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Published on: January 20, 2017
Chicken anaemia virus evades host immune responses in transformed lymphocytes
Efstathios S Giotis1, Alistair Scott2,3, Lisa Rothwell4,5
1Section of Virology, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK.
Abstract:
Chicken anaemia virus (CAV) is a lymphotropic virus that causes anaemia and immunosuppression in chickens. Previously, we proposed that CAV evades host antiviral responses in vivo by disrupting T-cell signalling, but the precise cellular targets and modes of action remain elusive. In this study, we examined gene expression in Marek's disease virus-transformed chicken T-cell line MSB-1 after infection with CAV using both a custom 5K immune-focused microarray and quantitative real-time PCR at 24, 48 and 72 h post-infection. The data demonstrate an intricate equilibrium between CAV and the host gene expression, displaying subtle but significant modulation of transcripts involved in the T-cell, inflammation and NF-κB signalling cascades. CAV efficiently blocked the induction of type-I interferons and interferon-stimulated genes at 72 h. The cell expression pattern implies that CAV subverts host antiviral responses and that the transformed environment of MSB-1 cells offers an opportunistic advantage for virus growth.
Insights
Chicken anaemia virus (CAV) disrupts T-cell signaling to evade immune responses. This study reveals CAV modulates host gene expression, blocking antiviral defenses in chickens.
Area of Science:
- * Virology
- * Immunology
- * Molecular Biology
Background:
- * Chicken anaemia virus (CAV) causes anemia and immunosuppression in poultry.
- * CAV's mechanism of evading host antiviral responses by disrupting T-cell signaling is not fully understood.
- * Identifying cellular targets and modes of action is crucial for understanding CAV pathogenesis.
Purpose of the Study:
- * To investigate the impact of CAV infection on host gene expression in a chicken T-cell line.
- * To elucidate the intricate molecular interactions between CAV and host antiviral pathways.
- * To understand how CAV subverts host immune responses.
Main Methods:
- * Gene expression analysis in MSB-1 cells (Marek's disease virus-transformed chicken T-cell line) infected with CAV.
- * Utilized a custom 5K immune-focused microarray for broad transcript profiling.
- * Quantitative real-time PCR (qRT-PCR) was employed for specific gene validation at 24, 48, and 72 hours post-infection.
Main Results:
- * CAV infection induced subtle but significant modulation of host gene expression.
- * Transcripts involved in T-cell, inflammation, and NF-κB signaling cascades were affected.
- * CAV effectively inhibited the induction of type-I interferons and interferon-stimulated genes by 72 hours post-infection.
Conclusions:
- * CAV establishes an intricate equilibrium with host gene expression, subverting antiviral responses.
- * The transformed environment of MSB-1 cells provides an advantage for CAV replication.
- * Findings provide insights into CAV's immune evasion strategies and viral pathogenesis.
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