Our strategy successfully identified two novel antiviral effectors: DHX9 and UPF1, both RNA helicases. While these proteins are known to participate in RNA detection and degradation, their precise mechanism of action against SFTSV remains unclear... Stay tuned for the next chapter! 🔍 #TickVirology

Finally we finalized our omics characterization by looking at the interactors of SFTSV N protein during an active infection. N interactors were mostly related to stress, or RNA regulation pathways. We identified interactors conserved in human, and other associated with immune response to bunyavirus.

To understand our tick cell infection we focused on immune related pathways. We were able to map innate immune pathways (Jak-STAT, Toll, Imd). Interestingly little regulation was observed. Regulation was more important for stress-associated pathways suggesting a role in viral regulation.

Using this novel knowledge we studied the impact of SFTSV infection dynamics on tick cells. While the infection is asymptomatic in cells, we observed large change at 3 and 6 days post-infection. With little conservation of those changes overtime, suggesting large changes in infected cells.

Our first objective was to generate a better transcriptome and the first reference proteome for BME/CTVM6 tick cells. Following RNA and protein extraction, we performed proteomic informed by transcriptomic analysis. This approach brings insights into the molecular biology of our tick vector system.

Ticks are vector of many pathogens including hemorrhagic fever virus like SFTSV. Identified in 2009, SFTSV interaction with its tick vector remains understudied. To bypass limited understanding and tools available I used my system virology expertise to explore tick-virus interactions!

A huge thank you to @microbiologysociety.org for an incredible meeting! This was the first chance for all members of the Petit Lab to showcase their work! #TickVirology #ProudPI #NewPI