Evidence map›Paper›PMID 15507627›Full record

ArticleJournal of virology2004

Functions of the C-terminal domain of varicella-zoster virus glycoprotein E in viral replication in vitro and skin and T-cell tropism in vivo.

Jennifer Moffat, Chengjun Mo, Jason J Cheng, Marvin Sommer, Leigh Zerboni, Shaye Stamatis, Ann M Arvin

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

49 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
  2. Development of mRNA vaccines against herpes zoster.Human vaccines & immunotherapeutics · 2026
    Review
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  14. Review
  15. Article
  16. The Structures and Functions of VZV Glycoproteins.Current topics in microbiology and immunology · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

7 authors at 2 institutions in 1 country.

Jennifer MoffatDepartment of Microbiology and Immunology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA. moffatj@upstate.edu
Chengjun Mo
Jason J Cheng
Marvin Sommer
Leigh Zerboni
Shaye Stamatis
Ann M Arvin
Stanford University · USSUNY Upstate Medical University · US

Funding

Varicella-Zoster Virus: T Cell/Skin Tropisms &ImmunityR01AI020459 · NIAID · STANFORD UNIVERSITY · PI OLIVER, STEFAN LYNE · 1985 to 2023
$6.4M
Varicella-Zoster Virus: T Cell/Skin Tropisms & ImmunityR37AI020459 · NIAID · STANFORD UNIVERSITY · PI ARVIN, ANN · 2016 to 2020
$2.0M
SCID/HU MOUSE MODEL FOR VZV INFECTIONF32AI009195 · NIAID · STANFORD UNIVERSITY · PI MOFFAT, JENNIFER F. · 1995 to 1997
–
NIAID NIH HHS AI 09195NIAID NIH HHS AI 20459NIAID NIH HHS F32 AI009195NIAID NIH HHS R01 AI020459NIAID NIH HHS R37 AI020459
6 · The paper itself

Abstract

Varicella-zoster virus (VZV) glycoprotein E (gE) is essential for VZV replication. To further analyze the functions of gE in VZV replication, a full deletion and point mutations were made in the 62-amino-acid (aa) C-terminal domain. Targeted mutations were introduced in YAGL (aa 582 to 585), which mediates gE endocytosis, AYRV (aa 568 to 571), which targets gE to the trans-Golgi network (TGN), and SSTT, an "acid cluster" comprising a phosphorylation motif (aa 588 to 601). Substitutions Y582G in YAGL, Y569A in AYRV, and S593A, S595A, T596A, and T598A in SSTT were introduced into the viral genome by using VZV cosmids. These experiments demonstrated a hierarchy in the contributions of these C-terminal motifs to VZV replication and virulence. Deletion of the gE C terminus and mutation of YAGL were lethal for VZV replication in vitro. Mutations of AYRV and SSTT were compatible with recovery of VZV, but the AYRV mutation resulted in rapid virus spread in vitro and the SSTT mutation resulted in higher virus titers than were observed for the parental rOka strain. When the rOka-gE-AYRV and rOka-gE-SSTT mutants were evaluated in skin and T-cell xenografts in SCIDhu mice, interference with TGN targeting was associated with substantial attenuation, especially in skin, whereas the SSTT mutation did not alter VZV infectivity in vivo. These results provide the first information about how targeted mutations of this essential VZV glycoprotein affect viral replication in vitro and VZV virulence in dermal and epidermal cells and T cells within intact tissue microenvironments in vivo.

Indexed as

Virus ReplicationAnimalsCell LineHerpesvirus 3, HumanHumansMiceMice, SCIDRecombination, GeneticSkinStructure-Activity RelationshipT-LymphocytesTropismViral Envelope Proteinsglycoprotein E, varicella-zoster virusViral Envelope Proteins

Identifiers

PMID15507627
PMCPMC525039
OpenAlexW2108957284

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.