Rinderpest infection series: Difference between revisions
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|species=Human (Homo sapiens) | |species=Human (Homo sapiens) | ||
|zenbu_config=http://fantom.gsc.riken.jp/zenbu/gLyphs/#config=F3ezuq6nIV3kT_N9qJhN2C | |zenbu_config=http://fantom.gsc.riken.jp/zenbu/gLyphs/#config=F3ezuq6nIV3kT_N9qJhN2C | ||
|TCOverview=Morbilliviruses including measles virus and rinderpest virus (RPV) are one of the most important pathogens in their respective hosts. In particular, transient strong immunosuppression is the most characteristic feature. Morbillivirus infection induces cell-type-dependent immune responses. However, the molecular mechanisms have not been elucidated. Morbillivirus possesses two nonstructural accessory proteins, V and C. These proteins have been shown to inhibit interferon induction and signaling, although their full functions are unclear. To resolve the complexity and multidimensionality of virus–host interactions, we established recombinant RPV that lacked V and C proteins, and searched for the cell-type-specific transcriptional regulatory network after infection with the FANTOM5 time course analysis. Our study provides a new insight that an accessory protein is one of the virulence factors that define a cell-type-specific response of morbillivirus. This high-throughput experiment uncovers a novel host response against virus infection, and will be useful for understanding the whole picture of virus pathogenesis.<br> | |||
|TCSample_description=We used two major target cell type for RPV infection, a lymphoid cell line (COBL-a cells) and an epithelial cell line (HEK293 cells stably expressing receptor SLAM; 293SLAM cells) [1]. In addition, we established a reverse genetics for RPV-L strain, which is highly virulent against rabbit [2,3], and succeeded in generating recombinant RPV lacking C protein. Cells were infected with each RPV at a multiplicity of infection of 2, and were harvested at 6, 12, 24 and 48 h post infection. Three biological triplicates were performed.<br> | |||
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References:<br> | |||
[1] Measles virus induces cell-type specific changes in gene expression. Sato H1, Honma R, Yoneda M, Miura R, Tsukiyama-Kohara K, Ikeda F, Seki T, Watanabe S, Kai C. Virology. 2008 Jun 5;375(2):321-30. PMID:18374960<br> | |||
[2] Rinderpest virus H protein: role in determining host range in rabbits. Yoneda M, Bandyopadhyay SK, Shiotani M, Fujita K, Nuntaprasert A, Miura R, Baron MD, Barrett T, Kai C. J Gen Virol. 2002 Jun;83(Pt 6):1457-63. PMID:12029161<br> | |||
[3] Rinderpest virus phosphoprotein gene is a major determinant of species-specific pathogenicity. Yoneda M, Miura R, Barrett T, Tsukiyama-Kohara K, Kai C. J Virol. 2004 Jun;78(12):6676-81. PMID:15163758<br> | |||
|TCQuality_control=No marker genes are established yet. Infection, replication and growth of virus were verified by cytopathic effect of cells (formation of multinuclear giant cells). | |||
}} | }} |
Revision as of 19:38, 10 December 2014
Series: | IN_VITRO DIFFERENTIATION SERIES |
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Species: | Human (Homo sapiens) |
Genomic View: | Zenbu |
Expression table: | [{{{tet_config}}} FILE] |
Link to TET: | [{{{tet_file}}} TET] |
Sample providers : | Michiko Kai |
Germ layer: | {{{germ_layer}}} |
Primary cells or cell line: | {{{primary_cells}}} |
Time span: | {{{time_span}}} |
Number of time points: | {{{number_time_points}}} |
Overview |
---|
