Effect of hookworm infection and anthelmintic treatment on naturally acquired antibody responses against the GMZ2 malaria vaccine candidate and constituent antigens.


Journal

BMC infectious diseases
ISSN: 1471-2334
Titre abrégé: BMC Infect Dis
Pays: England
ID NLM: 100968551

Informations de publication

Date de publication:
08 Apr 2021
Historique:
received: 13 11 2020
accepted: 30 03 2021
entrez: 9 4 2021
pubmed: 10 4 2021
medline: 4 5 2021
Statut: epublish

Résumé

Malaria and helminths diseases are co-endemic in most parts of sub-Saharan Africa. Immune responses from each of these pathogens interact, and these interactions may have implications on vaccines. The GMZ2 malaria vaccine candidate is a fusion protein of Plasmodium falciparum merozoite surface protein 3 (MSP3) and glutamate rich protein (GLURP R0). GMZ2 has recently showed modest efficacy in a phase IIb multicenter trial. Here, we assessed the effect of hookworm (Necator americanus) infection and anthelmintic treatment on naturally acquired antibody responses against GMZ2 and constituent antigens. This longitudinal cross-sectional study was conducted in the Kintampo North Municipality of Ghana. Blood and stool samples were taken from 158 individuals (4-88 years old) infected with either P. falciparum alone (n = 59) or both hookworm and P. falciparum (n = 63) and uninfected endemic controls (n = 36). Stool hookworm infection was detected by the Kato-Katz method and PCR. Malaria parasitaemia was detected by RDT, light microscopy and P. falciparum-specific 18S rRNA gene PCR. Serum samples were obtained prior to hookworm treatment with a single dose of albendazole (400 mg) and 3 weeks (21 days) after treatment. Levels of IgG1, IgG3 and IgM against GMZ2, MSP3 and GLURP R0 were measured by ELISA and compared among the groups, before and after treatment. Participants with P. falciparum and hookworm co-infection had significantly higher IgG3 levels to GMZ2 than those with only P. falciparum infection and negative control (p < 0.05) at baseline. Treatment with albendazole led to a significant reduction in IgG3 levels against both GMZ2 and GLURP R0. Similarly, IgM and IgG1 levels against MSP3 also decreased following deworming treatment. Individuals with co-infection had higher antibody responses to GMZ2 antigen. Treatment of hookworm/malaria co-infection resulted in a reduction in antibody responses against GMZ2 and constituent antigens after albendazole treatment. Thus, hookworm infection and treatment could have a potential implication on malaria vaccine efficacy.

Sections du résumé

BACKGROUND BACKGROUND
Malaria and helminths diseases are co-endemic in most parts of sub-Saharan Africa. Immune responses from each of these pathogens interact, and these interactions may have implications on vaccines. The GMZ2 malaria vaccine candidate is a fusion protein of Plasmodium falciparum merozoite surface protein 3 (MSP3) and glutamate rich protein (GLURP R0). GMZ2 has recently showed modest efficacy in a phase IIb multicenter trial. Here, we assessed the effect of hookworm (Necator americanus) infection and anthelmintic treatment on naturally acquired antibody responses against GMZ2 and constituent antigens.
METHODS METHODS
This longitudinal cross-sectional study was conducted in the Kintampo North Municipality of Ghana. Blood and stool samples were taken from 158 individuals (4-88 years old) infected with either P. falciparum alone (n = 59) or both hookworm and P. falciparum (n = 63) and uninfected endemic controls (n = 36). Stool hookworm infection was detected by the Kato-Katz method and PCR. Malaria parasitaemia was detected by RDT, light microscopy and P. falciparum-specific 18S rRNA gene PCR. Serum samples were obtained prior to hookworm treatment with a single dose of albendazole (400 mg) and 3 weeks (21 days) after treatment. Levels of IgG1, IgG3 and IgM against GMZ2, MSP3 and GLURP R0 were measured by ELISA and compared among the groups, before and after treatment.
RESULTS RESULTS
Participants with P. falciparum and hookworm co-infection had significantly higher IgG3 levels to GMZ2 than those with only P. falciparum infection and negative control (p < 0.05) at baseline. Treatment with albendazole led to a significant reduction in IgG3 levels against both GMZ2 and GLURP R0. Similarly, IgM and IgG1 levels against MSP3 also decreased following deworming treatment.
CONCLUSION CONCLUSIONS
Individuals with co-infection had higher antibody responses to GMZ2 antigen. Treatment of hookworm/malaria co-infection resulted in a reduction in antibody responses against GMZ2 and constituent antigens after albendazole treatment. Thus, hookworm infection and treatment could have a potential implication on malaria vaccine efficacy.

Identifiants

pubmed: 33832450
doi: 10.1186/s12879-021-06027-5
pii: 10.1186/s12879-021-06027-5
pmc: PMC8028774
doi:

Substances chimiques

Anthelmintics 0
Antibodies, Protozoan 0
Antigens, Protozoan 0
GMZ2 vaccine 0
Immunoglobulin G 0
Malaria Vaccines 0
Protozoan Proteins 0
merozoite surface protein 3, Plasmodium 0
glutamate-rich protein, Plasmodium 145112-81-8
Albendazole F4216019LN

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

332

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Auteurs

Benjamin Amoani (B)

Department of Biomedical Science, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana.
Department of Molecular Medicine, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.

Ben Gyan (B)

Department of Immunology, Noguchi Memorial Institute for Medical Research, College of Health Sciences, University of Ghana, Legon, Ghana.

Samuel Asamoah Sakyi (SA)

Department of Molecular Medicine, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana. samasamoahsakyi@yahoo.co.uk.

Emmanuel Kwasi Abu (EK)

Department of Optometry, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana.

Samuel Victor Nuvor (SV)

Department of Microbiology and Immunology, School of Medical Sciences, University of Cape Coast, Cape Coast, Ghana.

Precious Barnes (P)

Department of Physician Assistant, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana.

Tracy Sarkodie-Addo (T)

Department of Immunology, Noguchi Memorial Institute for Medical Research, College of Health Sciences, University of Ghana, Legon, Ghana.

Benjamin Ahenkorah (B)

Department of Molecular Medicine, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.
Department of Medical Laboratory Science, Bolgatanga Technical University, Bolgatanga, Upper East Region, Ghana.

Christian Sewor (C)

Department of Biomedical Science, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana.

Duah Dwomoh (D)

Department of Biostatistics, School of Public Health, University of Ghana, Accra, Ghana.

Michael Theisen (M)

Department for Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark.
Centre for Medical Parasitology at Department of International Health, Immunology, and Microbiology, University of Copenhagen, and Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.

Michael Cappello (M)

Partnerships for Global Health, Department of Pediatrics, Yale School of Medicine, Yale University, New Haven, CT, USA.

Michael D Wilson (MD)

Parasitology Department, Noguchi Memorial Institute for Medical Research, College of Health Sciences, University of Ghana, Legon, Ghana.

Bright Adu (B)

Department of Immunology, Noguchi Memorial Institute for Medical Research, College of Health Sciences, University of Ghana, Legon, Ghana.

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