Research Article
AssociationofTNF-Alpha,MBL2,NOS2,andG6PDwith
MalariaOutcomesinPeopleinSouthernGhana
GodfredFugtagbi,
1
PaulinaSOtu,
2
MubarakAbdul-Rahman ,
3
EbenezerKAidoo,
4
AminataCLo ,
5,6
BenAGyan ,
5
YawAAfrane ,
2
andLindaEAmoah
5,7
1
Department of Animal Biology and Conservation Science, College of Basic and Applied Sciences, University of Ghana,
Accra, Ghana
2
Department of Medical Microbiology, University of Ghana Medical School, University of Ghana, Accra, Ghana
3
Department of Pathology, University of Ghana Medical School, University of Ghana, Accra, Ghana
4
Department of Medical Laboratory, Accra Technical University, Accra, Ghana
5
Immunology Department, Noguchi Memorial Institute for Medical Research, University of Ghana, Accra, Ghana
6
Department of Medical Parasitology, Faculty of Medicine, University Cheikh Anta Diop, Dakar, Senegal
7
West Africa Center for Cell Biology of Infectious Pathogens, University of Ghana, Accra, Ghana
Correspondence should be addressed to Linda E Amoah; lamoah@noguchi.ug.edu.gh
Received 4 December 2020; Revised 11 January 2022; Accepted 10 February 2022; Published 28 February 2022
Academic Editor: Abd El-Latif Hesham
Copyright © 2022 Godfred Fugtagbi et al. is is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
Background. One major issue that has set back the gains of the numerous malaria control interventions that national malaria
control programs have implemented is asymptomatic malaria. Certain host genetic factors are known to influence symptomatic
malaria; however, not much is known about how host genetics influences the acquisition of asymptomatic malaria. Methods.
Genomic DNA was extracted from whole blood collected from 60 symptomatic and 149 nonfebrile (asymptomatic, N � 109, and
uninfected, N � 40) volunteers aged between 2 and 69 years from a high (Obom) and a low (Asutsuare) malaria transmission
setting in Southern Ghana. Restriction fragment length polymorphism (RFLP) was used to determine polymorphisms at the
MBL2 54, TNF-α 308, NOS2 954, and G6PD 202/376 gene loci. Results. Polymorphisms at the MBL2 54 and TNF-α 308 loci were
significantly different amongst the three categories of volunteers in both Asutsuare (p � 0.006) and Obom (p � 0.05). In
Asutsuare, a low malaria transmission area, the allele G has significantly higher odds (3.15) of supporting asymptomatic malaria as
against symptomatic malaria. ere were significantly higher odds of TNF-α genotype GA being associated with symptomatic
malaria as against asymptomatic malaria in both sites, Obom (p � 0.027) and Asutsuare (p � 0.027). e allele B of the G6PD
gene was more prevalent in symptomatic rather than asymptomatic parasite-infected individuals in both Obom (p � 0.001) and
Asutsuare (p � 0.003). Conclusion. Individuals in Southern Ghana carrying the TNF-α 308 GA genotype are more likely to exhibit
symptoms of malaria when infected with the malaria parasite as opposed to harboring an asymptomatic infection. Also, the B
allele of the G6PD gene is likely to prevent a P. falciparum-infected person from exhibiting symptoms and thereby promote
asymptomatic parasite carriage.
1.Background
Millions of individuals, particularly children and expectant
mothers, suffer from malaria in areas of Africa known for
Plasmodium falciparum endemicity. Ghana is one of the
countries hardest hit by malaria, accounting for about 2% of
global malaria cases. Despite successes in malaria control in
Ghana over the past decade, there were 161 cases per 1000 of
the population at risk as of 2019 [1]. Infections of humans
with Plasmodium falciparum (P. falciparum) can result in
different manifestations of malaria: asymptomatic and
symptomatic. Symptomatic cases could be uncomplicated or
complicated, and complicated cases could be severe malaria
or cerebral malaria [2]. Asymptomatic malaria infections are
Hindawi
Genetics Research
Volume 2022, Article ID 6686406, 11 pages
https://doi.org/10.1155/2022/6686406