Severe COVID-19 and long COVID are associated with high expression of STING, cGAS and IFN-α, 2024, Queiroz et al.

Severe COVID-19 and long COVID are associated with high expression of STING, cGAS and IFN-α
Queiroz, Maria Alice Freitas; Brito, Wandrey Roberto dos Santos; Pereira, Keise Adrielle Santos; Pereira, Leonn Mendes Soares; Amoras, Ednelza da Silva Graça; Lima, Sandra Souza; Santos, Erika Ferreira dos; Costa, Flávia Póvoa da; Sarges, Kevin Matheus Lima de; Cantanhede, Marcos Henrique Damasceno; Brito, Mioni Thieli Figueiredo Magalhães de; Silva, Andréa Luciana Soares da; Leite, Mauro de Meira; Viana, Maria de Nazaré do Socorro de Almeida; Rodrigues, Fabíola Brasil Barbosa; Silva, Rosilene da; Viana, Giselle Maria Rachid; Chaves, Tânia do Socorro Souza; Veríssimo, Adriana de Oliveira Lameira; Carvalho, Mayara da Silva; Henriques, Daniele Freitas; Silva, Carla Pinheiro da; Nunes, Juliana Abreu Lima; Costa, Iran Barros; Cayres-Vallinoto, Izaura Maria Vieira; Brasil-Costa, Igor; Quaresma, Juarez Antônio Simões; Falcão, Luiz Fábio Magno; Santos, Eduardo José Melo dos; Vallinoto, Antonio Carlos Rosário

The cGAS-STING pathway appears to contribute to dysregulated inflammation during coronavirus disease 2019 (COVID-19); however, inflammatory factors related to long COVID are still being investigated.

In the present study, we evaluated the association of cGAS and STING gene expression levels and plasma IFN-α, TNF-α and IL-6 levels with COVID-19 severity in acute infection and long COVID, based on analysis of blood samples from 148 individuals, 87 with acute COVID-19 and 61 in the post-COVID-19 period. Quantification of gene expression was performed by real-time PCR, and cytokine levels were quantified by ELISA and flow cytometry.

In acute COVID-19, cGAS, STING, IFN-α, TNF-α, and IL-6 levels were higher in patients with severe disease than in those with nonsevere manifestations (p < 0.05). Long COVID was associated with elevated cGAS, STING and IFN-α levels (p < 0.05). Activation of the cGAS-STING pathway may contribute to an intense systemic inflammatory state in severe COVID-19 and, after infection resolution, induce an autoinflammatory disease in some tissues, resulting in long COVID.

Link | PDF (Nature Scientific Reports) [Open Access]

 

This looks very interesting.
It seems a pity they keep talking about inflammation.
It looks to me that cGAS - STING and IFN-a may be involved in a protective or scavenging signalling response that, like complement in the circulation, may be more about anti-inflammation than inflammation. But it may still make you feel dreadful.

I would not be at all surprised if a pathway like this was involved in ME signalling. It looks relevant to lupus and other ANA associated diseases like Sjogren's.

 

Oops - trying to recycle a standard message to NIH to look at this as a possible research area!

https://twitter.com/user/status/1763705506844098874

 

Could you say anything more about your thoughts on anti -inflammation, would it feel like inflammation?


Would this be one part of the reason why when people with ME report all these pain symptoms, especially the more local ones, and our doctors are, like oh yeah okay give us a look, but then they see no swelling or no inflammation markers and convert to thinking we must have conversation disorder to be reporting all his stuff?

Do our symptoms sound like inflammation and then we don’t have it we’re just a big letdown?

 

See Chloride Homeostasis Regulates cGAS-STING Signaling (2024, Preprint: BioRxiv)