ArticleJournal of virology2023
A viral lncRNA tethers HSV-1 genomes at the nuclear periphery to establish viral latency.
Article in Journal of virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Analysis of host and viral nascent and steady-state RNA levels in a human neuronal model of herpes simplex virus 1 infection.PLoS pathogens · 2026Article
- Impact of HSV-1 Infection on Alzheimer's Disease Neurodegeneration Markers: Insights from LUHMES 2D and 3D Neuronal Models.International journal of molecular sciences · 2026Article
- The dynamic interplay between viruses and host non-coding RNA species.FEMS microbiology reviews · 2026Review
- The H4K20-mono-methyltransferase SETD8 promotes global accessibility of infecting herpes simplex virus genomes.Journal of virology · 2025Article
- Comprehensive analysis of lncRNAs and mRNAs revealed potential participants in the process of avian reovirus infection.Frontiers in microbiology · 2025Article
- Roles of SNORD115 and SNORD116 ncRNA clusters during neuronal differentiation.Nature communications · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
importanceHerpes simplex virus 1 (HSV-1) establishes lifelong latency in neuronal cells. Following a stressor, the virus reactivates from latency, virus is shed at the periphery and recurrent disease can occur. During latency, the viral lncRNA termed the latency-associated transcript (LAT) is known to accumulate to high abundance. The LAT is known to impact many aspects of latency though the molecular events involved are not well understood. Here, we utilized a human neuronal cell line model of HSV latency and reactivation (LUHMES) to identify the molecular-binding partners of the LAT during latency. We found that the LAT binds to both the cellular protein, TMEM43, and HSV-1 genomes in LUHMES cells. Additionally, we find that knockdown of TMEM43 prior to infection results in a decreased ability of HSV-1 to establish latency. This work highlights a potential mechanism for how the LAT facilitates the establishment of HSV-1 latency in human neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.