Haemoglobinopathies and glucose-6-phosphate dehydrogenase deficiency in a malaria endemic region of Manipur, northeast India

Achoubi, Nongthombam; Asghar, Mohammad; Meitei, Sanjenbam Yaiphaba; Sachdeva, M.P.; Sarawathy, Kallur Nava; Murry, Benrithung

doi:10.1537/ase.090408

Cited by 7 publications

(3 citation statements)

References 14 publications

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“…19 A study conducted in Manipur in 2010 by Achoubi among the different communities found high prevalence among the Manipuri Muslims (21.32%) followed by the Brahmins (9.45%) and Kabui (7.84%). 20 In Mizoram also, a high prevalence of 17.5% was found in the population. 21 In this study, it has been seen that among the tea garden labourers 7.6% of them had G6PD deficiency.…”

Section: Discussionmentioning

confidence: 92%

Study of Glucose 6-Phosphate Dehydrogenase (G6pd) Deficiency in Jaundiced Neonates of a Tertiary Care Centre of North-East India

Islam¹,

Bora²,

Ramasamy³

et al. 2016

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Section: Discussionmentioning

confidence: 92%

Study of Glucose 6-Phosphate Dehydrogenase (G6pd) Deficiency in Jaundiced Neonates of a Tertiary Care Centre of North-East India

Islam¹,

Bora²,

Ramasamy³

et al. 2016

jemds

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“…Gene frequency was calculated by simple gene count method. Several reports regarding G6PD deficiency were published in several caste groups/tribes like Parsee [13], Muslim [20], Brahmin [21][22][23], Jat [22], Rajputs [18], Vatalya Prajapati [24], Nagas [25], Kharia [26], Bhuyan [26], Danguria tharu [27], Kabui [20], and so forth. The frequency is higher among the tribals than the caste populations [15].…”

Section: Methodsmentioning

confidence: 99%

Epidemiological Study of Glucose-6-phosphate Dehydrogenase Deficiency in Scheduled Caste Population of India

Rai

Kumar

2012

Journal of Anthropology

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The aim of the present study was to determine the glucose-6-phostphate dehydrogenase (G6PD) deficiency in scheduled caste (SC) population of eastern Uttar Pradesh, India. After taking clearance certificate from the Institutional Ethics Committee, blood samples were collected from total 200 healthy individuals belonging to scheduled caste. G6PD deficiency analysis was done by methemoglobin test according to the method of Brewer et al. (1962). Out of 200 samples, 20 individuals were glucose-6-phosphate dehydrogenase deficient and 22 samples were heterozygous that is, carriers. The percentage of G6PD deficient (Gd+/+) and G6PD carrier (Gd+/Gd−) phenotypes were 10% and 11%, respectively. The frequency of mutant allele (Gd−) was observed 0.172. Early detection and prevention is the key strategy for successful management and control of this genetic disease.

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“…These sickle genes are responsible and capable of protecting these tribals from deadly malaria [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21]. In addition to the sickle cell gene, some other genes for red cell genetic disorders, such as Hb-C, β-thalassaemia, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, and blood groups are also found for genetic resistance to malaria in human populations [22][23][24][25][26][27][28][29][30][31][32][33][34][35][36]. This current communication provides factual and scientific information about the origin of sickle cell genes in the context of natural selection and how these genes protect tribal individuals from malaria.…”

Section: Introductionmentioning

confidence: 99%

How Do Sickle Cell Genes Protect Tribal People from Deadly Malaria? Is This a Type of Natural Selection?

Choubisa

2023

annhematoloncol

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In humans, genetic mutations have led to the formation of several haemoglobin (Hb) variants during human evolution. These mutations usually occur in the genes for a and Β- polypeptide or globin chains of haemoglobin located on chromosomes 11 and 16, respectively. Among these haemoglobin variants, sickle cell haemoglobin (Hb-S) is highly significant in the humans. In fact, this abnormal or mutant haemoglobin is the resultant of a point mutation in the gene for Β-globin, located on chromosome 11. No doubt, this sickle cell gene is relatively more prevalent among tribal people and widely distributed in those geographic regions where the dreaded Plasmodium falciparum-malaria is hyperendemic. In the human population, this mutant gene exists in two forms, the heterozygous (Hb-AS) and homozygous (Hb-SS) states. But this sickle cell gene is also found in association with other mutant genes of erythrocyte or red cell genetic disorders, such as abnormal Hb-C, Β-thalassemia, G-6-PD enzyme deficiency, etc. It is well known that tribal people generally live in forest ecosystem where dreaded malaria is also found to be endemic. How have these tribal people been able to protect themselves from this dreaded malaria for thousands of years in such a hostile environment, when they were most likely to be infected with the malaria parasite? Actually, its secret is hidden in these sickle cell genes only. Tribal individuals who have these genes in the heterozygous state (Hb-AS) do not get malaria or are protected from malaria and lead a healthy life. Several studies have confirmed that AS heterozygote people are protected against malaria. In contrast, those who have these genes in the homozygous (Hb-SS) state (homozygotes) develop sickle cell anaemia, which is fatal. Such patients die early due to severe malaria i.e AS heterozygotee individuals have a double advantages. In fact, it is a type of natural selection and also shows a balanced polymorphism in tribal people which is based on Darwin’s theory. This current communication provides factual and scientific information about the origin of sickle cell genes in the context of natural selection and how these genes protect tribal individuals from malaria. This communication is useful and important for zoologists, scientists working on human evolution, and medical scientists.

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Haemoglobinopathies and glucose-6-phosphate dehydrogenase deficiency in a malaria endemic region of Manipur, northeast India

Cited by 7 publications

References 14 publications

Study of Glucose 6-Phosphate Dehydrogenase (G6pd) Deficiency in Jaundiced Neonates of a Tertiary Care Centre of North-East India

Study of Glucose 6-Phosphate Dehydrogenase (G6pd) Deficiency in Jaundiced Neonates of a Tertiary Care Centre of North-East India

Epidemiological Study of Glucose-6-phosphate Dehydrogenase Deficiency in Scheduled Caste Population of India

How Do Sickle Cell Genes Protect Tribal People from Deadly Malaria? Is This a Type of Natural Selection?

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