By: Richard Paul, Functional Genetics of Infectious Diseases Unit, Institut Pasteur, Paris
Mutating ourselves into a corner: Malaria parasite responses to haematological modifications
As encapsulated by the Red Queen hypothesis, hosts and their pathogens are locked into a co-evolutionary arms race with adaptation and counter-adaptation to promote survival. The human genome has been thus remodelled over the millennia and haemoglobinopathies, such as Sickle cell trait, are quintessential examples of this, protecting from severe malaria.
However, haemoglobinopathies can come at a cost and humans have evolved suites of successive mutations to counter such negative side-effects. Hereditary persistence of foetal haemoglobin is a benign condition where the production of foetal haemoglobin (HbF) continues into adulthood and alleviates the severity of sickle cell disease and β-thalassemias.
The protective effect afforded by these haemoglobinopathies against malaria has additionally been suggested to be in part due to HbF. Malaria parasites have evolved strategies to respond to a hostile hematological environment by increasing investment in transmission.
Study of genetic determinants of prolonged fetal hemoglobin production in two populations with endemic malaria showed that whilst increased fetal hemoglobin afforded protection from disease, it increased transmissibility and enabled parasite persistence in red cells normally deleterious for the parasite. Personal protection seemingly comes at a cost to the community.
Hosts: Joacim Rocklöv, Oliver Billker Contact: Nóra Lehotai, email@example.com
Joint Seminar by The Department of Public Health and Clinical Medicine & Molecular Infection Medicine Sweden (MIMS)