Don’t forget to check the OE social corner at #ESEB2025 for some behind the scenes on science..

Great talk and suggestions (!!!) for a responsible open publishing by @jacek-radwan.bsky.social

Going to eseb2025.bsky.social? 🇪🇸
Into heterogeneity in parasite transmission? 🦠
Or just feel like playing a board game? 🎲

Then come say hi and check what @kayla-king.bsky.social and I have been cooking! 🧪✨

Poster P01.365 in session 1 (Monday 18, 5pm)
See u there ✌️ 🌞 🍻

#EvoSky #ESEB2025

2/4 Here, we show that #Dexrazoxane suppresses microsporidian proliferation in mosquitoes without affecting the infection establishment

3/6 By zooming further, we can pinpoint target effectors associated with the specific host response to infection by early or late-selected parasites - marked with an asterisk. While early- elicit a stronger immune response, late-selected seem to evade it, if not even modulate it.

2/6 When looking at the response to infection by early- or late-parasites, some interesting changes started to appear, particularly regarding Golgi-ER immune signalling, immunity and response to ROS.

1/6 Using #RNAseq, I addressed the host response to different V. culicis lines we evolved and studied before in previous studies (Silva & Koella 2024a&b, bioRxiv). First, infection by the reference parasite did not elicit a large immune response.

And I also advice you to check Tiago’s work, also from Koella’s lab for some nice insights into parasite evolution, its adaptation potential and how it might affect vector control :)

in the same room, just a bit before!

Attending this weekend’s @evolmtg.bsky.social #Evol2024 ?

Pass by room 525AB on July 28th 11:20-11:45 for some nice results and discussions surrounding virulence evolution and parasite transmission presented by yours truly :) from my postdoc in Koella lab

5/Differences in virulence could be decomposed into parasite growth differences within the host, and not to changes in per parasite pathogenicity - probably due to the tiny genome of this parasite. Our data also agrees with the uncontrollable growth hypothesis.

4/Late-transmitted spores had faster growth rate and produced higher numbers than any of the other treatments.

3/Higher virulence also sped up the host larvae-to-pupae development but at a low cost in larvae or pupae mortality.

2/Contrary to the trade-off virulence hypothesis, late spores selected for higher virulence than early ones. Higher virulence led the host to shift investment in fecundity adequately, with late spores almost fully ameliorating the cost of infection during early stages.

1/We selected a microsporidian parasite to a) spend less time within-host and kill faster or b)spend more time and kill later. After 6 generations we quantified their virulence and pathogen changes, as well as consequent host responses