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