Written by Girish Khera on June 19, Biochemical as well as demographic evidence substantiates the theory that sickle-cell anemia imparts resistance to malaria. The relationship between malaria and sickle cell anemia, therefore, needs to be studied in detail. The Atlantic states that as per the research published in the last few years, tolerance may be a crucial factor in determining whether individuals will survive infections such as malaria, cholera, and sepsis. Therefore, by better understanding the tolerance mechanisms, new ways can be figured out to enhance them and also open unexpected avenues for drug development. The researchers have envisioned the journey from infection to illness to recovery as a loop. The infected mosquito bites the person and transfers the malarial parasite into his bloodstream that keeps multiplying inside the cell, hidden from the immune system. The parasite ultimately ruptures its own cellular refuge and, in the process, releases toxins which damage the surrounding tissue. These variables, when plotted on a graph, resembled the above recovery loop.
Sickle cell anaemia is a major chapter within haemolytic anaemias; at the same time, its epidemiology is a remarkable signature of the past and present world distribution of Plasmodium falciparum malaria. In this brief review, in keeping with the theme of this journal, we focus on the close and complex relationship betweeen this blood disease and this infectious disease. On one hand, heterozygotes for the sickle gene AS are relatively protected against the danger of dying of malaria, as now firmly established through a number of clinical field studies from different parts of Africa. In addition, experimental work is consistent with a plausibile mechanism: namely, that in AS heterozygotes P falciparum -infected red cells sickle preferentially and are then removed by macrophages. On the other hand, patients who are homozygous for the sickle gene and therefore suffer from sickle cell anaemia SCA are highly susceptible to the lethal effects of malaria. The simplest explanation of this fact is that malaria makes the anaemia of SCA more severe; in addition, in SCA there is often hyposplenism, which reduces clearance of parasites. From the point of view of public health it is important that in malaria-endemic countries patients with SCA, and particularly children, be protected from malaria by appropriate prophylaxis. The history of sickle cell anaemia SCA lists several gold medals.
Sickle cell malaria protect how does against
A linkage between presence of Sickle Haemoglobin HbS and protection from malaria infection and clinical manifestations in certain areas was suspected from early observations and progressively elucidated by more recent studies. Research has confirmed the abovementioned connection, but also clarified how such protection may be abolished by coexistence of sickle cell trait HbS trait and alpha thalassemia, which may explain the relatively low incidence of HbS trait in the Mediterranean. The mechanisms of such protective effect are now being investigated: factors of genetic, molecular and immunological nature are prominent. As for genetic factors attention is given to the role of the red blood cell RBC membrane complement regulatory proteins as polymorphisms of these components seem to be associated with resistance to severe malaria; genetic ligands like the Duffy group blood antigen, necessary for erythrocytic invasion, and human protein CD36, a major receptor for P. Genome-wide linkage and association studies are now carried out too, in order to identify genes associated with malaria resistance. Only a minor role is attributed to intravascular sickling, phagocytosis and haemolysis, while specific molecular mechanisms are the object of intensive research: among these a decisive role is played by a biochemical sequence, involving activation of haeme oxygenase HMO-1, whose effect appears mediated by carbon monoxide CO.