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Farrell, H.

Publications and source records attributed to Farrell, H..

2 recordsLinked to original sources

A catastrophic marine mortality event caused by a complex algal bloom including the novel brevetoxin producer, Karenia cristata (Dinophyceae)

Harmful algal blooms of Karenia brevis (Dinophyceae) are a global anomaly, occurring in one location worldwide, causing severe marine and acute human impacts via brevetoxins (BTX). During 2025 an unprecedented, currently ongoing, mass marine mortality occurred in South Australia, across an area of [~]20,000 km2, persisting for >6 months, resulting in the deaths of [~]106 marine animals of >550 taxa, with human health impacts. Using custom metabarcoding, long-read sequencing and targeted quantitative PCR, we characterized the microalgal assemblage. Karenia cristata dominated over the sampling area, in an assemblage with four other Karenia species with varied abundances spatially and temporally. High abundances of K. cristata appeared in the austral autumn, and hydrodynamic processes appear to have entrained cells coastward in the semi-enclosed seas. We isolated the species and characterized it using light and electron microscopy, liquid chromatography mass spectrometry and toxicity assays. We show for the first time that the rare and little known K. cristata produces significant BTX with a profile (BTX-2, -3, -B5), differing from K. brevis, with toxicological effects. These findings reveal a novel, significant BTX-producing Karenia, which considering its substantial detrimental marine ecosystem impacts, is an emerging international threat with unknown consequences in changing ocean conditions.

ecology↗

Olfactory host entry supports herpesvirus recombination

Herpesvirus genomes record abundant recombination. Its impact on infection remains ill-defined. When co-infecting mice by the natural olfactory route, individually incapacitated Murid Herpesvirus-4 (MuHV-4) mutants routinely recombined to restore normal host colonization. Lung infection rescued much less well. Murine cytomegalovirus mutants deficient in salivary gland colonization also showed rescue via the nose but not the lungs. As nose and lung infections show similar spread, efficient recombination seemed specific to olfactory entry. Rescue of replication-deficient MuHV-4 implied co-infection of the first encountered cells, and this worked also with asynchronous inoculation, suggesting that latent virus could lie in wait for later reactivation. Inhaled MuHV-4 is commonly caught on respiratory mucus, which epithelial cilia push back towards the olfactory surface, and infection was correspondingly frequent at the anterior olfactory edge. Thus olfactory entry provides a general means for herpesviruses to meet. Author summaryInter-strain recombination allows viruses to optimise infection in diverse hosts. Many herpesviruses show past recombination. Yet they are ancient pathogens, so this past may be remote and recombination rare. Diverse herpesviruses enter new hosts via olfactory cells. We show that such entry routinely allows recombination between co-infecting virus strains, even when one strain cannot spread. Recombination was contrastingly rare after lung infection. Thus, entry via olfactory cells specifically supports frequent herpesvirus recombination.

microbiology↗