Project description:To discover the mechanism by which herpes simplex virus type 1 (HSV-1) drastically reshapes the host cell transcriptional patterns during infection, we performed RNAseq. We infected A549 cells with HSV-1, and analized host and viral expression at 1, 3 and 8 hours post infection. We report both a drastical human transcription shutoff parallel with an increase in viral transcription.
Project description:The purpose of this study was to determine what are the effects of Src deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV, MOI=1) or herpes simplex virus 1 (HSV-1, MOI=5) for 6h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.
Project description:This is a part of the study that shows that a host gene,FOXF1, promote herpes simplex virus 1 (HSV-1) genome accessibility. These ATAC analyses viral and host genome accessibility in Neuro-2a cells. Neuro-2a cells were transfected with pFOXF1 and pcDNA plasmids for 42 hours then infected with herpes simple virus1 for 3 hours.
Project description:This is a part of the study that shows that a host gene,ONECUT2( OC2), promotes herpes simplex virus 1 (HSV-1) genome accessibility. These ATAC analyses are for viral and host genome accessibility in Neuro-2a cells. Neuro-2a cells were transfected with pOC2△HOX2 and pcDNA plasmids for 42 hours then infected with herpes simple virus1 for 2 hours.
Project description:We show that Herpes simplex virus 1 (HSV-1) induces the expression of about 1000 antisense transcripts from the human host cell genome.
Project description:Herpes simplex virus type 1 (HSV-1) infects dendritic cells (DCs), professional antigen-presenting cells that initiate and regulate host antiviral responses. HSV-1 infects DCs limiting their maturation, migration to draining lymph nodes and T cell activation capacity, ultimately promotes their apoptosis. Here, we investigated the impact of HSV-1 infection over neutral lipid metabolism in DCs and their function. We found that HSV-1 significantly alters neutral lipid metabolism in infected DCs and promotes LD accumulation. Pharmacological inhibition of cholesterol ester synthesis, or fatty acid transporter proteins in infected DCs reduced LD accumulation and viral replication, enhanced DC viability and DC migration to draining lymph nodes and promoted DC priming of virus-specific CD8+ T cells. These findings highlight the role of neutral lipid metabolism in HSV-1-infected DCs and its impact over host immunity against this virus, underscoring lipid metabolism in DCs as a potential therapeutical target for triggering antiviral immunity against HSV-1.
2025-04-03 | MTBLS5163 | MetaboLights
Project description:Antiviral resistance evolution in hypermutator herpes simplex virus
