Categorical complexities of Plasmodium falciparum malaria in individuals is associated with genetic variations in ADORA2A and GRK5 genes

Gupta, Himanshu; Jain, Aditya; Saadi, Abdul Vahab; Vasudevan, Thanvanthri Gururajan; Hande, Manjunath; D’Souza, Sydney C.; Ghosh, Susanta Kumar; Umakanth, Shashikiran; Satyamoorthy, Kapaettu

doi:10.1016/j.meegid.2015.06.010

Cited by 17 publications

(9 citation statements)

References 62 publications

(59 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the same study, a severe malaria protective effect of the SNP rs201346212 heterozygous genotype ( CD36 gene) was described. Other possible evidences on P. falciparum malaria resistance include additional genes such as GRK5 , a G protein receptor (mutation rs2230345) 52 , IL-10 (rs1800890), FCGR2B (rs105050) and TIRAP (rs8177374).…”

Section: Methodsmentioning

confidence: 99%

Malaria was a weak selective force in ancient Europeans

Gelabert

Olalde

de-Dios

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Malaria, caused by Plasmodium parasites, is thought to be one of the strongest selective forces that has shaped the genome of modern humans and was endemic in Europe until recent times. Due to its eradication around mid-twentieth century, the potential selective history of malaria in European populations is largely unknown. Here, we screen 224 ancient European genomes from the Upper Palaeolithic to the post-Roman period for 22 malaria-resistant alleles in twelve genes described in the literature. None of the most specific mutations for malaria resistance, like those at G6PD, HBB or Duffy blood group, have been detected among the available samples, while many other malaria-resistant alleles existed well before the advent of agriculture. We detected statistically significant differences between ancient and modern populations for the ATP2B4, FCGR2B and ABO genes and we found evidence of selection at IL-10 and ATP2B4 genes. However it is unclear whether malaria is the causative agent, because these genes are also involved in other immunological challenges. These results suggest that the selective force represented by malaria was relatively weak in Europe, a fact that could be associated to a recent historical introduction of the severe malaria pathogen.The malaria parasite Plasmodium falciparum is one of the main causes of child mortality worldwide, although other species from the same genus, P. vivax, P. malariae and P. ovale are also causative agents of the disease. Therefore, it is not surprising that malaria is one of the strongest known selective pressures that have recently shaped the human genome. Malaria is the evolutionary driving force behind sickle-cell disease (HbS), thalassemia, glucose-6-phosphatase deficiency (G6PD) and other erythrocyte defects that together comprise the most common Mendelian diseases of humankind. Remarkably, populations from different geographical areas have developed different genetic mechanisms adapted to malaria resistance; for instance, the HbS allele at the HBB gene is common in Africa but rare in Southeast Asia, whereas the HbE alelle shows a reversed pattern. Resistance to malaria includes primarily genes involved in immunological response, but also some involved in inflammation and cell adhesion and even genes related to metabolic pathways. The fact that different malaria-resistance alleles have arisen in different places suggests that this adaptation occurred relatively recent in human history, at least well after the Out of Africa migration 1 . P. falciparum may have rapidly spread from its African tropical origins to other tropical and subtropical regions of the world only within the last 6,000 years 2 . The recent origin of the worldwide P. falciparum populations, which are the most malignant of human malarial parasites, may account for its virulence 3 . Thus, haplotype analysis at the G6PD locus suggests that the African resistance allele to P. falciparum originated within the last 10,000 years 4 while a similar analysis at the HbE alleles (variants of the HBB gene) in...

show abstract

Section: Methodsmentioning

confidence: 99%

Malaria was a weak selective force in ancient Europeans

Gelabert

Olalde

de-Dios

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Adora2a has been shown to be involved in the infection of Plasmodium falciparum, a common pathogen of malaria (Auburn et al, 2010;Gupta et al, 2015). The ligand adenosine activates the Adora2a receptor, which in turn triggers other downstream processes.…”

Section: Blood-brain Barrier Disruption In Response To Borrelia Infecmentioning

confidence: 99%

A Transcriptome Study of Borrelia burgdorferi Infection in Murine Heart and Brain Tissues

Carey¹,

Ho²

2017

View full text Add to dashboard Cite

“…This includes parasite genes, and var groups A, B, as well as domain cassette (DC) 8, DC11 and DC13 have been shown to be associated with SM [ 7 , 8 ]. Similarly, among host genes, polymorphisms in intercellular adhesion molecule 1 (ICAM-1), cluster of differentiation 36 (CD36), tumor necrosis factor-alpha (TNF-α), Interferon-gamma (IFN-γ), interleukin-1β, complement receptor-1 (CR-1), ATP binding cassette subfamily B member 1 (ABCB1) and adenosine A2a receptor (ADORA2A) have linked to the development of SM [ 9 – 16 ]. Ribonuclease 3 ( RNASE 3 ), which encodes eosinophil cationic protein (ECP), an important protein produced by eosinophils during inflammation and infection [ 17 , 18 ], was found to increase susceptibility to SM [ 19 – 22 ].…”

Section: Introductionmentioning

confidence: 99%