ArticleCellular and molecular life sciences : CMLS2024
VZV IE4 downregulates cellular surface MHC-I via sequestering it to the Golgi complex.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- The race between viral immune evasion and the MHC class I antigen processing pathway.FEMS microbiology reviews · 2026Review
- High-Throughput Yeast Two-Hybrid Technology for Investigating Molecular Virology.Methods in molecular biology (Clifton, N.J.) · 2025Article
- No Evidence for a Causal Association Between Depression and Herpes Zoster or Post-Herpetic Neuralgia: A Mendelian Randomization Study.Journal of pain research · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
Abstract
Varicella-zoster virus (VZV) infection downregulates surface major histocompatibility complex class I (MHC-I) expression and retains MHC-I in the Golgi complex of infected cells. However, the underlying mechanism is not fully understood. The VZV IE4 protein is a multifunctional protein that is essential for VZV infection. In this study, the human leucocyte antigen C (HLA-C) protein was identified as a novel cellular factor associated with IE4. Ectopically expressed IE4 co-localizes with HLA-C, sequesters HLA-C to the Golgi complex and downregulates cellular surface MHC-I. VZV, with a mutated Golgi localization signal in IE4, denoted as mutated IE4 (mIE4) VZV, was constructed. In mIE4 VZV-infected cells, the cellular surface MHC-I was restored, and HLA-C was not retained in the Golgi complex. In summary, for the first time, we demonstrate a novel role of VZV IE4 in interfering with the MHC-I presentation pathway, suggesting that it may contribute to the evasion of host antiviral adaptive immunity.
Indexed as
Identifiers
What OpenQuestion holds
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.