Officially out in @CellCellPress: Systematic comparison of SARS-CoV-2 variants of concern (Alpha, Beta, Gamma, Delta, & Omicron) using global proteomic and genomic analyses during infection to understand the molecular responses driving viral evolution 🧵👇 cell.com/cell/fulltext/… We quantitatively compared the host response to infection in Calu-3 cells using abundance proteomics, phosphoproteomics, APMS, and transcriptomics. We observed equivalent replication kinetics for all VOCs except for Omicron BA.1, showing lower replication.

In this new preprint we systematically compared SARS-CoV-2 variants of concern (Alpha, Beta, Gamma, Delta, and Omicron) during infection using global proteomic and genomic analyses to understand the molecular responses driving viral evolution 🧵👇🏾biorxiv.org/content/10.110… We found increased replication for the Variants of Concern (VOCs) in primary cells and quantitatively compared the host response to infection in Calu-3 cells using transcriptomics, abundance proteomics, and phosphoproteomics analyses.

How do SARS-CoV-2 variants evolve to become more transmissible? One contributor, which we report today in @Nature, is increased innate immune antagonism likely driven by selective upregulation of viral proteins Orf9b, Orf6 and N. nature.com/articles/s4158… We directly compared the SARS-CoV-2 Alpha variant to early lineage strains VIC and IC19 and found no differences in viral replication in Calu-3 cells but did find differences in interferon production.

We previously published a virus-human SARS-CoV-2 protein interaction map in @Nature (Gordon et al., 2020a). In our @ScienceMagazine article out today, we compared these interactions to those from other lethal coronaviruses, SARS-CoV-1 and MERS-CoV. More @ kroganlab.ucsf.edu/network-maps We have a library of viral protein plasmids that we are happy to distribute to the research community free of charge until @Addgene takes over. Email Dr. Krogan at UCSF to request these.

In this new article, we map global phosphorylation profiles induced by #SARSCoV2 infection to kinase activities, identifying kinase inhibitors with potential to treat #COVID19. See thread for findings
cell.com/cell/fulltext/… #SARSCoV2 infection activated the p38/MAPK signaling pathway. Abrogation of p38 signaling with drugs/compounds, or knockdown of p38 pathway members, possessed an antiviral effect and reduced cytokine production.

In collaboration with @ZoicLabs, we produced an interactive rendition of our #SARSCoV2 Protein Interaction Map to facilitate the exploration of our dataset. Explore host targets, corresponding drugs/compounds, and other pathogen interactions. Link: ppi.zoiclabs.io/#/ This interactive map corresponds to our paper published today @nature (nature.com/articles/s4158…). The map contains clickable nodes to explore the known functions of #SARSCoV2 viral proteins and host targets, including host protein complexes and biological processes.