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Reposted by LabzInnate Lab

Brian Ferguson @viropractor.bsky.social · 11/02/2025

There is a Postdoc job available in my lab to study fundamental mechanisms of antiviral immunity, specifically in the context of viral nucleic acid sensing. Please take a look here and contact me if interested: #immunosky #virology 🧪 www.jobs.cam.ac.uk/job/50254/

jobs.cam.ac.uk

Research Assistant / Research Associate (Fixed Term) - Job Opportunities - University of Cambridge

Research Assistant / Research Associate (Fixed Term) in the Department of Pathology at the University of Cambridge.

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LabzInnate Lab @labzinnate.bsky.social · 20/12/2024

Thanks! We think the TBK1 (likely IFN-dependent) restriction therefore happens at assembly (post RNA replication anyway) but we never followed that up…it’d be cool to define that though and find out what happens to all that viral RNA 😀

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LabzInnate Lab @labzinnate.bsky.social · 06/12/2024

Thanks @ausvirologysoc.bsky.social for a great meeting. Where else can you turn the evolution of flu A vs flu B strains as described by @marioskoutsakos.bsky.social into a dance move. Having Jenna Guthmiller here from the US was a highlight for me! See you all in Adelaide in 2026

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LabzInnate Lab @labzinnate.bsky.social · 17/11/2024

Thanks Natalia! The most important starter pack of all 😉

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LabzInnate Lab @labzinnate.bsky.social · 11/11/2024

Huge thanks to all of the people who contributed to this project including my fantastic lab, brilliant collaborators and the imaging and microscopy experts at IMB, UQ because seeing is believing.

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LabzInnate Lab @labzinnate.bsky.social · 11/11/2024

These ACE2-pos macs CAN make new infectious virions, BUT, all those anti-viral cytokines the macs make stop new virion release. If we block cytokine induction with a TBK1 inhibitor (BX795) then we rescue ACE2-pos mac virus production.

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LabzInnate Lab @labzinnate.bsky.social · 11/11/2024

But SARS-CoV-2 can enter ACE2-pos macs (maybe even fuse at the plasma membrane) AND trigger macrophage cytokine release.

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LabzInnate Lab @labzinnate.bsky.social · 11/11/2024

Macrophages are of course big eaters, and we saw some virus in ACE2-neg HMDM, but we speculate it doesn’t make it into the cytosol to trigger macrophage sensors. Accordingly, ACE2-neg macs don’t make any cytokines.

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LabzInnate Lab @labzinnate.bsky.social · 11/11/2024

Huge scRNA seq efforts from many groups found macrophages with lots of viral RNA in COVID-19 patients, but not many macrophages expressing ACE2. So, we modelled some ACE2-neg (incl. HMDM) and ACE2-pos macs and saw that SARS-COV-2 only replicates in ACE2-pos Macs (THP-1 ACE2).

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LabzInnate Lab @labzinnate.bsky.social · 11/11/2024

Macrophages are key players in COVID-19, so we asked the crucial questions 1) does SARS-CoV-2 need ACE2 to replicate in macrophages 2) does ACE2 enable macrophage cytokine responses?

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LabzInnate Lab @labzinnate.bsky.social · 11/11/2024

How do macrophages sense SARS-CoV-2 infection to drive inflammation (protective or disease causing) in COVID-19? Our 2023 paper in Science Signalling helps explain 🧵 www.science.org/doi/10.1126/...

science.org

Macrophage ACE2 is necessary for SARS-CoV-2 replication and subsequent cytokine responses that restrict continued virion release

ACE2 in macrophages promotes infection that enables an intrinsic antiviral response to SARS-CoV-2.

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LabzInnate Lab @labzinnate.bsky.social · 11/11/2024

If you've wondered how antibodies can work against us during infectious disease, please check out our recent review in Nature Reviews Immunology: Mechanisms of antibody-dependent enhancement of infectious disease | Nature Reviews Immunology www.nature.com/articles/s41...

nature.com

Mechanisms of antibody-dependent enhancement of infectious disease - Nature Reviews Immunology

This Review discusses the different mechanisms of antibody-dependent enhancement (ADE) of infectious disease, including how antibodies can increase the pathogen load, protect bacteria from the immune ...

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