MRNA-Sequencing data of herpes simplex virus type 1 (HSV1)-infected primary mouse microglia
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE278015 | GEO | 2024/12/31
REPOSITORIES: GEO
Similar Datasets
Project description:mRNA-Sequencing data of herpes simplex virus type 1 (HSV1)-infected primary mouse microglia
| PRJNA1165223 | ENA
Project description:Gene expression analysis of wild type and STING knock-out Mouse Embryonic Fibroblasts (MEFs) infected with γ34.5 deleted HSV1. Genes whose expression that are affected by HSV1 in a STING dependent manner will be identified and signaling pathways regulated by STING will be elucidated. Primary MEFs were mock treated or infected with γ34.5 deleted HSV1 at M.O.I. 1. Total RNA was extracted 3 hours post infection for array analysis.
2013-01-15 | E-GEOD-43479 | biostudies-arrayexpress
Project description:Gene expression analysis of wild type and STING knock-out Mouse Embryonic Fibroblasts (MEFs) infected with γ34.5 deleted HSV1. Genes whose expression that are affected by HSV1 in a STING dependent manner will be identified and signaling pathways regulated by STING will be elucidated.
2013-01-15 | GSE43479 | GEO
Project description:We hypothesize that human RIPK3 deficiency does not result in impairment of type I IFN mediated antiviral immunity, contrasting with the situation in deficiencies of the TLR3-IFNAR1 circuit. To test the cellular responses to HSV1 at the wide transcriptome level, bulk RNA sequencing was performed with human primary fibroblasts without or with HSV-1 infection for 24 hours, in cells from healthy controls, RIPK3 HSE patient and other patients with recessive TLR3, IFNAR1 or NEMO deficiency.
2023-03-29 | GSE228495 | GEO
Project description:Herpes simplex virus types 1 and 2 (HSV1 and HSV2) are common infectious agents in both industrialized and developing countries. They cause recurrent asymptomatic and/or symptomatic infections, and life-threatening diseases and death in newborns and immunocompromised patients. Current treatment for HSV relies on antiviral medications, which can halt the symptomatic diseases but cannot prevent the shedding that occurs in asymptomatic patients or, consequently, the spread of the viruses. Therefore, prevention rather than treatment of HSV infections has long been an area of intense research, but thus far effective anti-HSV vaccines still remain elusive. One of the key hurdles to overcome in anti-HSV vaccine development is the identification and effective use of strategies that promote the emergence of Th1-type immune responses against a wide range of epitopes involved in the control of viral replication. Since the HIV1 Tat protein has several immunomodulatory activities and increases CTL recognition of dominant and subdominant epitopes of heterologous antigens, we generated and assayed a recombinant attenuated replication-competent HSV1 vector containing the tat gene (HSV1-Tat). In this proof-of-concept study we show that immunization with this vector conferred protection in 100% of mice challenged intravaginally with a lethal dose of wild-type HSV1. We demonstrate that the presence of Tat within the recombinant virus increased and broadened Th1-like and CTL responses against HSV-derived T-cell epitopes and elicited in most immunized mice detectable IgG responses. In sharp contrast, a similarly attenuated HSV1 recombinant vector without Tat (HSV1-LacZ), induced low and different T cell responses, no measurable antibody responses and did not protect mice against the wild-type HSV1 challenge. These findings strongly suggest that recombinant HSV1 vectors expressing Tat merit further investigation for their potential to prevent and/or contain HSV1 infection and dissemination.
