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Interferon inhibits a model RNA virus via a limited set of inducible effector genes [GW_CRISPR_Screen]

ABSTRACT: Host cells produce interferon (IFN) in response to viral infections. Secreted interferon results in the transcription and production of hundreds of interferon-stimulated genes (ISGs). A genome-wide CRISPR screen using IFN beta-treated U-2 OS cells was performed to determine which ISGs were required in order for host cells to suppress Venezuelan equine encephalitis virus (VEEV) infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE233195 | GEO | 2023/05/26

REPOSITORIES: GEO

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Interferon inhibits a model RNA virus via a limited set of inducible effector genes [ISG_CRISPR_Screen]

Project description:Host cells produce interferon (IFN) in response to viral infections. Secreted interferon results in the transcription and production of hundreds of interferon-stimulated genes (ISGs). An ISG-targeted CRISPR screen using IFN beta-treated U-2 OS cells was performed to determine which ISGs were required in order for host cells to suppress Venezuelan equine encephalitis virus (VEEV) infection.

2023-05-26 | GSE233196 | GEO

Spatial Transcriptomics of Brains Infected with VEEV

Project description:Venezuelan equine encephalitis virus (VEEV) is a neurotropic alphavirus that causes neurological disease in both humans and equine. In this study we paired spatial transcriptomics and a mouse model of VEEV to generate a transcriptomic profile of infected or control brains at 6 days post infection. We identified regionally distinct myeloid and lymphocyte populations, contributing to our understanding of the neuroinflammation caused by VEEV.

2024-12-09 | GSE275201 | GEO

Characterization of genetic variability of Venezuelan equine encephalitis viruses

Project description:We performed whole genome single nucleotide polymorphism (SNP) based analysis of all available Venezuelan equine encephalitis (VEE) virus antigenic complex genomes and developed a high resolution genome-wide SNP microarray. We used the SNP microarray to analyze a broad panel of VEEV isolates, found excellent concordance between array and sequence based genotypes for previously sequenced strains, and genotyped unsequenced strains.

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The transcriptional landscape of Venezuelan equine encephalitis virus infection

Project description:No vaccines or antivirals are approved against Venezuelan equine encephalitis virus (VEEV) infection in humans. To improve our understanding of VEEV-host interactions, we simultaneously profiled host transcriptome and viral RNA (vRNA) in thousands of single cells during infection of human astrocytes. Host transcription was suppressed, and “superproducer cells” with extreme vRNA abundance and altered transcriptome emerged during the first viral life cycle. Cells with increased structural-to-nonstructural transcript ratio demonstrated upregulation of trafficking genes at later time points. Loss- and gain-of-function experiments confirmed pro- and antiviral host factors. Single-cell deep sequencing analysis identified a viral E3 protein mutation altering host gene expression. Lastly, comparison with data from other viruses highlighted common and unique pathways perturbed by infection across evolutionary scales. This study provides a high-resolution characterization of the cellular response to VEEV infection, identifies candidate targets for antivirals, and establishes a comparative single-cell approach to study the evolution of virus-host interactions.

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Single-cell transcriptomic profiling of brain immune infiltration following Venezuelan equine encephalitis virus infection

Project description:Neurotropic alphaviruses such as Venezuelan equine encephalitis virus (VEEV) are critical human pathogens that continually expand to naïve populations and for which there are no licensed vaccines or therapeutics. The neuropathology of VEEV has been attributed to the immune response in the brain yet the underlying mechanisms and specific immune cell populations involved are not fully elucidated. In this study, a murine model of lethal VEEV infection is paired with single-cell RNA sequencing to transcriptionally profile the immune response longitudinally in the brain following infection. Infection-induced immune changes in the brain was also compared to changes in peripheral blood mononuclear cells (PBMCs). The results define an inflammatory response involving transcriptionally distinct subpopulations of activated microglia and infiltrating proinflammatory myeloid populations and cytotoxic lymphocytes. This study advances our understanding of the immune mechanisms underlying viral encephalitis toward the goal of identifying new therapeutic targets.

