Evidence map›Paper›PMID 32072172›Full record

ArticleThe Journal of infectious diseases2020

Kaposi Sarcoma-Associated Herpesvirus Infection and Endemic Burkitt Lymphoma.

Peter O Oluoch, Cliff I Oduor, Catherine S Forconi, John M Ong'echa, Christian Münz, Dirk P Dittmer, Jeffrey A Bailey, Ann M Moormann

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Journal of infectious diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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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

8 authors at 5 institutions in 3 countries.

Peter O OluochDivision of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Cliff I OduorKenya Medical Research Institute/Center for Global Health Research, Kisumu, Kenya.
Catherine S ForconiDivision of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
John M Ong'echaKenya Medical Research Institute/Center for Global Health Research, Kisumu, Kenya.
Christian MünzViral Immunobiology, Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Dirk P DittmerDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, USA.
Jeffrey A BaileyDepartment of Pathology and Laboratory Medicine, Warren Alpert Medical School, Brown University, Providence, Rhode Island, USA.
Ann M MoormannDivision of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
University of Massachusetts Chan Medical School · USBrown University · USKenya Medical Research Institute · KEUniversity of North Carolina at Chapel Hill · USUniversity of Zurich · CH

Funding

Vironomics and Biostatistics CoreP01CA019014 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, NANCY JOAN RAAB-TRAUB · 1985 to 2026
$43.8M
Impact of malaria on shaping immunity to EBV in the etiology of Burkitt lymphomaR01CA189806 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MOORMANN, ANN M · 2014 to 2024
$5.7M
Mechanisms of KSHV TransmissionR01CA239583 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAMANIA, BLOSSOM A, DITTMER, DIRK P · 2019 to 2023
$2.8M
NCI NIH HHS P01 CA019014NCI NIH HHS R01 CA189806NCI NIH HHS R01 CA239583
6 · The paper itself

Abstract

backgroundEndemic Burkitt lymphoma (eBL) is associated with Epstein-Barr virus (EBV) and Plasmodium falciparum malaria coinfections. However, the role of Kaposi sarcoma-associated herpesvirus (KSHV), also endemic in Africa, has not been evaluated as a cofactor in eBL pathogenesis.

methodsMultiplexed seroprofiles for EBV, malaria, and KSHV were generated for 266 eBL patients, 78 non-eBL cancers, and 202 healthy children. KSHV and EBV loads were quantified by PCR.

resultsKSHV seroprevalence did not differ by study group but was associated with age. Seropositivity, defined by K8.1/LANA or in combination with 5 other KSHV antigens (ORF59, ORF65, ORF61, ORF38, and K5) was associated with antimalarial antibody levels to AMA1 (odds ratio [OR], 2.41, P < .001; OR, 2.07, P < .001) and MSP1 (OR, 2.41, P = .0006; OR, 5.78, P < .001), respectively. KSHV loads did not correlate with antibody levels nor differ across groups but were significantly lower in children with detectable EBV viremia (P = .014).

conclusionsAlthough KSHV-EBV dual infection does not increase eBL risk, EBV appears to suppress reactivation of KSHV while malaria exposure is associated with KSHV infection and/or reactivation. Both EBV and malaria should, therefore, be considered as potential effect modifiers for KSHV-associated cancers in sub-Saharan Africa.

Indexed as

AdolescentAge FactorsBurkitt LymphomaChildChild, PreschoolCoinfectionFemaleHerpesviridaeHerpesviridae InfectionsHumansInfantKenyaMaleSarcoma, KaposiSeroepidemiologic Studiesendemic Burkitt lymphomaEpstein-Barr virusKaposi sarcoma-associated herpesvirusKenyaPlasmodium falciparum malaria

Identifiers

PMID32072172
PMCPMC7296861
OpenAlexW3008784427

What Socratic 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 Socratic graph.