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Andisi, C.

Publications and source records attributed to Andisi, C..

2 recordsLinked to original sources

The complete mitochondrial genome of Tunga penetrans and insights into flea phylogeny

Tungiasis, one of the oldest and most neglected tropical diseases endemic to sub-Saharan Africa and the Americas, is caused by the female parasitic flea, Tunga penetrans. The flea burrows into the skin, leading to acute and chronic inflammation, often exacerbated by bacterial superinfection. Despite its significant public health impact, genomic studies on T. penetrans are scarce. Here, we present the first complete mitochondrial genome of T. penetrans, comprising 17,279 base pairs and encoding 13 protein-coding genes, 22 transfer RNAs and 2 ribosomal RNAs. Phylogenetic analysis of the cox2 gene revealed a divergent basal lineage from Brazil, supporting a South American origin of T. penetrans and highlights genetic differentiation within the Americas. Clustering of the Ecuadorian and African isolates further suggests historical connections, likely linked to transatlantic maritime trade. The tree highlights a strong South American origin and evidence of migration and diversification, facilitated by human and animal movement. Phylogenetic analysis of the complete genomes relying on the protein-coding genes of other fleas revealed that T. penetrans is closely related to Dorcadia ioffi, a semi-sessile flea of goats and sheep in China. This mitochondrial genome provides a critical resource for future studies on molecular epidemiology, evolutionary history, and control of tungiasis.

genomics↗

Plasmodium falciparum adapts its investment into replication versus transmission according to the host environment

The malaria parasite life cycle includes asexual replication in human blood, with a proportion of parasites differentiating to gametocytes required for transmission to mosquitoes. Commitment to differentiate into gametocytes, which is marked by activation of the parasite transcription factor ap2-g, is known to be influenced by host factors but a comprehensive model remains uncertain. Here we analyze data from 828 children in Kilifi, Kenya with severe, uncomplicated, and asymptomatic malaria infection over 18 years of falling malaria transmission. We examine markers of host immunity and metabolism, and markers of parasite growth and transmission investment. We find that inflammatory responses and reduced plasma lysophosphatidylcholine levels are associated with markers of increased investment in parasite sexual reproduction (i.e., transmission investment) and reduced growth (i.e., asexual replication). This association becomes stronger with falling transmission and suggests that parasites can rapidly respond to the within-host environment, which in turn is subject to changing transmission.

microbiology↗