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.
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.
Project description:Purpose: To compare single cell transcriptional profiling (scRNAseq) of different murine genital herpes infection models with HSV1-McKrae and HSV2-186. Method: DMPA-treated WT C57BL/6 mice were infected with HSV1-McKrae, HSV2-186 or PBS intravaginally. Vaginal tissues were harvested at 5 days post infection, live cells were sorted, a minimum of 16,000 cells were used for scRNAseq. Results: By tSNE visualization of 21,633 cells across all samples, 17 distinct clusters were resolved. We found significantly increased levels of Interferons-Stimulated-Genes (ISGs) in the neutrophils potentially contributing to disease onset and progression in HSV2 genital infections. Conclusion: Our study is the first comparison between the transcriptional signature of two genital herpes model- namely HSV1 and HSV2. Generated by scRNAseq, this study would provide researchers with gene candidates associated with the disease progression and inflammation induced by genital infections with HSV1 and HSV2.
Project description:We report mRNA-Sequencing analysis of primary mouse microglia infected with HSV1 and/or treated with ALT001, which is mitophagy inducing drug
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.