I was skiing with friends, after being super sick for a week with my son Martin and nearly missing our yearly ski-trip (#privilege). The news were coming from everywhere: a deadly virus was striking the world. Or was it a small flu? Nah, a tiny bug? Oh no, a massive pandemic? Back in February 2020 the news were incoherent and completely polarized... But by June 2020 we knew Covid was there to stay. We were in lockdown, I had to take care of my two boys (3 and 6 at the time) and work (ha ha ha!). But then came my brilliant post-doc, Mariana, who asked me to join her on a hackaton on Covid RNA analysis, overly excited by the idea that we could try to help, and do something, and clearly stating I wouldn't need to worry about having too much work as she would take care of everything. And she did. She spearheaded a group of scientists from all over the world to analyze the first Sars-Cov-2 RNAseq dataset that were available. After the hackaton's week was over, we decided to continue the work. We were lucky to find efficient, competent and highly motivated individuals, and together with Mariana they all put up with late nights, weekends, and after-work hours to finish a very thorough pipeline for RNAseq and donwstream analysis, covering genes, isoforms, RNA binding proteins and much more. I am beyond proud of Mariana, and although I did not have a doubt of how competent a researcher she is, her input in this covid-related project confirmed what a brilliant PI she aready is.
Regarding TEs, probably the less thorough analysis of the paper (yeah, my bad...) we find very few TE families upregulated in Sars-Cov-2 infected cells specifically. No LINE1s are upregulated at all (wink wink to claims of Sars-Cov-1 being LINE-1 retrotransposed), and many old LTR families with well known immunoregulatory functions are upregulated specifically in Sars-Cov-2 infected cells (binding sites for STAT1, IRF regulation etc). The caveats in these analysis are of course related to the TE family analysis (and not TE copy analysis), meaning that a couple of copies could be responsible for the higher TE family expression observed. Of course those copies could be the result of pervasive transcription, so not associated with TE regulation per se. In our TE family analysis we are not removing reads that could be associated with TE-gene transcripts either. Finally, the association between TE family expression and nearby genes, although interesting to pinpoint potential pathways upregulated (as we do, and it actually worked pretty well recapitulating the DE gene pathways) suffers from the same caveat of a TE family and not a TE copy analysis. So I'm hoping other researchers will carry this on, and possibly finish this properly.
Oh, the figures of the paper <3, Mariana in all her splendeur!
oh crap, I need to go, despite being March 2021, my 4 year old's class is closed because of a covid case, and I'm just... surviving!
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