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Genome-wide analysis of interferon-stimulated genes in primary cells and immortalized cell lines

ABSTRACT: Analysis of interferon-stimulated genes (ISGs) in various primary cells and immortalized cell lines, following type 1 interferon (IFN) treatment. Some cell types become resistant to HIV-1 infection following type 1 interferon treatment (such as macrophages, THP-1, PMA-THP-1, U87-MG cells and to a lesser extent, primary CD4+ T cells) while others either become only partially resistant (e.g., HT1080, PMA-U937) or remain permissive (e.g., CEM, CEM-SS, Jurkat T cell lines and U937); for more information see (Goujon and Malim, Journal of Virology 2010) and (Goujon and Schaller et al., Retrovirology 2013). We hypothesized that the anti-HIV-1 ISGs are differentially induced and expressed in restrictive cells compared to permissive cells and performed a whole genome analysis following type 1 IFN treatment in cell types exhibiting different HIV-1 resistance phenotypes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE46599 | GEO | 2013/09/13

SECONDARY ACCESSION(S): PRJNA201063

REPOSITORIES: GEO

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Project description:HIV is able to outpace the innate immune response, including the response mediated by interferon (IFN), to establish a productive infection. However, monocyte derived macrophages (MDMs) may be protected from HIV infection by treatment with type I IFN before virus exposure. The ability of HIV to modulate the type I IFN-mediated innate immune response when it encounters a cell that has already been exposed to IFN was investigated. To investigate the presence of HIV on an established IFN response, MDMs were subjected to four different conditions: (1) IFN-treated only, (2) IFN-treated followed by HIV infection, (3) HIV infected only, and (4) a mock-treated and mock-infected control. Microarray gene expression analysis was performed on a total of 24 samples derived from the 4 conditions assessed at 3 time points (1, 4 and 8 days following treatment/infection) for both IFN-α2 or -ω. Initially, ISGs were identified as those that were upregulated greater than 2-fold by IFN alone (condition 1) at both Days 4 and 8. Then, the IFN-treated condition was compared to the IFN-treated followed by HIV-infection condition in order to identify those ISGs that were downregulated at least 1.5-fold by the presence of HIV at both days. Assuming that it would be counterproductive for HIV infection by itself to induce the expression of ISGs with putative anti-HIV effects, those ISGs that were upregulated greater than 2-fold in the HIV control were removed. Finally, ISGs that passed these filters and were concordant with both IFN-treatments (IFN-α2 and -ω) were identified and corresponded to the following 8 ISGs: AXL receptor tyrosine kinase (AXL), interferon-alpha inducible protein 27 (IFI27), interferon-induced protein 44 (IFI44), interferon-induced protein 44-like (IFI44L), ISG15, OAS1, OAS3 and XIAP associated factor 1 (XAF1). It should be noted that the IFN-α2 and -ω microarray experiments were performed in different batches but batch effects were not corrected since genes were identified by the filtering approach just described within each batch.

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Genome-wide analysis of interferon-stimulated genes in primary cells and immortalized cell lines

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