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Satu Latvala

Researcher at Natural Resources Institute Finland

Publications -  29
Citations -  406

Satu Latvala is an academic researcher from Natural Resources Institute Finland. The author has contributed to research in topics: Fusarium oxysporum & Virus. The author has an hindex of 10, co-authored 28 publications receiving 298 citations. Previous affiliations of Satu Latvala include University of Turku.

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Purification and properties of a new virus from black currant, its affinities with nepoviruses, and its close association with black currant reversion disease.

TL;DR: The data suggest that this virus may be the causal agent of reversion disease, and it is tentatively called black currant reversion associated virus.
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Genetic Variation of 'Candidatus Liberibacter solanacearum' Haplotype C and Identification of a Novel Haplotype from Trioza urticae and Stinging Nettle.

TL;DR: 'Candidatus Liberibacter solanacearum' (CLso) haplotype C is associated with disease in carrots and transmitted by the carrot psyllid Trioza apicalis, and samples were taken of wild plants within and near the carrot fields, the psyllids feeding on these plants, parsnips growing next to carrots, and carrot seeds.
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Fusarium oxysporum, F. proliferatum and F. redolens associated with basal rot of onion in Finland

TL;DR: Fusarium proliferatum seems to be more aggressive on onion, and some of the F. redolens isolates were highly virulent, killing onion seedlings, and more research is required to determine to what extent Fusarium infections spoiling onions originate from infected onion sets rather than the field soil.
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Ribes host range and erratic distribution within plants of blackcurrant reversion associated virus provide further evidence for its role as the causal agent of reversion disease

TL;DR: The detection of BRAV by immuno-capture reverse-transcriptase PCR (IC-RT-PCR) in redcurrant and in the wild species, Ribes spicatum and R. alpinum, but not in the non-host, gooseberry, graft-inoculated with scions from reverted blackcurrant plants, adds further support to the suggestion that BRAV is the causal agent of reversion disease.