In particular, they examined two parasite genes: ap2-g (a transcription factor required for gametocyte activation) and PfSir2a (an environmental sensor linked to regulation of antigenic variation and replication), and a marker for parasite biomass. Across this cohort, they examined markers of host immune responses and metabolism and compared markers of parasite growth and transmission investment. To address this gap, Abdi and colleagues analysed data from 828 children in Kilifi, Kenya with severe, mild and asymptomatic malaria between 19. However, the factors that lead to activation of this gene have not previously been well characterised.”
“Differentiation in gametocytes is known to be marked by the activation of a gene called ap2-g in the parasite. falciparum has a complex life cycle, involving asexual replication in human blood, and differentiation into gametocytes required for transmission to mosquitoes,” explains lead author Abdirahman Abdi, a Senior Research Scientist at the KEMRI Wellcome Trust Research Programme, Kilifi, Kenya and the Pwani University Biosciences Research Centre, Pwani University, Kilifi, Kenya. This requires the parasite to differentiate into specialised cells called gametocytes – cells which eventually become gametes which are necessary for sexual reproduction. In order to transmit from one human host to another, the parasite must first transfer to a mosquito. Around 70% of malaria deaths occur in children under the age of five in Africa and are caused by a single parasite, P.
Malaria represents one of the world’s greatest public health concerns In 2021, an estimated 619,000 deaths and 247 million cases were reported. These low levels of LPC are associated with increased parasite investment into transmission to another host, by increasing sexual reproduction and decreasing asexual replication.
The research shows that the inflammatory responses to malaria infection in the human body during low transmission are associated with reduced levels of a chemical called lysophospatidylcholine (LPC) in the blood plasma. The findings, published in eLife and led by researchers at the KEMRI-Wellcome Trust and the University of Glasgow, shed further light on how malaria parasites adapt to changing within-human environments as a result of changing transmission intensity – a measure of the level of transmission of the malaria parasite in a particular area. New research sheds light on how malaria parasites adapt to their human hostsĪ study has characterised the factors that cause the malaria parasite, Plasmodium falciparum, to invest resources into reproduction – to maximise transmission to other hosts – or replication – to ensure survival within its current human host.
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