4/ Shedding explained how many parasites reached the next host. But it didn’t explain what those parasites did once they got there. The quantity of transmission and the quality of transmission turned out to be different things.

3/ The surprise? Host rankings kept changing. The hosts releasing the most parasites were often not the hosts causing the highest infection burden or the most severe disease in the next host.

2/ We followed transmission across the infection cycle for a panel of hosts strains: • susceptibility to different routes • parasite shedding • infection-induced dispersal • recipient virulence • recipient parasite burden Instead of assuming these processes covary, we measured each one separately.

Going to #ISEMPH2026 ? 💉🦠 Come by my poster (n90) and check what we have been up to :) @evmed.bsky.social #EvolutionaryMedicine

4/Rather than focusing on single genes, I combinied differential expression with WGCNA to identify coordinated biological programmes. These reflected traits associated with pathogen exploitation, transmission, and env. persistence, providing a view of how pathogen evolution changes host biology.

3/I found a common transcriptional response to infection, but beyond that, different evolutionary strategies consistently activated different host gene programmes. Evolution wasn’t simply changing infection. It was changing the biology of the host.

2/To test this, I experimentally evolved a mosquito pathogen for either early or late transmission, infected mosquitoes, and sequenced the host transcriptome. Same host. Same pathogen species. Different evolutionary histories.

Aging is messier, and more interesting, than a simple oxidative-stress story. @natureportfolio.nature.com #Aging #EvoSky #Aedes

Scientists, more than ever, have a responsibility to bridge the gap between science and the public, for more reasons than I could ever list. Very grateful for the chance to give back to my hometown, Porto, last week — and hopefully inspire and educate a new generation of young minds 🫶 #AcademicSky

4/5. Treatments did not differ in any of the 5 redox markers. Using a PCA, we described an antioxidant-to-oxidant PC gradient. However, this gradient only explains some differences between early/young and late/aged individuals.

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