Biology subjects

Athni, T. S.

Publications and source records attributed to Athni, T. S..

3 recordsLinked to original sources

bioRxiv2024

Australian vertebrate hosts of Japanese encephalitis virus; a review of the evidence

Japanese Encephalitis Virus (JEV) transmission in temperate Australia has underscored a critical need to characterise transmission pathways and identify probable hosts of infection within the country. This systematic review consolidates existing research on the vertebrate hosts of JEV that are known to exist in Australia. Specifically, we aim to identify probable species for JEV transmission, their potential role as either a spillover or maintenance host and identify critical knowledge gaps. Data were extracted from studies involving experimental infection, seroprevalence, and virus isolation and were available for 22 vertebrate species known to reside in Australia. A host competence score was calculated to assess the potential for a given species to infect JEV vectors and to quantity their possible role in JEV transmission. Based on the host competence score and ecology of each species, we find ardeid birds, feral pigs, and flying foxes have potential as maintenance hosts for JEV in the Australian context. We also note that brushtail possums and domestic pigs have potential as spillover hosts under certain outbreak conditions. However, evidence to confirm these roles in localized transmission or outbreaks is sparse, emphasizing the need for further targeted research. This review provides a foundation for future investigations into JEV transmission in Australia, advocating for enhanced surveillance and standardized research methodologies to better understand and mitigate the viruss impact.

ecology↗

bioRxiv2024

Climate variables and urbanization drive changes in the distribution of S. mansoni competent snails in Brazil: novel results from a counterfactual analysis

Schistosomiasis is a neglected tropical disease caused by Schistosoma parasites. Schistosoma are obligate parasites of freshwater Biomphalaria snails, so controlling snail populations is critical to reducing transmission risk. As snails are sensitive to environmental conditions, we expect their distribution is significantly impacted by global change. Here, we leveraged machine learning, remote sensing, and 30 years of snail occurrence records to map the historical and current distribution of competent Biomphalaria throughout Brazil. We identified key features influencing the distribution of suitable habitat and determined how Biomphalaria habitat has changed with climate and urbanization over the last three decades. Our models show that climate change has driven broad shifts in snail host range, whereas expansion of urban and peri-urban areas has driven localized increases in habitat suitability. Elucidating change in Biomphalaria distribution - while accounting for non-linearities that are difficult to detect from local case studies - can help inform schistosomiasis control strategies.

ecology↗

bioRxiv2020

A ubiquitin-based mechanism for the oligogenic inheritance of heterotaxy and heart defects

The etiology of congenital heart defects (CHDs), amongst the most common human birth defects, is poorly understood partly because of its complex genetic architecture. Here we show that two genes previously implicated in CHDs, Megf8 and Mgrn1, interact genetically and biochemically to regulate the strength of Hedgehog signaling in target cells. MEGF8, a single-pass transmembrane protein, and MGRN1, a RING superfamily E3 ligase, assemble to form a transmembrane ubiquitin ligase complex that catalyzes the ubiquitination and degradation of the Hedgehog pathway transducer Smoothened. Homozygous Megf8 and Mgrn1 mutations increased Smoothened abundance and elevated sensitivity to Hedgehog ligands. While mice heterozygous for loss-of-function Megf8 or Mgrn1 mutations were normal, double heterozygous embryos exhibited an incompletely penetrant syndrome of CHDs with heterotaxy. Thus, genetic interactions between components of a receptor-like ubiquitin ligase complex that tunes morphogen signaling strength can cause a birth defect syndrome inherited in an oligogenic pattern.

developmental biology↗