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MX1 is Silenced in Permissive HRP4 Cells Supporting HCV Replication

ABSTRACT: MX1 is a well-characterized interferon-induced antiviral gene. MX1 is activated by viral infection due to interferon production in cells. We treated non-permissive Huh7 cells and permissive HRP4 cells with interferon. We compared the expression of genes induced by interferon to determine host factors affecting HCV replication.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31903 | GEO | 2013/07/03

SECONDARY ACCESSION(S): PRJNA155073

REPOSITORIES: GEO

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MX1 is Silenced in Permissive HRP4 Cells Supporting HCV Replication

Project description:MX1 is a well-characterized interferon-induced antiviral gene. MX1 is activated by viral infection due to interferon production in cells. We treated non-permissive Huh7 cells and permissive HRP4 cells with interferon. We compared the expression of genes induced by interferon to determine host factors affecting HCV replication. Huh7 cells and HRP4 cells were treated with 40U/ml interferon-Î± for 6h. RNA was extracted and hybridized on Affymetrix microarrays

2013-07-03 | E-GEOD-31903 | biostudies-arrayexpress

Host Factors with Reduced Expression in Two HCV Permissive Cell Lines as Compared to the Non-Permissive Parent Cell Line Huh7

Project description:Drugs directly targeting Hepatitis C (HCV) are often rendered useless by the high mutation rate of the virus. Thus, we deduce that targeting of host factor that affect HCV replication may provide enhanced therapy fort HCV infection. Hepatocyte cell line Huh7 is known to be non-permissive for Hepatits C (HCV) replication. Through a method developed by the Rice laboratory (Blight, K.J., et al., J Virol, 2002), selection of a small subset of permissive hepatocytes is possible. The Rice laboratory generated the first permissive cell line, Huh7.5, using this method. We generated another permissive cell line, HRP1, using the same method. With microarray, we compared the expression of host mRNAs in non-permissive Huh7 to both Huh7.5 and HRP1 searching for host factors lost in the cell lines permisive for HCV replication. Non-permissive cell line Huh7 and permissive cell lines Huh7.5 and HRP1 were harvested for RNA extraction and hybridization on Affymetrix microarrays.

2011-05-01 | E-GEOD-25156 | biostudies-arrayexpress

Host Factors with Reduced Expression in Two HCV Permissive Cell Lines as Compared to the Non-Permissive Parent Cell Line Huh7

2011-05-01 | GSE25156 | GEO

Huh7 cells exist as a mixed population of cells with distinct patterns of gene methylation

Project description:A powerful approach to study innate antiviral response is to compare the difference between wild type Huh7 cells, which do not support robust replication of hepatitis C virus (HCV)2, versus certain subclones of Huh7 cells that are permissive for HCV replication. We generated two permissive cell lines and two independent non-permissive subclone from Huh7 cells. We compared the global methylation pattern of these different cells and find that Huh7 cells exist as a heterogeneous population of cells with distinct patterns of gene methylation. Comparison of Huh7, HRP1, HRP4, Huh7-pNeo1 and Huh7-pNeo2 cells.

2013-07-03 | E-GEOD-31960 | biostudies-arrayexpress

Huh7 cells exist as a mixed population of cells with distinct patterns of gene methylation

2013-07-03 | GSE31960 | GEO

Expression data from HCV infected hepatoma carcinoma cell line Huh7-MAVSR cells

Project description:Hepatitis C virus (HCV) infection is a major cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. HCV can be sensed by host innate immunity to induce expression of interferons (IFNs) and a number of antiviral effectors. HCV-encoded NS3/4 serine protease can subvert host innate immune responses by cleaving MAVS, a critical adaptor protein in the RLR-mediated IFN signaling. To study innate immunity in the context of HCV infection, we constructed Huh7-MAVSR cells which express a mutant MAVS resistant to NS3/4A cleavage. HCV infection induces robust IFN response in Huh7-MAVSR cells, providing a cellular system to study antiviral innate immune response against HCV infection. To analyze host innate antiviral effectors against HCV infection, we performed an mRNA microarray analysis in the HCV-infected Huh7-MAVSR cells.

2018-02-08 | GSE110312 | GEO

Molecular signatures associated with Mx1-mediated resistance to highly pathogenic influenza virus infection: mechanisms of survival

2012-02-20 | GSE35933 | GEO

Molecular signatures associated with Mx1-mediated resistance to highly pathogenic influenza virus infection: mechanisms of survival

Project description:Understanding the role of host factors during lethal influenza virus infection is critical to deciphering the events that will determine the fate of the host. One such factor is encoded by the Mx1 gene, which confers resistance to influenza virus infection. Here, we compared pathology and global gene expression profiles in lung tissue from BALB/c (Mx1(-)) and BALB•A2G-Mx1 mice (Mx1(+/+)) infected with the fully reconstructed 1918 pandemic influenza virus with an without interferon-alpha pretreatment. Mx1(+/+) mice showed less tissue damage than Mx(-) animals, and pathology and mortality were further reduced by treating the mice with interferon prior to infection. The goal of the global transcriptional profiling was to identify distinct molecular signatures associated with partial protection, complete protection, and the contribution of interferon to the host response. BALB/c mice carrying a defective allele of the Mx1 resistance gene or congenic Balb.A2G-Mx1 mice carrying the functional Mx1 allele. Half of the animals in each group were intranasally treated with 10,000 units of recombinant human IFN-α A/D (R&D Systems, Minneapolis, MN). Animals were anesthetized by IP injection and inoculated intranasally with 3.2 × 10^5 PFU (One hundred times 50% lethal dose (LD50)) of the reconstructed 1918 infectious virus diluted in 50 μl phosphate-buffered saline (PBS) or mock infected with PBS. To assess gene expression in response to r1918 virus with and without IFN treatment, lungs were harvested at 12hr, 24hr, and 72hr post-innoculation (n=3 per group at each time point). To assess gene expression in the context of IFN treatment only, lungs were harvested at 8h and 24hr post-treatment (n=3 per group at each time point). To assess gene expression without IFN or virus infection, lungs were harvested from mock-infected animals at 12h, 24h and 72hr from both Balb/c (n=2 per at each time point) and Mx1+/+ (n=3 at each time point).

2012-02-20 | E-GEOD-35933 | biostudies-arrayexpress