WASHINGTON, May 9, 2022 (Newswire.com) - A recently published article in Experimental Biology and Medicine (Volume 247, Issue 8, April, 2022) identifies a new target for malaria treatment. The study, led by Dr. Evans Raballah in the University of New Mexico-Kenya Global Health Program in Kisumu and Siaya (Kenya), reports that variations in the C3 gene, an immune response gene, impacts the susceptibility to and mortality of malaria in children.
Most global malaria deaths occur in African children less than five years of age. African children with malaria suffer from severe malarial anemia, which is caused by both the destruction and reduced production of red blood cells. Natural protection against malaria and vaccine-induced immunity rely on the generation of antibodies that activate the complement system, a complex part of the immune system. Therefore, genetic variation in immune genes can impact malaria disease outcomes.
In this study, Dr. Raballah and colleagues examined the role of two mutations in the immune response gene complement component 3 (C3) in malarial immunity in Kenyan children. Children who inherited the most common combination of these mutations had a decreased risk of malaria. In contrast, children who inherited less common combinations of these mutations had an increased risk of contracting malaria. While there are currently approved immunotherapies for malaria, these findings suggest that efforts aimed at targeting the complement system may offer important treatment alternatives for Malaria. Dr. Raballah said, "We are grateful to have the opportunity to address the challenges of severe malaria in one of the most vulnerable pediatric populations around the globe. It is our sincere hope that our novel discoveries on the pathogenesis of severe malaria can foster the development of future therapeutics to reduce the burden of morbidity and mortality due to malaria."
Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said, "Dr. Raballah and colleagues have demonstrated that C3 variants, in the MG1 and thioester-containing domain, influence the risk of developing both malaria and severe malarial anemia during the stage at which children develop naturally acquired immunity. These important studies provide a potential target for immunotherapy against malaria."
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Source: Experimental Biology and Medicine