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Transcriptional profiling of the host cell response to feline immunodeficiency virus infection
BACKGROUND: Feline immunodeficiency virus (FIV) is a widespread pathogen of the domestic cat and an important animal model for human immunodeficiency virus (HIV) research. In contrast to HIV, only limited information is available on the transcriptional host cell response to FIV infections. This stud...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999937/ https://www.ncbi.nlm.nih.gov/pubmed/24642186 http://dx.doi.org/10.1186/1743-422X-11-52 |
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author | Ertl, Reinhard Klein, Dieter |
author_facet | Ertl, Reinhard Klein, Dieter |
author_sort | Ertl, Reinhard |
collection | PubMed |
description | BACKGROUND: Feline immunodeficiency virus (FIV) is a widespread pathogen of the domestic cat and an important animal model for human immunodeficiency virus (HIV) research. In contrast to HIV, only limited information is available on the transcriptional host cell response to FIV infections. This study aims to identify FIV-induced gene expression changes in feline T-cells during the early phase of the infection. Illumina RNA-sequencing (RNA-seq) was used identify differentially expressed genes (DEGs) at 24 h after FIV infection. RESULTS: After removal of low-quality reads, the remaining sequencing data were mapped against the cat genome and the numbers of mapping reads were counted for each gene. Regulated genes were identified through the comparison of FIV and mock-infected data sets. After statistical analysis and the removal of genes with insufficient coverage, we detected a total of 69 significantly DEGs (44 up- and 25 down-regulated genes) upon FIV infection. The results obtained by RNA-seq were validated by reverse transcription qPCR analysis for 10 genes. DISCUSSION AND CONCLUSION: Out of the most distinct DEGs identified in this study, several genes are already known to interact with HIV in humans, indicating comparable effects of both viruses on the host cell gene expression and furthermore, highlighting the importance of FIV as a model system for HIV. In addition, a set of new genes not previously linked to virus infections could be identified. The provided list of virus-induced genes may represent useful information for future studies focusing on the molecular mechanisms of virus-host interactions in FIV pathogenesis. |
format | Online Article Text |
id | pubmed-3999937 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-39999372014-04-26 Transcriptional profiling of the host cell response to feline immunodeficiency virus infection Ertl, Reinhard Klein, Dieter Virol J Research BACKGROUND: Feline immunodeficiency virus (FIV) is a widespread pathogen of the domestic cat and an important animal model for human immunodeficiency virus (HIV) research. In contrast to HIV, only limited information is available on the transcriptional host cell response to FIV infections. This study aims to identify FIV-induced gene expression changes in feline T-cells during the early phase of the infection. Illumina RNA-sequencing (RNA-seq) was used identify differentially expressed genes (DEGs) at 24 h after FIV infection. RESULTS: After removal of low-quality reads, the remaining sequencing data were mapped against the cat genome and the numbers of mapping reads were counted for each gene. Regulated genes were identified through the comparison of FIV and mock-infected data sets. After statistical analysis and the removal of genes with insufficient coverage, we detected a total of 69 significantly DEGs (44 up- and 25 down-regulated genes) upon FIV infection. The results obtained by RNA-seq were validated by reverse transcription qPCR analysis for 10 genes. DISCUSSION AND CONCLUSION: Out of the most distinct DEGs identified in this study, several genes are already known to interact with HIV in humans, indicating comparable effects of both viruses on the host cell gene expression and furthermore, highlighting the importance of FIV as a model system for HIV. In addition, a set of new genes not previously linked to virus infections could be identified. The provided list of virus-induced genes may represent useful information for future studies focusing on the molecular mechanisms of virus-host interactions in FIV pathogenesis. BioMed Central 2014-03-19 /pmc/articles/PMC3999937/ /pubmed/24642186 http://dx.doi.org/10.1186/1743-422X-11-52 Text en Copyright © 2014 Ertl and Klein; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Ertl, Reinhard Klein, Dieter Transcriptional profiling of the host cell response to feline immunodeficiency virus infection |
title | Transcriptional profiling of the host cell response to feline immunodeficiency virus infection |
title_full | Transcriptional profiling of the host cell response to feline immunodeficiency virus infection |
title_fullStr | Transcriptional profiling of the host cell response to feline immunodeficiency virus infection |
title_full_unstemmed | Transcriptional profiling of the host cell response to feline immunodeficiency virus infection |
title_short | Transcriptional profiling of the host cell response to feline immunodeficiency virus infection |
title_sort | transcriptional profiling of the host cell response to feline immunodeficiency virus infection |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999937/ https://www.ncbi.nlm.nih.gov/pubmed/24642186 http://dx.doi.org/10.1186/1743-422X-11-52 |
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