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The general population will keep on getting infected, most probably without any effects for the vast majority of them. I think it's unrealistic to hope or demand anything else. I believe things such as ultra-sensitive single molecule array assays, maybe even PET scans, old data and other things...

I'm not able to comprehend that. We need good controls now, what is the impact of future generations on that?

I hope the researchers become more aware of the limitations of such studies. People that haven't had Covid hardly exist anymore. Even at the End of 2021 it's not unlikely that less than 50% of controls are actually controls. I don't know how this can be managed. Of course there can be the...

Prevalence of long-term symptoms varies by using different post-COVID-19 definitions in positively and negatively tested adults: the PRIME post-COVID study Abstract Background Long-term symptoms after a SARS-CoV-2 infection (i.e., post-COVID-19 condition or long COVID), constitute a substantial...

VEGF-A plasma levels are associated with impaired DLCO and radiological sequelae in long COVID patients Background Long COVID, also known as post-acute sequelae of COVID-19 (PASC), is characterized by persistent clinical symptoms following COVID-19. Objective To correlate biomarkers of...

I can't judge the relevance of this work, especially not without reading it, but just reading the abstract it seems to be slightly in line with Rob Wüsts work?

Long-Covid symptoms mainly being neurological or neuropsychiatric in nature seems like a bold if not simply wrong statement. Considering that in the RECOVER 12 symptom study only 2 of those 12 symptoms, I would consider to be neurological or neuropsychiatric and with those you don't come...

Whilst the study is very much appreciated, to me this doesn't rule out the value of studying a pathogen. Conduct the same study for post-Ebola and your results will also be negative.

The study has now been published in Nature https://www.nature.com/articles/s41598-023-39049-x.

With the caveat that tissue biopsies were only looking at Long-Covid patients, this study looks very substantial. I don't recall a similar PET study in post-Ebola, if someone knows of one, could they please direct me to it to see how well they line up?

Abstract The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern such as Omicron hampered efforts in controlling the ongoing coronavirus disease 2019 pandemic due to their ability to escape neutralizing antibodies induced by vaccination or prior...

A significant factor in this study seems to be that ME/CFS Long-Covid patients are obese in this study (compared to the remaing Long-Covid patients). This has implications on the results as many other studies suggest https://pubmed.ncbi.nlm.nih.gov/29743194/. Of course this doesn't have...

I've heard that Scheibenbogen is using RVA as part of her Biomarker platform (apart from EndoPAT for endothelial dysfunction assessment). So hopefully we will see some replication of this work from other labs soon.

Harald Prüss and his group also do some associated research on autoantibodies in the CSF and associations to Long-Covid. They published https://www.sciencedirect.com/science/article/pii/S0889159123000065?via%3Dihub and are currently doing a follow-up of this work.

Akiko Iwasaki actually has alpha-gal syndrome. Makes it less suprising to me, that she's sympathetic to "mysterious illnesses" triggered by a sudden onset others don't believe in .

I still feel like this discussion is largely going in circles and all the research doesn't add too much to the discussion. Pretorius et al. have been studying these "microclots" way before Covid came around and argue that these Long-Covid microclots are somehow slightly different (resistant to...

Iwasaki was also very recently asked about microclots since her team are investigating them as well . I thought her opinion would be a decent reflection of their current research as she has a better tone than some of the “Twitter scientists”. The gist of it (or my interpretation of it) is that...

That I don't know, but I certainly would like to know how this data matches with that of Phair/Davis/Armstrong. My phrasing wasn't good, what I want to say is that Phair's and Davis' own measurements didn't corroborate their own theories (I think the Kynurenine trial was particularly dissapointing).

From what I’ve understood the IDO2, Kynurenine and Tryptophan measurements didn’t corroborate Davis & Phair’s theories. Was anything published or is the data available somewhere? The researchers of this paper are also ME/CFS researchers.

Prolonged indoleamine 2,3-dioxygenase-2 activity and associated cellular stress in post-acute sequelae of SARS-CoV-2 infection Background Post-acute sequela of SARS-CoV-2 infection (PASC) encompass fatigue, post-exertional malaise and cognitive problems. The abundant expression of the...