Preprint Divergent inflammatory and neurology-related plasma protein profiles in LC following primary and breakthrough infections., 2024, Bansal+

SNT Gatchaman

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Divergent inflammatory and neurology-related plasma protein profiles in individuals with long COVID following primary and breakthrough SARS-CoV-2 infections.
Amit Bansal; Sam W.Z. Olechnowicz; Nicholas Kiernan-Walker; Jacob Cumming; Ramin Mazhari; COVID PROFILE consortium; Rebecca J. Cox; Ivo Mueller; Rory Bowden; Emily M Eriksson

Long COVID is a complex condition where symptoms persist for more than 3 months after SARS-CoV-2 infection and affects an estimated 5-30% of individuals. While the pathobiology of long COVID is still evolving, persistent inflammation has emerged as an important feature of this condition. However, it is unclear if immune responses from COVID-19 vaccination or SARS-CoV-2 re-infection exacerbate or mirror the initial inflammatory responses.

To address this question, we quantified 182 inflammatory and neurology-related proteins in plasma using multiplexed affinity proteomics. Plasma samples were collected 6-9 months after first infection, but before COVID-19 vaccination from individuals who had recovered from COVID-19 (n=21) or from individuals with long COVID (n=12). This was benchmarked against plasma from unvaccinated, SARS-CoV-2 naive individuals (n=24). In addition to this cross-sectional analysis, we performed longitudinal analysis in a subset of individuals (n=34), where paired samples collected 2-4 weeks after a third COVID-19 vaccine dose and after SARS-CoV-2 breakthrough infection were available.

Boruta feature selection and lasso regression models identified a distinct plasma profile in long COVID individuals, characterised by elevated IL-20, HAGH, NAAA, CLEC10A, LXN, and MCP-1 and reduced TRAIL, G-CSF, NBL1, and CCL23 protein concentrations. Notably, longitudinal analysis demonstrated that neither COVID-19 booster vaccination nor breakthrough infection replicated inflammatory and neurology-related plasma protein profiles observed after primary infection suggesting an altered immune response outcome in individuals with long COVID upon re-exposure.


Link | PDF (Preprint: MedRxiv) [Open Access]
 
In this study, we leveraged access to samples collected from an Australian population with low community transmission during the two first years of the COVID-19 pandemic. Using a multiplexed affinity proteomics approach […] and longitudinal plasma samples from initially SARS-CoV-2 naïve individuals, COVID-19 recovered and long COVID individuals, we explored inflammatory and neurology-related plasma protein profiles not only following a primary infection with the SARS-CoV-2 ancestral strain, but also after COVID-19 booster vaccination and breakthrough infections. Our study design provided a rare opportunity to understand how circulating protein profiles after vaccination and re-exposure in the same individual compare to plasma profiles after primary SARS-CoV-2 infections in long COVID individuals.
 
To me the abstract is completely opaque. What diverged from what? The overall impression is that they didn't find much other than a few odd patterns with statistics I have never heard of.

I prefer papers to present data rather than waffling about leveraging and rare opportunities.
 
identified a distinct plasma profile in long COVID individuals, characterised by elevated IL-20, HAGH, NAAA, CLEC10A, LXN, and MCP-1

Elevated MCP-1 was also found in the following thesis paper.
Paper : Role for EBV- & HHV-6A-dUTPases on Immune Dysfunction in ME/CFS and other Chronic Multi-Symptom Illnesses, 2024, Cox
Thread : https://www.s4me.info/threads/role-...ronic-multi-symptom-illnesses-2024-cox.40309/

The CMI cohort exhibited elevated levels of monocyte chemoattractant protein 1 (MCP-1) when comparted to the GWI and control cohorts.
 
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