Abstract
Human African trypanosomiasis (HAT), or sleeping sickness, caused by Trypanosoma brucei gambiense, is associated with diverse clinical outcomes. Host’s genetic factors involved in immunity are potential factors that can regulate infection. Genetic polymorphisms within HLA-G could influence the level of HLA-G expression and therefore play a critical role in infection outcomes. The goal of our study was to investigate the association of 14 bp Indel HLA-G polymorphism with the susceptibility/resistance to HAT. DNA samples were collected from 119 cases, 221 controls and 43 seropositive individuals living in Ivorian HAT foci. The 14 bp Indel polymorphism was determined by PCR. Homozygous individuals for 14 bp insertion had a lower risk of progressing to active HAT (p = 0.012, OR = 0.27, 95% CI: 0.09 - 0.8). Moreover, the frequency of 14 bp insertion homozygous genotype was higher in the seropositive group (11%) than in the HAT cases group (3%) (p = 0.043, OR = 0.27, 95% CI: 0.07 - 0.99), which suggested a protective effect of 14 bp insertion homozygous genotype. Genetic polymorphisms in HLA-G may be associated with a variable risk to develop HAT. The 14 bp insertion appears to favour the occurrence of long-lasting T. b. gambiense latent infections.
Highlights
Homozygous individuals for 14 bp insertion had a lower risk of progressing to active Human African trypanosomiasis (HAT) (p = 0.012, odds ratios (OR) = 0.27, 95% confidence intervals (CI): 0.09 - 0.8)
Human African trypanosomiasis (HAT), or sleeping sickness, caused by Trypanosoma brucei gambiense (T. b. gambiense) is classically described as a chronic infection characterized by an early hemolymphatic stage associated with nonspecific symptoms such as intermittent fevers and headaches, followed by a meningoencephalitic stage in which the parasite invades the central nervous system and causes neurological disorders and death if left untreated
[16] Among the 17 variation sites that have been identified in 3’ untranslated region (3’UTR), the 14 bp Insertion/Deletion polymorphism has been extensively studied in different pathologies including infectious diseases and seems to play an important role on Human leucocyte antigen (HLA)-G alternative splicing and HLA-G messenger RNA stability [16] [17] [18]
Summary
Human African trypanosomiasis (HAT), or sleeping sickness, caused by Trypanosoma brucei gambiense (T. b. gambiense) is classically described as a chronic infection characterized by an early hemolymphatic stage (stage 1) associated with nonspecific symptoms such as intermittent fevers and headaches, followed by a meningoencephalitic stage (stage 2) in which the parasite invades the central nervous system and causes neurological disorders and death if left untreated. Human African trypanosomiasis (HAT), or sleeping sickness, caused by Trypanosoma brucei gambiense HLA-G is a non-classical major histocompatibility complex (MHC) class I gene. It is located on chromosome 6p21.3 and encompasses 4144 nucleotides distributed across eight exons and seven introns. Exon 8 consists in a regulatory 3’ untranslated region (3’UTR) that plays an important role in gene expression [16] Among the 17 variation sites that have been identified in 3’UTR, the 14 bp Insertion/Deletion polymorphism has been extensively studied in different pathologies including infectious diseases and seems to play an important role on HLA-G alternative splicing and HLA-G messenger RNA stability [16] [17] [18]
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