| S-EPMC4102458 | biostudies-literature
Project description:We describe the cellular response to HSV-1 infection in human iPSC-derived brain organoids
2021-01-22 | GSE163952 | GEO
Project description:Infected-cell protein 0 (ICP0) is a RING finger E3 ligase that regulates herpes simplex virus (HSV) mRNA synthesis, and strongly influences the balance between latency and replication of HSV. For 25 years, the nuclear functions of ICP0 have been the subject of intense scrutiny. To obtain new clues about ICP0's mechanism of action, we constructed HSV-1 viruses that expressed GFP-tagged ICP0. To our surprise, both GFP-tagged and wild-type ICP0 were predominantly observed in the cytoplasm of HSV-infected cells. Although ICP0 is exclusively nuclear during the immediate-early phase of HSV infection, further analysis revealed that ICP0 translocated to the cytoplasm during the early phase where it triggered a previously unrecognized process; ICP0 dismantled the microtubule network of the host cell. A RING finger mutant of ICP0 efficiently bundled microtubules, but failed to disperse microtubule bundles. Synthesis of ICP0 proved to be necessary and sufficient to disrupt microtubule networks in HSV-infected and transfected cells. Plant and animal viruses encode many proteins that reorganize microtubules. However, this is the first report of a viral E3 ligase that regulates microtubule stability. Intriguingly, several cellular E3 ligases orchestrate microtubule disassembly and reassembly during mitosis. Our results suggest that ICP0 serves a dual role in the HSV life cycle, acting first as a nuclear regulator of viral mRNA synthesis and acting later, in the cytoplasm, to dismantle the host cell's microtubule network in preparation for virion synthesis and/or egress.
| S-EPMC2882321 | biostudies-literature
Project description:Here we integrate immune profiling and computational approaches to study responses to a replication-defective herpes simplex virus (HSV) 2 vaccine, in men and women either naive or previously exposed to HSV. Subjects were recipients of a herpes simplex virus (HSV) 2 vaccine in a phase 1 clinical trial where comparisons could be made between three groups of human volunteers based on their HSV serostatus prior to vaccination: HSV1-/HSV2- , HSV1+/HSV2-, or HSV1±/HSV2+ Peripheral blood transcriptomics and cell population frequencies showed the greatest changes on day 1 after vaccination. Prior exposure status and gender were independently associated with responses, but the magnitude of innate responses including type I interferon signatures and TLR7 were greatest in HSV naive women. In contrast, subjects previously infected with HSV had more prominent interferon-I responses. Thus, prior exposure and gender interact to shape innate responses that may also impact adaptive immune phenotypes, such as the neutralizing antibody response which was also faster in HSV naive women than men.
2023-01-04 | GSE185341 | GEO
Project description:The Latency-Associated Transcript Locus of Herpes Simplex Virus 1 is a Virulence Determinant in Human Skin
| PRJNA338711 | ENA
Project description:BACKGROUND:We previously reported reduced prefrontal cortex (PFC) grey matter volume among first episode, antipsychotic-naïve schizophrenia subjects (SZ) exposed to HSV1 but not among healthy subjects (HS) (Prasad et al., 2007). Independently, rs1051788, an exonic polymorphism of the MHC Class I polypeptide-related sequence B (MICB) gene was associated with HSV1 seropositivity, as well as SZ risk. In this study, we examined whether PFC grey matter changes associated with HSV1 exposure varied against the background of MICB genotypes. METHODS:We examined Caucasian individuals from the sample we studied in our previous report (Prasad et al., 2007) (SZ, n=21 and HS, n=19). Whole brain voxelwise analysis of structural MRI scans was conducted using Statistical Parametric Mapping, ver 5 (SPM5). The impact of rs1051788 variation and HSV1 seropositivity on grey matter volumes was examined using regression models on the combined sample of cases and controls, and then within each diagnostic group. RESULTS:In the combined sample of cases and controls, we observed the main effects of HSV1 seropositivity and genotypes, and a significant joint effect of HSV1 seropositivity and genotype mainly in the PFC. The joint effect was more prominent among cases than among controls. DISCUSSION:Our observations suggest that rs1051788 and HSV1 seropositivity are associated individually and jointly with reduced PFC grey matter volume. The patterns of these associations differ by diagnostic status, and these factors explain only a "small" portion of the variance in the grey matter volume reductions.
| S-EPMC2856756 | biostudies-literature