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:Viruses have evolved sophisticated immune evasion strategies to establish persistent and latent infections. While type I interferon (IFN-I) signaling through the IFNAR–JAK–STAT axis constitutes a major antiviral defense, IFNAR-independent mechanisms also play complementary roles in restricting viral replication. Herpes simplex virus type 1 (HSV-1), a widespread DNA virus capable of lifelong latency, can exploit the host nuclear transport machinery to facilitate its replication. Here, we identify a distinct IFNAR-independent antiviral mechanism mediated by the nuclear-enriched microRNA miR-29b. We show that miR-29b, but not its closely related family member miR-29a, restricts HSV-1 replication by targeting the nuclear transport receptor Importin-5 (IPO5). Proteomic, imaging, and biochemical analyses reveal that miR-29b binds to IPO5 and disrupts IPO5-mediated nuclear import of the HSV-1 protein UL47, a key regulator of viral genome packaging. Notably, mutation of the hexanucleotide element “AGUGUU” in miR-29b by using Prime editing technology, which governs its nuclear localization, abolishes both its interaction with IPO5 and its antiviral activity in vitro and in vivo, exacerbating the progression of herpes simplex encephalitis. Our findings uncover a previously unrecognized miRNA–protein regulatory axis, in which miR-29b interferes with viral hijacking of host nuclear import pathways to selectively block viral protein trafficking, highlighting miR-29b and IPO5 as promising targets for antiviral intervention.
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.
