Preprint Transfer of IgG from Long COVID patients induces symptomology in mice, 2024, Vidarsson+

[butter.]

Have previously measured NFL in ME/CFS patient serum vs controls. Found no difference. Didn't measure GFAP though.

I have measured all of them and GFAP in my own samples (very severe ME), all negative, but again, I did not expect them to be elevated, as I think we deal with something more akin to past 'acute injury' as opposed to 'neurodegeneration'. I think 'time of sampling' is paramount.

PS: If LC mouse models are somewhat informative about ME/CFS we would not expect to see Nfl but GFAP to be elevated.

 

[Denise]

I haven't had a chance to read the preprint yet so apologies if my question is answered in it.
Did they by chance monitor the mice to see if their LC resolved over time?

 

[Paraprosdokian]

I haven't had a chance to read the preprint yet so apologies if my question is answered in it.
Did they by chance monitor the mice to see if their LC resolved over time?

They monitored the mice for 12 weeks (iirc) and stopped after that. The mice had LC symptoms over that whole period, but they did seem to improve over that period.

 

[Denise]

They monitored the mice for 12 weeks (iirc) and stopped after that. The mice had LC symptoms over that whole period, but they did seem to improve over that period.

Thank you very much.

 

[SNT Gatchaman]

Commentary in Nature News —

Danny Altmann, an immunologist at Imperial College London, is more sceptical. “Things like long COVID are really, really hard to reiterate in animal models,” he says, and it is unclear how well the symptoms observed in mice really reflect what’s going on in humans. “We’ve invested almost zero in building up those models,” he says, owing to a lack of government interest and “policymaker fatigue” in funding long COVID research. So even “if this study catalyses debate about the vacuum of small-animal models that are really holding back the field, I think it’s helpful”, he adds.

 

[ryanc97]

I would contrast this paper with the sort of paper that one found in a journal of 1974 - where a single simple experiment was reported and in six cases out of ten became a classic piece of evidence that everyone learnt about. These days we see thirty seven graphs in colour about various things not directly related to the main experiment but not much detail on the finding of interest. In 99 out of 100 cases the papers are forgotten.

I am not aware of any disease in which transfer of human antibodies to mice has been critical in our understanding. Human immunoglobulin in mice will form immune complexes, fix complement, activate Fc receptors and generally cause a nuisance, whatever it is against.

I just don't see this sort of paper as a serious attempt to convey a simple, sound, scientific observation. It is more like what pops up when you try to read a newspaper - all sorts of flashing advertisements here there and everywhere making it impossible tor read what you wanted to look at. It is bad manners apart from anything.

We all used to do bad experiments in the 1970s but didn't bombard people with all this stuff and didn't expect anyone to take much notice. Now people spend millions of dollars on studies like this and nobody has any idea what to make of it.

If antibody transfer from human to mice always causes problems because it is mice, why didn't the authors do a transfer of IGG of healthy people to mice and compare that as well? Because that would pretty much prove whether the first statement is true or not. @Jonathan Edwards

If there are overlapping effects from just the antibody being from a human to mice and also the faulty antibodies from CFS, then doing a healthy transfer would allow the researchers to extract out the two effects, similar to how you look at regression coefficients.