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Gene expression in the brains of different strains of laboratory mice upon intranasal infection with vaccine strain (TC83) of Venezuelan equine encephalitis virus

Project description:Differing from other experimental models, intranasal infection with vaccine strain of Venezuelan equine encephalitis virus, VEEV, (TC83) caused high titer infection in the brain and 90–100% mortality in the C3H/HeN murine model. Intranasal infection with VEEV (TC83) caused persistent viral infection in the brains of mice without functional αβ T-cells (αβ-TCR -/-). While wild-type C57BL/6 mice clear infectious virus in the brain by 13 dpi, αβ-TCR -/- maintain infectious virus in the brain to 92 dpi. To better characterize the susceptibility to disease development in different strains of mice, we have analyzed the gene transcriptomes in the brains of infected mice.

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Deep Spatial Profiling of Venezuelan Equine Encephalitis Virus Reveals Increased Genetic Diversity Amidst Neuroinflammation and Cell Death During Brain Infection

Project description:Venezuelan equine encephalitis virus (VEEV) causes a febrile illness that can progress to neurological disease with the possibility of death in human cases. The evaluation and optimization of therapeutics that target brain infections demands knowledge of the host’s response to VEEV, the dynamics of infection, and the potential for within-host evolution of the virus. We hypothesized that selective pressures during infection of the brain may differ temporally and spatially and so we investigated the dynamics of the host response, viral transcript levels, and genetic variation of VEEV TC-83 in eight areas of the brain in mice over 7 days post-infection (dpi). Viral replication increased throughout the brain until 5-6 dpi and decreased thereafter with neurons as the main site of viral replication. Low levels of genetic diversity were noted on 1 dpi, and was followed by an expansion in the genetic diversity of VEEV and nonsynonymous mutations (Ns) that peaked by 5 dpi. The proinflammatory response and the influx of immune cells mirrored the levels of virus and correlated with substantial damage to neurons by 5 dpi and increased activation of microglial cells and astrocytes. The prevalence and dynamics of Ns mutations suggests that the VEEV is under selection within the brain and that progressive neuroinflammation may play a role in acting as a selective pressure.

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Insect-Specific Chimeric Viruses Potentiated Antiviral Responses and Inhibited Pathogenic Alphavirus Growth in Mosquito Cells

Project description:Most alphaviruses are transmitted by mosquito vectors and infect a wide range of vertebrate hosts, with a few exceptions. Eilat virus (EILV) in this genus is characterized by a host range restricted to mosquitoes. Its chimeric viruses have been developed as safe and effective vaccine candidates and diagnostic tools. Here, we investigated the interactions between these insect-specific viruses (ISVs) and mosquito cells, unveiling their potential roles in determining vector competence and arbovirus transmission. By RNA sequencing, we found that these ISVs profoundly modified host cell gene expression profiles. Two EILV-based chimeras, consisting of EILV’s nonstructural genes and the structural genes of Chikungunya virus (CHIKV) or Venezuelan equine encephalitis virus (VEEV), namely EILV/CHIKV (E/C) and EILV/VEEV (E/V), induced more intensive transcriptome regulation than parental EILV and activated different antiviral mechanisms in host cells. We demonstrated that E/C robustly promoted antimicrobial peptide production and E/V strongly upregulated the RNA interference pathway components. This also highlighted the intrinsic divergences between CHIKV and VEEV, representatives of the Old World and New World alphaviruses. In contrast, EILV triggered a limited antiviral response. We further showed that initial chimera infections efficiently inhibited subsequent pathogenic alphavirus replication, especially in the case of E/V infection, which almost prevented VEEV and Sindbis virus (SINV) superinfections. Altogether our study provided valuable information on developing ISVs as biological control agents.

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Project description:Venezuelan equine encephalitis virus passaging

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| PRJNA157941 | ENA