ArticleJournal of virology2021
Prohibitin-1 Contributes to Cell-to-Cell Transmission of Herpes Simplex Virus 1 via the MAPK/ERK Signaling Pathway.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 20 citations in OpenAlex.
- MEK/ERK-Mediated Transcriptional Repression of Metabolic Genes Confers Host Defense AgainstMicroorganisms · 2026Article
- Novel Hsp90 inhibitor JD‑02 inhibits HSV‑1 infection via the Raf/MEK/ERK signaling pathway.International journal of molecular medicine · 2026Article
- Proximity labelling identifies proteins associated with HSV-2 pUL21 at early and late times after infection.PLoS pathogens · 2026Article
- Prohibitins: emerging host targets of bacteria and viruses at the plasma membrane, mitochondria, and cytoplasm.Microbial cell (Graz, Austria) · 2026Article
- Development of a Piezoelectric Immunosensor to Rapidly Measure Prohibitin‑1 as a Prognostic Biomarker for Sepsis and Other Serious Infectious Diseases.ACS applied electronic materials · 2025Article
- Article
- Herpes simplex virus 1 evades APOBEC1-mediated immunity via its uracil-DNA glycosylase in mice.Nature microbiology · 2025Article
- Review
- Prohibitins in infection: potential therapeutic targets.Future microbiology · 2025Review
- Impact of the interaction between herpes simplex virus 1 ICP22 and FACT on viral gene expression and pathogenesis.Journal of virology · 2024Article
- Identification of a novel neurovirulence factor encoded by the cryptic orphan gene UL31.6 of herpes simplex virus 1.Journal of virology · 2024Article
- Synthetic dibenzylideneketones as promising anti-herpes simplex virus type 1 agents.Archives of virology · 2023Article
- Network pharmacology-based exploration identified the antiviral efficacy of Quercetin isolated from mulberry leaves against enterovirus 71 via the NF-κB signaling pathway.Frontiers in pharmacology · 2023Article
- ATF1 Restricts Human Herpesvirus 6A Replication via Beta Interferon Induction.Journal of virology · 2022Article
- Genome-wide CRISPR screen for HSV-1 host factors reveals PAPSS1 contributes to heparan sulfate synthesis.Communications biology · 2022Article
- Role of the Orphan Transporter SLC35E1 in the Nuclear Egress of Herpes Simplex Virus 1.Journal of virology · 2022Article
- Evaluation of the Safety and Immunogenicity of Duck-Plague VirusFrontiers in immunology · 2022Article
- Berberine Inhibits Herpes Simplex Virus 1 Replication in HEK293T Cells.Computational and mathematical methods in medicine · 2022Article
- The Intricacy of the Viral-Human Protein Interaction Networks: Resources, Data, and Analyses.Frontiers in microbiology · 2022Review
- Transcriptome-wide N6-methyladenosine modification profiling of long non-coding RNAs during replication of Marek's disease virus in vitro.BMC genomics · 2021Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral cell-to-cell spread, a method employed by several viral families for entrance via cell junctions, is highly relevant to the pathogenesis of various viral infections. Cell-to-cell spread of herpes simplex virus 1 (HSV-1) is known to depend greatly on envelope glycoprotein E (gE). However, the molecular mechanism by which gE acts in HSV-1 cell-to-cell spread and the mechanisms of cell-to-cell spread by other herpesviruses remain poorly understood. Here, we describe our identification of prohibitin-1 as a novel gE-interacting host cell protein. Ectopic expression of prohibitin-1 increased gE-dependent HSV-1 cell-to-cell spread. As observed with the gE-null mutation, decreased expression or pharmacological inhibition of prohibitin-1 reduced HSV-1 cell-to-cell spread without affecting the yield of virus progeny. Similar effects were produced by pharmacological inhibition of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, wherein prohibitin-1 acts as a protein scaffold and is required for induction of this pathway. Furthermore, artificial activation of the MAPK/ERK pathway restored HSV-1 cell-to-cell spread impaired by the gE-null mutation. Notably, pharmacological inhibition of prohibitins or the MAPK/ERK pathway reduced viral cell-to-cell spread of representative members in all herpesvirus subfamilies. Our results suggest that prohibitin-1 contributes to gE-dependent HSV-1 cell-to-cell spread via the MAPK/ERK pathway and that this mechanism is conserved throughout the
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