Morbilliviruses including measles virus and rinderpest virus (RPV) are one of the most important pathogens in their respective hosts. In particular, transient strong immunosuppression is the most characteristic feature. Morbillivirus infection induces cell-type-dependent immune responses. However, the molecular mechanisms have not been elucidated. Morbillivirus possesses two nonstructural accessory proteins, V and C. These proteins have been shown to inhibit interferon induction and signaling, although their full functions are unclear. To resolve the complexity and multidimensionality of virus–host interactions, we established recombinant RPV that lacked V and C proteins, and searched for the cell-type-specific transcriptional regulatory network after infection with the FANTOM5 time course analysis. Our study provides a new insight that an accessory protein is one of the virulence factors that define a cell-type-specific response of morbillivirus. This high-throughput experiment uncovers a novel host response against virus infection, and will be useful for understanding the whole picture of virus pathogenesis. |
Sample description |
---|
We used two major target cell type for RPV infection, a lymphoid cell line (COBL-a cells) and an epithelial cell line (HEK293 cells stably expressing receptor SLAM; 293SLAM cells) [1]. In addition, we established a reverse genetics for RPV-L strain, which is highly virulent against rabbit [2,3], and succeeded in generating recombinant RPV lacking C protein. Cells were infected with each RPV at a multiplicity of infection of 2, and were harvested at 6, 12, 24 and 48 h post infection. Three biological triplicates were performed. |
Quality control |
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No marker genes are established yet. Infection, replication and growth of virus were verified by cytopathic effect of cells (formation of multinuclear giant cells). |
Profiled time course samples
Only samples that passed quality controls (Arner et al. 2015) are shown here. The entire set of samples are downloadable from FANTOM5 human / mouse samples
13541-145H4 | 293SLAM rinderpest infection | 00hr | biol_rep1 |
13542-145H5 | 293SLAM rinderpest infection | 00hr | biol_rep2 |
13543-145H6 | 293SLAM rinderpest infection | 00hr | biol_rep3 |
13544-145H7 | 293SLAM rinderpest infection | 06hr | biol_rep1 |
13545-145H8 | 293SLAM rinderpest infection | 06hr | biol_rep2 |
13546-145H9 | 293SLAM rinderpest infection | 06hr | biol_rep3 |
13547-145I1 | 293SLAM rinderpest infection | 12hr | biol_rep1 |
13548-145I2 | 293SLAM rinderpest infection | 12hr | biol_rep2 |
13549-145I3 | 293SLAM rinderpest infection | 12hr | biol_rep3 |
13550-145I4 | 293SLAM rinderpest infection | 24hr | biol_rep1 |
13551-145I5 | 293SLAM rinderpest infection | 24hr | biol_rep2 |
13552-145I6 | 293SLAM rinderpest infection | 24hr | biol_rep3 |
13553-145I7 | COBL-a rinderpest infection | 00hr | biol_rep1 |
13554-145I8 | COBL-a rinderpest infection | 00hr | biol_rep2 |
13555-145I9 | COBL-a rinderpest infection | 00hr | biol_rep3 |
13556-146A1 | COBL-a rinderpest infection | 06hr | biol_rep1 |
13557-146A2 | COBL-a rinderpest infection | 06hr | biol_rep2 |
13558-146A3 | COBL-a rinderpest infection | 06hr | biol_rep3 |
13559-146A4 | COBL-a rinderpest infection | 12hr | biol_rep1 |
13560-146A5 | COBL-a rinderpest infection | 12hr | biol_rep2 |
13561-146A6 | COBL-a rinderpest infection | 12hr | biol_rep3 |
13562-146A7 | COBL-a rinderpest infection | 24hr | biol_rep1 |
13563-146A8 | COBL-a rinderpest infection | 24hr | biol_rep2 |
13564-146A9 | COBL-a rinderpest infection | 24hr | biol_rep3 |
13565-146B1 | COBL-a rinderpest infection | 48hr | biol_rep1 |
13566-146B2 | COBL-a rinderpest infection | 48hr | biol_rep2 |
13567-146B3 | COBL-a rinderpest infection | 48hr | biol_rep3 |
13568-146B4 | COBL-a rinderpest(-C) infection | 06hr | biol_rep1 |
13569-146B5 | COBL-a rinderpest(-C) infection | 06hr | biol_rep2 |
13570-146B6 | COBL-a rinderpest(-C) infection | 06hr | biol_rep3 |
13571-146B7 | COBL-a rinderpest(-C) infection | 12hr | biol_rep1 |
13572-146B8 | COBL-a rinderpest(-C) infection | 12hr | biol_rep2 |
13573-146B9 | COBL-a rinderpest(-C) infection | 12hr | biol_rep3 |
13574-146C1 | COBL-a rinderpest(-C) infection | 24hr | biol_rep1 |
13575-146C2 | COBL-a rinderpest(-C) infection | 24hr | biol_rep2 |
13576-146C3 | COBL-a rinderpest(-C) infection | 24hr | biol_rep3 |
13577-146C4 | COBL-a rinderpest(-C) infection | 48hr | biol_rep1 |
13578-146C5 | COBL-a rinderpest(-C) infection | 48hr | biol_rep2 |
13579-146C6 | COBL-a rinderpest(-C) infection | 48hr | biol_rep3 |