Malaria parasite triggers changes in gene regulators

Malaria affects more than 200 million people annually and is one of the leading causes of child death from infectious diseases. Understanding how the parasite evades the host immune system and why individuals and populations differ in their ability to respond to the infection could pinpoint genes and biological pathways for the development of therapeutics and vaccines. 

A study, led by researchers at New York University Abu Dhabi (NYUAD), investigated the immune responses, genetic profiles, and parasite loads of children infected with the malaria parasite in rural Burkina Faso.  

The analyses showed that the infection triggered changes in the expression of a group of short RNA molecules, microRNAs, that regulate genes involved in the adaptive immune response. Some of these microRNAs were involved in triggering the death of lymphocytes, immune cells responsible for producing parasite-specific antibodies and long-term memory. This helps the parasite evade the immune response to invade and then proliferate in other blood cells. 

“Our results highlight the importance of host immunity. We argue that boosting adaptive immunity is as important as reducing the parasite load,” says NYUAD biologist, Youssef Idaghdour.

Further analyses showed that small individual genetic variations in the children’s DNA alter the expression levels of some of the microRNAs investigated in the study. Genetic variations were also associated with the parasite load. These findings could explain why some children withstand infection better than others. 

“We have initiated similar work on other ethnic groups to understand why some populations in Africa are more immune to the disease than others,” says Idaghdour.

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