Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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FIV host cell response

ABSTRACT: Transcriptional profiling of the host cell response to feline immunodeficiency virus (FIV) infection. Feline T-cells were infected with FIV and virus-induced gene expression changes were investigated at 24 hours post infection.

INSTRUMENT(S): Illumina Genome Analyzer IIx

ORGANISM(S): Felis catus

SUBMITTER: Reinhard Ertl

PROVIDER: E-MTAB-2083 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional profiling of the host cell response to feline immunodeficiency virus infection.

Ertl Reinhard R Klein Dieter D

Virology journal 20140319

<h4>Background</h4>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 ge ...[more]

PMID: 24642186

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Project description:HIV-infected persons are at increased risk for developing pulmonary diseases including chronic obstructive pulmonary disease (COPD), and the fungal opportunistic pathogen, Pneumocystis jirovecii (Pc) has been implicated in the pathogenesis of HIV-related COPD. We previously developed a non-human primate model of HIV-related COPD using simian-human immunodeficiency virus (SHIV) and Pc co-infection in cynomolgus macaques. In the present study we examined gene expression profiles in lung tissue from SHIV/Pc co-infected monkeys with COPD and compared them to SHIV-infected monkeys infected with normal lung function. Microarray technology was used to develop gene profiles, and differential gene expression was determined by a comparative evaluation of competing normalization methods applied to our expression data set followed by validation using quantitative real-time polymerase chain reaction analysis for select genes. Of over 52,000 transcripts representing more than 20,000 genes analyzed, the SHIV/Pc infected macaques with COPD exhibited 243 differentially expressed (DE) genes compared to SHIV-infected monkeys with normal lung function. DE genes fell into a number of functional categories which may be important in COPD development including: inflammation (pulmonary surfactants A2, B, C, D, upregulated; alternative macrophage activation-associated CC chemokine, upregulated), protease/antiprotease balance (cathepsin H, upregulated; alpha-1-chymotrypsin and secretory leukocyte peptidase inhibitor, downregulated), redox balance (glutathione peroxidase 4 and mitochondrial aldehyde dehydrogenase 2, upregulated) and tissue homeostasis (connective tissue growth factor, downregulated; ornithine decarboxylase antizyme, upregulated). These results identify factors and pathways that may be involved in early development of Pneumocystis and SHIV-associated COPD and reveal several novel, potential therapeutic targets. There are totally 11 samples in the experiment. The sample breakdown is as follows: KN14(group 1) is a true control in that the monkey was not infected with simian-human immunodeficiency virus (SHIV) nor was it colonized with Pneumocystis. KN02, KN03, KN07 and KN08 (group 2) are also controls of a sort. They were infected with SHIV but they did not become colonized with Pneumocystis. The remainder (KN01, KN04, KN06, KN11, KN12, KN13) (group3) were both infected with SHIV and colonized with Pneumocystis. The primary interest is in comparing the two SHIV-infected groups (2 and 3)

Project description:RNA-Seq was used to unveil the transcriptional profile of DF-1 cells at the early stage of cell-adapted Infectious Bursal Disease Virus (caIBDV) infection. Total RNAs were extracted from virus-infected cells at 0, 6 and 12 hpi. RNA-Seq datasets of respective samples mapped to 56.5 - 57.6% of isoforms in the reference genome Galgal4.73. At 6 hpi, 23 isoforms underwent an elevated expression, while 128 isoforms were up-regulated and 5 were down-regulated at 12 hpi in the virus-infected group. Besides, 10 isoforms were exclusively expressed in the virus-infected cells. Though no significant change was detected in cytokine and interferon expression levels at the first 12 hours of infection, modulations of the upstream regulators were observed. In addition to the reported regulatory factors including EIF2AK2, MX, OAS*A, GBP7 and IFIT, IBDV infection also triggered a IFIT5-IRF1/3-RSAD5 pathway in the DF-1 cells which potentially restricted the viral replication cycle in the early infection stage. Over-expression of LIPA and CH25H, together with the suppression of STARD4, LSS and AACS genes implied a modulation of membrane fluidity and lipid raft arrangement in the infected cells. Alternative splicing of the EFR3 homolog A gene was also through to be involved in the lipid membrane regulation, and these cumulative responses projected an inhibition of viral endocytosis. Recognition of viral RNA genomes and intermediates was presumably enhanced by the elevated levels of IFIH1, DHX58 and TRIM25 genes which possess properties on detecting viral dsRNA. On the other hand, the caIBDV arrested the host's apoptotic process by inducing the expression of apoptosis inhibitors including NFKBIA/Z, TNFAIP2/3 and ITA at the first 12 hours of infection. In conclusion, the differential expression landscape demonstrated with RNA-Seq provides a comprehensive picture on the molecular interactions between host cells and virus at the early stage of infection. Two sample groups (infected and mock-infected) at three time points (0, 6, 12 hpi) were analysed.

Dataset Information

FIV host cell response

Publications

Transcriptional profiling of the host cell response to feline immunodeficiency virus infection.

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