Evidence map›Paper›PMID 15613312›Full record

ArticleJournal of virology2005

Epstein-Barr virus gp42 is posttranslationally modified to produce soluble gp42 that mediates HLA class II immune evasion.

Maaike E Ressing, Daphne van Leeuwen, Frank A W Verreck, Sinéad Keating, Raquel Gomez, Kees L M C Franken, Tom H M Ottenhoff, Melanie Spriggs, Ton N Schumacher, Lindsey M Hutt-Fletcher and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.8field-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

57 citing papers in PubMed, 99 citations in OpenAlex.

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  9. Neutralizing antibodies against EBV gp42 show potentEmerging microbes & infections · 2023
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  19. Inferring the Urban Transmission Potential of Bat Influenza Viruses.Frontiers in cellular and infection microbiology · 2020
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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

12 authors at 5 institutions in 3 countries.

Maaike E RessingDepartment of Medical Microbiology, Leiden University Medical Center, Bldg. 1 E4, P P.O. Box 9600, 2300 RC Leiden, The Netherlands. m.ressing@lumc.nl
Daphne van Leeuwen
Frank A W Verreck
Sinéad Keating
Raquel Gomez
Kees L M C Franken
Tom H M Ottenhoff
Melanie Spriggs
Ton N Schumacher
Lindsey M Hutt-Fletcher
Martin Rowe
Emmanuel J H J Wiertz
Leiden University Medical Center · NLThe Netherlands Cancer Institute · NLUniversity of Wales · GBAmgen (United States) · USLouisiana State University Health Sciences Center Shreveport · US

Funding

INITIATION OF CELL INFECTION WITH EPSTEIN-BAR VIRUSR01AI020662 · NIAID · UNIVERSITY OF MISSOURI KANSAS CITY · PI HUTT-FLETCHER, LINDSEY M. · 1985 to 2004
$1.4M
NIAID NIH HHS R01 AI020662
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) resides as a persistent infection in human leukocyte antigen (HLA) class II+ B lymphocytes and is associated with a number of malignancies. The EBV lytic-phase protein gp42 serves at least two functions: gp42 acts as the coreceptor for viral entry into B cells and hampers T-cell recognition via HLA class II molecules through steric hindrance of T-cell receptor-class II-peptide interactions. Here, we show that gp42 associates with class II molecules at their various stages of maturation, including immature alphabetaIi heterotrimers and mature alphabeta-peptide complexes. When analyzing the biosynthesis and maturation of gp42 in cells stably expressing the viral protein, we found that gp42 occurs in two forms: a full-length type II membrane protein and a truncated soluble form. Soluble gp42 is generated by proteolytic cleavage in the endoplasmic reticulum and is secreted. Soluble gp42 is sufficient to inhibit HLA class II-restricted antigen presentation to T cells. In an almost pure population of Burkitt's lymphoma cells in the EBV lytic cycle, both transmembrane and soluble forms of gp42 are detected. These results imply that soluble gp42 is generated during EBV lytic infection and could contribute to undetected virus production by mediating evasion from T-cell immunity.

Indexed as

Protein Processing, Post-TranslationalAmino Acid SequenceB-LymphocytesCell Line, TumorGlycoproteinsHistocompatibility Antigens Class IIHumansMolecular Sequence DataT-LymphocytesViral ProteinsBZLF2 protein, Herpesvirus 4, HumanGlycoproteinsHistocompatibility Antigens Class IIViral Proteins

Identifiers

PMID15613312
PMCPMC538541
OpenAlexW2138822872

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.