Evidence map›Paper›PMID 25535384›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Autophagic flux without a block differentiates varicella-zoster virus infection from herpes simplex virus infection.

Erin M Buckingham, John E Carpenter, Wallen Jackson, Leigh Zerboni, Ann M Arvin, Charles Grose

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Erin M BuckinghamVirology Laboratory, Department of Pediatrics, University of Iowa Children's Hospital, Iowa City, IA 52242; and.
John E CarpenterVirology Laboratory, Department of Pediatrics, University of Iowa Children's Hospital, Iowa City, IA 52242; and.
Wallen JacksonVirology Laboratory, Department of Pediatrics, University of Iowa Children's Hospital, Iowa City, IA 52242; and.
Leigh ZerboniDepartments of Pediatrics and Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305.
Ann M ArvinDepartments of Pediatrics and Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305.
Charles GroseVirology Laboratory, Department of Pediatrics, University of Iowa Children's Hospital, Iowa City, IA 52242; and charles-grose@uiowa.edu.
University of Iowa Stead Family Children’s Hospital · USStanford University · US

Funding

Autophagy and ER stress during varicella infectionR01AI089716 · NIAID · UNIVERSITY OF IOWA · PI GROSE, CHARLES F. · 2011 to 2015
$1.9M
Request for Funds to Purchase a Replacement Laser Scanning Confocal MicroscopeS10RR025439 · NCRR · UNIVERSITY OF IOWA · PI ZABNER, JOSEPH · 2009 to 2009
$500k
NCRR NIH HHS 1S10RR025439-01NCRR NIH HHS S10 RR025439NIAID NIH HHS AI89716NIAID NIH HHS R01 AI089716
6 · The paper itself

Abstract

Autophagy is a process by which misfolded and damaged proteins are sequestered into autophagosomes, before degradation in and recycling from lysosomes. We have extensively studied the role of autophagy in varicella-zoster virus (VZV) infection, and have observed that vesicular cells are filled with >100 autophagosomes that are easily detectable after immunolabeling for the LC3 protein. To confirm our hypothesis that increased autophagosome formation was not secondary to a block, we examined all conditions of VZV infection as well as carrying out two assessments of autophagic flux. We first investigated autophagy in human skin xenografts in the severe combined immunodeficiency (SCID) mouse model of VZV pathogenesis, and observed that autophagosomes were abundant in infected human skin tissues. We next investigated autophagy following infection with sonically prepared cell-free virus in cultured cells. Under these conditions, autophagy was detected in a majority of infected cells, but was much less than that seen after an infected-cell inoculum. In other words, inoculation with lower-titered cell-free virus did not reflect the level of stress to the VZV-infected cell that was seen after inoculation of human skin in the SCID mouse model or monolayers with higher-titered infected cells. Finally, we investigated VZV-induced autophagic flux by two different methods (radiolabeling proteins and a dual-colored LC3 plasmid); both showed no evidence of a block in autophagy. Overall, therefore, autophagy within a VZV-infected cell was remarkably different from autophagy within an HSV-infected cell, whose genome contains two modifiers of autophagy, ICP34.5 and US11, not present in VZV.

Indexed as

AutophagyAnimalsCell-Free SystemCell LineDisease Models, AnimalFibroblastsGreen Fluorescent ProteinsHerpes SimplexHerpesvirus 3, HumanHerpes ZosterHeterograftsHumansMice, SCIDMicrotubule-Associated ProteinsPhagosomesPlasmidsGreen Fluorescent ProteinsMAP1LC3A protein, humanMicrotubule-Associated ProteinsautophagosomeautophagyEpstein–Barr virusICP34.5SCID-mouse

Identifiers

PMID25535384
PMCPMC4291665
OpenAlexW2039908848

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.