Evidence map›Paper›PMID 17559303›Full record

ArticlePLoS pathogens2007

A molecular link between malaria and Epstein-Barr virus reactivation.

Arnaud Chêne, Daria Donati, André Ortlieb Guerreiro-Cacais, Victor Levitsky, Qijun Chen, Kerstin I Falk, Jackson Orem, Fred Kironde, Mats Wahlgren, Maria Teresa Bejarano

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 181 citations in OpenAlex.

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  12. Aflatoxin B1 and Epstein-Barr virus-induced CCL22 expression stimulates B cell infection.Proceedings of the National Academy of Sciences of the United States of America · 2024
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20 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 2 countries.

Arnaud ChêneCenter for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Daria Donati
André Ortlieb Guerreiro-Cacais
Victor Levitsky
Qijun Chen
Kerstin I Falk
Jackson Orem
Fred Kironde
Mats Wahlgren
Maria Teresa Bejarano
Karolinska Institutet · SESwedish Institute · SEMakerere University · UGUganda Cancer Institute · UG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although malaria and Epstein-Barr (EBV) infection are recognized cofactors in the genesis of endemic Burkitt lymphoma (BL), their relative contribution is not understood. BL, the most common paediatric cancer in equatorial Africa, is a high-grade B cell lymphoma characterized by c-myc translocation. EBV is a ubiquitous B lymphotropic virus that persists in a latent state after primary infection, and in Africa, most children have sero-converted by 3 y of age. Malaria infection profoundly affects the B cell compartment, inducing polyclonal activation and hyper-gammaglobulinemia. We recently identified the cystein-rich inter-domain region 1alpha (CIDR1alpha) of the Plasmodium falciparum membrane protein 1 as a polyclonal B cell activator that preferentially activates the memory compartment, where EBV is known to persist. Here, we have addressed the mechanisms of interaction between CIDR1alpha and EBV in the context of B cells. We show that CIDR1alpha binds to the EBV-positive B cell line Akata and increases the number of cells switching to the viral lytic cycle as measured by green fluorescent protein (GFP) expression driven by a lytic promoter. The virus production in CIDR1alpha-exposed cultures was directly proportional to the number of GFP-positive Akata cells (lytic EBV) and to the increased expression of the EBV lytic promoter BZLF1. Furthermore, CIDR1alpha stimulated the production of EBV in peripheral blood mononuclear cells derived from healthy donors and children with BL. Our results suggest that P. falciparum antigens such as CIDR1alpha can directly induce EBV reactivation during malaria infection that may increase the risk of BL development for children living in malaria-endemic areas. To our knowledge, this is the first report to show that a microbial protein can drive a latently infected B cell into EBV replication.

Indexed as

AnimalsAntigens, ProtozoanCell Line, TumorChildChild, PreschoolDNA-Binding ProteinsDNA, ViralEpstein-Barr Virus InfectionsErythrocytesGene Expression Regulation, ViralHerpesvirus 4, HumanHumansLeukocytes, MononuclearMalariaPlasmodium falciparumProtozoan ProteinsAntigens, ProtozoanBZLF1 protein, Herpesvirus 4, HumanDNA-Binding ProteinsDNA, Viralerythrocyte membrane protein 1, Plasmodium falciparumProtozoan ProteinsTrans-ActivatorsViral Proteins

Identifiers

PMID17559303
PMCPMC1891325
OpenAlexW2014462867

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.