ArticleFrontiers in microbiology2014
Varicella-zoster virus glycoprotein expression differentially induces the unfolded protein response in infected cells.
Article in Frontiers in microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 27 citations in OpenAlex.
- Viral Infection and Antiviral Treatments in Ocular Pathologies.Microorganisms · 2022Review
- P2X7 receptor antagonist BBG inhibits endoplasmic reticulum stress and pyroptosis to alleviate postherpetic neuralgia.Molecular and cellular biochemistry · 2021Article
- Review
- The Epstein-Barr Virus Lytic Protein BMLF1 Induces Upregulation of GRP78 Expression through ATF6 Activation.International journal of molecular sciences · 2021Article
- Induction of the Unfolded Protein Response during Bovine Alphaherpesvirus 1 Infection.Viruses · 2020Article
- Porcine Circovirus Type 2 Induces ORF3-Independent Mitochondrial Apoptosis via PERK Activation and Elevation of Cytosolic Calcium.Journal of virology · 2019Article
- Virus and tumor microenvironment induced ER stress and unfolded protein response: from complexity to therapeutics.Oncotarget · 2018Review
- Programmed cell death: the battlefield between the host and alpha-herpesviruses and a potential avenue for cancer treatment.Oncotarget · 2018Review
- Cellular Stress Response to Varicella-Zoster Virus Infection of Human Skin Includes Highly Elevated Interleukin-6 Expression.Open forum infectious diseases · 2018Article
- Autophagy Quantification and STAT3 Expression in a Human Skin Organ Culture Model for Innate Immunity to Herpes Zoster.Frontiers in microbiology · 2018Article
- Gp78 E3 Ubiquitin Ligase: Essential Functions and Contributions in Proteostasis.Frontiers in cellular neuroscience · 2017Review
- Varicella-Zoster Virus Infectious Cycle: ER Stress, Autophagic Flux, and Amphisome-Mediated Trafficking.Pathogens (Basel, Switzerland) · 2016Review
- Role for the αV Integrin Subunit in Varicella-Zoster Virus-Mediated Fusion and Infection.Journal of virology · 2016Article
- Porcine Circovirus 2 Deploys PERK Pathway and GRP78 for Its Enhanced Replication in PK-15 Cells.Viruses · 2016Article
- Autophagic flux without a block differentiates varicella-zoster virus infection from herpes simplex virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The unfolded protein response in virus infections.Frontiers in microbiology · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Varicella-zoster virus (VZV) is a human herpesvirus that spreads to children as varicella or chicken pox. The virus then establishes latency in the nervous system and re-emerges, typically decades later, as zoster or shingles. We have reported previously that VZV induces autophagy in infected cells as well as exhibiting evidence of the Unfolded Protein Response (UPR): XBP1 splicing, a greatly expanded Endoplasmic Reticulum (ER) and CHOP expression. Herein we report the results of a UPR specific PCR array that measures the levels of mRNA of 84 different components of the UPR in VZV infected cells as compared to tunicamycin treated cells as a positive control and uninfected, untreated cells as a negative control. Tunicamycin is a mixture of chemicals that inhibits N-linked glycosylation in the ER with resultant protein misfolding and the UPR. We found that VZV differentially induces the UPR when compared to tunicamycin treatment. For example, tunicamycin treatment moderately increased (8-fold) roughly half of the array elements while downregulating only three (one ERAD and two FOLD components). VZV infection on the other hand upregulated 33 components including a little described stress sensor CREB-H (64-fold) as well as ER membrane components INSIG and gp78, which modulate cholesterol synthesis while downregulating over 20 components mostly associated with ERAD and FOLD. We hypothesize that this expression pattern is associated with an expanding ER with downregulation of active degradation by ERAD and apoptosis as the cell attempts to handle abundant viral glycoprotein synthesis.
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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.