5 and EIF2S3 than NDV challenged Leghorns. At 6 dpi, NDV challenged Fayoumis had lower expression of EIF2S3 and EIF2B4 than NDV challenged Leghorns. The genetic line differences in expression of eIF2-related genes may contribute to their differential resistance to NDV and also to understanding the interaction between protein synthesis shut-off and virus control in chickens.Newcastle disease virus (NDV) outbreaks have been reported in several countries in the last few decades and continue to cause economic losses around the world 1 . Newcastle disease virus can cause different symptoms depending on strain pathogenicity, concurrent diseases, avian species, and genetic resistance to the pathogen. Symptoms of NDV range from morbidity and respiratory signs associated with lentogenic strains to high mortality caused by velogenic strains 2 . Birds infected with NDV exhibit increased expression of cytokines 3 and genes related to antiviral action of interferons (IFNs) and chemokines 4 .As an sRNA virus belonging to the Paramyxoviridae family, NDV produces a double-stranded molecule (dsRNA) during its replication process 5 . To contain the virus and prevent it from spreading, type I interferons bind to their receptors and signal to downstream molecules to stimulate the transcription of several interferon-stimulated genes (ISGs) 6 . In chickens, some of the ISGs are 2′-5′-oligoadenylate synthetase (OAS) and protein kinase R (PKR). These ISGs act at different stages of the viral replication cycle and can be upregulated by NDV infection 7,8 ; OAS turns on degradation of viral RNA, and PKR acts to contain viral replication 9 .Newcastle disease virus replication depends on the translation machinery of the host cell and thus it is subject to the control mechanisms modulated by host translation factors 10 . The first stage of protein translation is the most regulated phase and eukaryotic initiation factor (eIF) family genes play important roles in this regulation 11 . Eukaryotic initiation factor 2 (eIF2) is a protein complex with three subunits, eIF2α, eIF2β and eIF2γ 12 encoded by EIFS1, EIFS2 and EIFS3 genes, res...

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“…Hu et al (2015) studied immune response of primary chicken lung cells infected with two HPAI H5N1 viruses using microarray technology (Hu et al, 2015). Ranaware et al (2016) studied global immune response of chicken infected with HPAI H5N1 (A/duck/India/02CA10/2011) virus infection (Ranaware et al, 2016). The microarray datasets were analysed in GEO2R online tool of the NCBI (http://www.ncbi.nlm.nih.gov/geo/geo2r/).…”

Section: Methodsmentioning

confidence: 99%

“…Bayesian networks were reconstructed for TLR, RLR, IL1R, NLR and JAK-STAT signaling pathways using ‘bnlearn’ package (Scutari, 2017). The networks were constructed based on intensity values of microarray dataset of our pervious published work (Ranaware et al, 2016). Bayesian network structure was learned from transcriptomic dataset with prior knowledge using Hill Climbing (HC) algorithm.…”

Section: Methodsmentioning

confidence: 99%

Proteomics Analysis of Differential Expression of Lung Proteins in Response to Highly Pathogenic Avian Influenza Virus Infection in Chicken

Vijayakumar

Raut

Chingtham

et al. 2019

Preprint

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12Elucidation of molecular pathogenesis underlying virus-host interaction is important for the 13 development of new diagnostic and therapeutic strategies against highly pathogenic avian 14 influenza (HPAI) infection in chicken. However, chicken HPAI viral pathogenesis is not 15 completely understood. To elucidate the intracellular signaling pathways and critical host 16 proteins associated with influenza pathogenesis, we characterized the lung proteome of 17 chicken infected with HPAI H5N1 virus (A/duck/India/02CA10/2011/Agartala). The chicken 18 mass spectra data sets comprised1, 47, 451 MS scans and 19, 917 MS/MS scans. At local 19 FDR 5% level, we identified total 3313 chicken proteins with presence of at least one unique 20 peptide. At 12 hrs, 247 proteins are downregulated while 1754 proteins are downregulated at 21 48 hrs indicating that the host has succumbed to infection. There is expression of proteins of 22 the predominant signaling pathways, such as TLR, RLR, NLR and JAK-STAT signaling.23Activation of these pathways is associated with cytokine storm effect and thus may be the 24 cause of severity of HPAI H5N1 infection in chicken. Further we identified proteins like 25 MyD88, IKBKB, IRAK4, RELA, and MAVS involved in the critical signaling pathways and 26 2 some other novel proteins(HNF4A, ELAVL1, FN1, COPS5, CUL1, BRCA1 and FYN) as 27 main hub proteins that might play important roles in influenza pathogenesis in chicken. 28Taken together, we characterized the signaling pathways and the proteomic determinants 29 responsible for disease pathogenesis in chicken infected with HPAI H5N1 virus. 30

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Genome wide host gene expression analysis in chicken lungs infected with avian influenza viruses

Cited by 5 publications

References 0 publications

Dynamic analysis of expression of chemokine and cytokine gene responses to H5N1 and H9N2 avian influenza viruses in DF‐1 cells

Dynamic analysis of expression of chemokine and cytokine gene responses to H5N1 and H9N2 avian influenza viruses in DF‐1 cells

Genetic responses of inbred chicken lines illustrate importance of eIF2 family and immune-related genes in resistance to Newcastle disease virus

Proteomics Analysis of Differential Expression of Lung Proteins in Response to Highly Pathogenic Avian Influenza Virus Infection in Chicken

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