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Malaria - What you need to know?

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Malarial Infections Drive the Incorporation of Gene Mutations into the Human Genome



Malaria is an infectious disease caused by Plasmodium, a genus of parasitic protozoa, and is among the most important infectious diseases in human history.1 Malaria has a long history of causing death and other devastating health problems, particularly in tropical and subtropical regions of the world such as Africa, Asia and South America. The plasmodium parasites that cause malaria have played an important role in shaping human evolution and hundreds of new mutations have arisen in the human genome due to selection by malaria.

There is growing evidence that malaria is the driving force for mutations that increase resistance and reduce susceptibility to human malaria.

Genes harboring malaria-driven mutations are often involved in immunity, inflammation, or cell adhesion. For example, glucose-6-phophatase deficiency, thalassemia, and sickle-cell anemia are diseases associated with erythrocyte defects and are also among the most common Mendelian or inherited diseases of humankind. Human erythrocytes (red blood cells) express large numbers of adhesion receptors and adhesion molecules on their surfaces which have important roles in normal human physiology and homeostasis. The development of underlying specific gene mutations causing glucose-6-phophatase deficiency, thalassemia, and sickle-cell anemia were all driven by malaria.

A mutation causing a change from valine to glutamate in the beta chain of the human hemoglobin gene resulted in the 'sickle cell gene' and causes sickle cell anemia when inherited as a homozygous mutation. An individual who inherits only one copy of the sickle cell gene, with the other copy being a normal hemoglobin gene, has the sickle cell trait. The sickle offers a protective immunity advantage against malaria and individuals carrying it may be less susceptible to contracting malaria than those who have two copies of the corresponding normal hemoglobin gene. It is not surprising that the frequency of sickle cell gene carriers may be highest in malaria-endemic regions of the world since the gene mutation was induced in response to malarial infection.

Malaria is carried and spread by mosquitos that host Plasmodium.

1 There are four species primarily infecting humans including Plasmodium falciparum (the most deadly form in humans) and Plasmodium vivax. However, there are more than 250 plasmodium species infecting other animals such as birds, lizards, non-human mammals such as gorillas, and snakes. Malaria is thought to have its origins in Africa from a single horizontal transfer between a gorilla infected with malaria who, in turn, infected a human. 2 Human migration led to malaria becoming a global problem.

Whereas malaria has been extensively studied, the mechanisms by which specific mutations offer protective immunity against malarial infection remain to be fully elucidated. Identifying additional malaria or other infectious agent-driven gene mutations that afford increased resistance or offer reduced susceptibility to infectious diseases may help researchers discover new mechanisms associated with protective immunity.

The threat of infection from a myriad of infectious agents is increasingly becoming a global problem, underscoring the importance of elucidating underlying mechanisms for infectious diseases. For example, Zika virus like malaria is carried and spread by mosquitos. The discovery in late 2015 that Zika virus infections in pregnant women in Brazil appeared to be associated with increased incidences of microcephaly in newborns set off worldwide panic. This led to some athletes and spectators opting out of the 2016 Summer Olympics, also known as the Games of the XXXI Olympiad, held in Rio de Janeiro, Brazil.

Although there is increasing evidence that

Zika can cause microcephaly in newborns

2 and other neurological diseases such as Guillain-Barré syndrome in adults, the underlying mechanisms of Zika viral infection remain to be elucidated. For example, why do some but not all women who were infected with Zika give birth to babies with microcephaly, a lifelong devastating neurological condition associated with brain defects? Why do some Zika-infected adults suffer only mild symptoms and others come down with as Guillain-Barré syndrome? Could it be throughout history that humankind has developed gene mutations, analogous to those developed in response to malarial infection, as common protective defenses against viral disease? Ongoing scientific research is needed to provide answers, and researchers are increasingly using reagents4 and kits3 from MyBioSource to study infectious diseases.

Products for Studying Malaria:


• Malaria Pv. MSP antigen (merozoite surface protein) (Catalog #MBS596068)
• Plasmodium falciparum LDH monoclonal antibody (Catalog #MBS832018)
• Plasmodium falciparum Real Time PCR Kit (Catalog #MBS486008)
• Plasmodium falciparum HSP70 Recombinant Protein (Catalog #MBS434231)
• Plasmodium Malariae Real Time PCR Kit (Catalog #MBS598091)
• Plasmodium vivax monoclonal antibody (Catalog #MBS838624)
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References
1. Faust C, Dobson AP Primate malarias: Diversity, distribution and insights for zoonotic Plasmodium. One Health 2016. doi:10.1016/j.onehlt.2015.10.001.
2. Molina-Cruz A, Canepa GE, Kamath N. et al. Plasmodium evasion of mosquito immunity and global malaria transmission: The lock-and-key theory. PNAS 2015. doi: 10.1073/pnas.1520426112 Molina-Cruz A, Canepa GE, Kamath N. et al.
3. Clinical and imaging finding in an infant with Zika embryopathy. Culjat M, Darling SE, VR Nerurkar et al. Clin Infect Dis 2016. doi: 10.1093/cid/ciw324. MyBioSource product cited: Zika IgM ELISA Kit Cat. no. MBS109003.
4. Markwalter CF, Davis KM, Wright DW. Immunomagnetic capture and colorimetric detection of malarial Biomarker Plasmodium falciparum lactate dehydrogenase. ?Anal Biochem
2015. doi:10.1016/j.ab.2015.10.003. MyBioSource product cited: Plasmodium falciparum LDH (PfLDH) monoclonal antibody, Cat. no. MBS832018.
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