Malaria Is Associated With Kaposi Sarcoma-Associated Herpesvirus Seroconversion in a Cohort of Western Kenyan Children.


Journal

The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675

Informations de publication

Date de publication:
15 07 2021
Historique:
received: 12 08 2020
accepted: 25 11 2020
pubmed: 30 11 2020
medline: 2 2 2022
entrez: 29 11 2020
Statut: ppublish

Résumé

We aimed to determine whether Plasmodium falciparum infection affects age of Kaposi sarcoma-associated herpesvirus (KSHV) seroconversion in Kenyan children. Kenyan children (n = 144) enrolled at age 1 month, from 2 sites with different levels of malaria transmission (stable/high vs unstable/low) were followed to age 24 months. Plasma was tested for KSHV antibodies using enzyme-linked immunosorbent assay (ELISA; K8.1 and LANA) and a multiplex bead-based assay (K8.1, K10.5, ORF38, ORF50, and LANA) and whole blood tested for P. falciparum DNA using quantitative PCR. Cox proportional hazards models were used to assess associations between P. falciparum DNA detection, malaria annualized rate (P. falciparum detections/person-years), and enrollment site (malaria-high vs malaria-low) with time to KSHV seroconversion. KSHV seroprevalence was 63% by age 2 years when assessed by multiplex assay. Children with P. falciparum were at increased hazards of earlier KSHV seroconversion and, among children with malaria, the hazard of becoming KSHV seropositive increased significantly with increasing malaria annualized rate. Children from the malaria-high transmission region had no significant difference in hazards of KSHV seroconversion at 12 months but were more likely to become KSHV seropositive by age 24 months. Malaria exposure increases the risk for KSHV seroconversion early in life.

Sections du résumé

BACKGROUND
We aimed to determine whether Plasmodium falciparum infection affects age of Kaposi sarcoma-associated herpesvirus (KSHV) seroconversion in Kenyan children.
METHODS
Kenyan children (n = 144) enrolled at age 1 month, from 2 sites with different levels of malaria transmission (stable/high vs unstable/low) were followed to age 24 months. Plasma was tested for KSHV antibodies using enzyme-linked immunosorbent assay (ELISA; K8.1 and LANA) and a multiplex bead-based assay (K8.1, K10.5, ORF38, ORF50, and LANA) and whole blood tested for P. falciparum DNA using quantitative PCR. Cox proportional hazards models were used to assess associations between P. falciparum DNA detection, malaria annualized rate (P. falciparum detections/person-years), and enrollment site (malaria-high vs malaria-low) with time to KSHV seroconversion.
RESULTS
KSHV seroprevalence was 63% by age 2 years when assessed by multiplex assay. Children with P. falciparum were at increased hazards of earlier KSHV seroconversion and, among children with malaria, the hazard of becoming KSHV seropositive increased significantly with increasing malaria annualized rate. Children from the malaria-high transmission region had no significant difference in hazards of KSHV seroconversion at 12 months but were more likely to become KSHV seropositive by age 24 months.
DISCUSSION
Malaria exposure increases the risk for KSHV seroconversion early in life.

Identifiants

pubmed: 33249494
pii: 6010567
doi: 10.1093/infdis/jiaa740
pmc: PMC8280487
doi:

Substances chimiques

Antibodies, Viral 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

303-311

Subventions

Organisme : CCR NIH HHS
ID : HHSN261200800001C
Pays : United States
Organisme : NCI NIH HHS
ID : HHSN261200800001E
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA239588
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA102667
Pays : United States

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

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Auteurs

Katherine R Sabourin (KR)

Department of Epidemiology, Colorado School of Public Health, Denver, Colorado, USA.
Department of Immunology and Microbiology, University of Colorado, Denver, Colorado, USA.

Ibrahim Daud (I)

Centre for Global Health Research, Kenya Medical Research Institute, Kisumu, Kenya.

Sidney Ogolla (S)

Centre for Global Health Research, Kenya Medical Research Institute, Kisumu, Kenya.

Nazzarena Labo (N)

Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Frederick, Maryland, USA.

Wendell Miley (W)

Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Frederick, Maryland, USA.

Molly Lamb (M)

Department of Epidemiology, Colorado School of Public Health, Denver, Colorado, USA.

Robert Newton (R)

Department of Health Sciences, University of York, York, United Kingdom.

Denise Whitby (D)

Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Frederick, Maryland, USA.

Rosemary Rochford (R)

Department of Immunology and Microbiology, University of Colorado, Denver, Colorado, USA.

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