Victoria Stuart 🇨🇦 🏳️‍⚧️Jul 24, 2024

Severe COVID-19: Researchers confirm 3 genes for increased risk in addition to TLR7
https://www.sciencedaily.com/releases/2024/07/240724123046.htm

* confirms role of TLR7 gene in severe courses of COVID in men
* evidence for a contribution of TLR7 in women
* changes in 3 other genes of innate immune system (IFNAR2; IFIH1; TBK1) contribute to severe COVID-19

Stratified analyses refine association between TLR7 rare variants & severe COVID-19
https://www.cell.com/hgg-advances/fulltext/S2666-2477(24)00063-0

https://www.sciencedaily.com/releases/2024/07/240724123046.htm

#COVID #COVID19 #TLR7 #IFNAR2 #IFIH1 #TBK1

Large genetic study on severe COVID-19

Whether or not a person becomes seriously ill with COVID-19 depends, among other things, on genetic factors. With this in mind, researchers investigated a particularly large group of affected individuals. They confirmed the central and already known role of the TLR7 gene in severe courses of the disease in men, but were also able to find evidence for a contribution of the gene in women. In addition, they were able to show that genetic changes in three other genes of the innate immune system contribute to severe COVID-19.

ScienceDaily
CellBioNewsMar 15, 2024

Research uncovers specific #protein interactions needed for #cells to break down and remove damaged #mitochondria.

#autophagy #TBK1 #mitophagy

https://phys.org/news/2024-03-uncovers-specific-protein-interactions-cells.html

Research uncovers specific protein interactions needed for cells to break down and remove damaged mitochondria

Autophagy is a process used by cells as a recycling system to transport and break down organelles and other cytosolic components, which become enveloped in a membrane called the autophagosome. When this involves the removal of damaged mitochondria, it is known as mitophagy.

Phys.org
Giuseppe MichieliJan 10, 2023
#TBK1 and #IRF3 are potential #therapeutic #targets in #EVA71-associated diseases https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011001
TBK1 and IRF3 are potential therapeutic targets in Enterovirus A71-associated diseases

Author summary EV-A71 is an important causative agent of HFMD. There is currently no specific antiviral agent to treat HFMD and the related severe complications. The underlying molecular mechanism controlling host innate immunity after EV-A71 infection is still not fully understood, especially the roles of TBK1 and IRF3. Here, we applied TBK1 inhibitor (TBK1/IKKε-IN-2) and IRF3 agonist (KIN1148) to evaluate the antiviral activities of TBK1 and IRF3 in vivo. We found through regulating EV-A71-induced type I IFN response, IRF3 agonist effectively alleviated EV-A71-induced illness, while TBK1 inhibitor aggravated disease progression. More severe pathological alterations of neuronal degeneration, muscle fiber breaks, fractured or fused alveolar walls and diffuse congestion occurred in EVA-71-infected mice with TBK1 inhibitor treatment, while no obvious pathological change occurred in EVA-71-infected mice with IRF3 agonist treatment and control mice. Furthermore, TBK1 inhibitor promoted EV-A71-induced inflammatory response, while IRF3 agonist alleviated it. Our findings suggest that TBK1 and IRF3 are potential therapeutic targets in EV-A71-induced illness for the development of new antiviral agents and therapeutic strategies.