The title here ("100% of Long Covid patients have GPCR-autoantibodies") is editorialized, making this sound interesting. The actual title is "Possible Impact of functional active GPCR-autoantibodies on retinal microcirculation in Long-COVID."
The study looked at 76 long covid patients with no control group, so you can't make a general conclusion from it. This post is a waste of time unless you're interested in obscure opthamological research.
I couldn't tell from the abstract (is there a link I missed), but I suspect that the test for GPCR-autoantibodies has a baseline (e.g. to test positive you must be 2-sd above the mean). From that if all 76 test positive you can know without a control group that that is otherwise very unlikely and a strong signal of correlation.
I've tested +ve for many GPCR-autoantibodies, I had it done at the CellTrend lab. I've never had covid but my pre-existing ME/CFS was made vastly worse from the booster shot, I have particularly high count of ACE2-AAb which seems to be associated with covid, and or the vaccine. I have the genetic predisposition called hEDS and knew the risks when I took them. It's taken 3 months of many powerful and experimental drugs and I'm just starting to get back to my normal baseline.
To the people wondering where the control group is; most people don't test positive to GPCR-autoantibodies. I don't know where the threshold is set but the probability that all 76 long-covid patients test positive is otherwise rather low.
Most probably not, at least not based on this study.
First of all, GPCRs are a class of many different receptors present in many different cells and with vastly different downstream effects, nothing that could easily be reversed with a targeted pharmacological intervention. Secondly, if there are general anti-GPCR antibodies present, it is most likely that they would inhibit the receptors or lead to damage of the cells expressing the receptors. Activating autoantibodies do exist (a form of hyperthyroidism being a common example) but are not the norm, so additional blocking would not be indicated. I also have some questions about the study as such. First of all, this is only an abstract that doesn’t describe all of their methods, it absolutely doesn’t allow any conclusions. My field of research is not GPCRs so I can’t say whether it’s common in that niche but their choice of using an in vitro rat (this cross-species) cardiomyocyte assay for antibody detection coupled with the absence of a proper control group or seropositivity threshold (at least not mentioned in the abstract) immediately makes me want to see further data before I trust anything described here. Their presentation style also seems confusing to me at a first glance and making it hard to tell what they did. Would have to spend more time on this and with the proper paper to disassemble everything. It also seems odd that they would not investigate this further if they indeed believed it to be involved in Long Covid at the systemic levels but rather chose to publish this in an ophthalmology journal.
There are experimental drugs that can neutralize AAbs. They were successfully tested on Long Covid patients, but this is very preliminary. See for instance
This paper here will fill in the gaps of why auto antibodies against GPCR could be a bad thing - initiating autoimmune disease.
"GPCRs are the largest superfamily of integral membrane proteins in humans10. GPCRs play an essential role in vertebrate physiology by sensing the external environment of a cell and responding to a variety of physiological stimuli11. For instance, GPCRs coordinate the cellular behavior involved in host immune responses."
" we suspect that the homeostasis of aab relationships, which are possibly a physiological part of our immune system, may break down, causing autoimmune disease."
I came here to say "sure. But what's the control group," and "this would be more interesting if 100% of non-long-covid sufferers didn't have the antibody."
Interesting work, but this seems like only the first half of the experiment. Would love to see the data when the experiment is completed.
This paper was from the journal "IOVS - Investigative ophthalmology and visual science". So, I sent a copy to my ophthalmologist and asked his opinion. He replied that he couldn't understand any of it.
No, of course not, unless you are funding him to research long Covid.
Some doctors are unwilling to admit when they don't know something. If he was like that, then maybe it would make sense to start looking for another ophthamologist.
Maybe? Reading the abstract, it seems to make sense to me how this paper ended up in this specific journal. From what I understand, the authors were specifically looking at one ophthalmology-related long COVID symptom (impaired retinal microcirculation) and found a common marker that is linked to that symptom.
Granted, I have 0 experience in any medical field, but it doesn't immediately look like a red flag to me?
Long covid is ongoing chronic illness symptoms following a covid infection, including but not limited to fatigue, heart problem, lung problems, brain fog, and auto-immune problems.
Well for a study trying to find biological markers of a condition, I imagine the only way to source people is by self reporting. Because they haven’t found the markers yet…
Not sure why this is downvoted. I am not qualified to read the paper but I have the same question. My impression was that "long covid" was self reported and there is no way to medically confirm if someone is actually has "long covid"
[+] [-] kens|3 years ago|reply
The study looked at 76 long covid patients with no control group, so you can't make a general conclusion from it. This post is a waste of time unless you're interested in obscure opthamological research.
[+] [-] dang|3 years ago|reply
Submitters: please follow the site guidelines, which ask: "Please use the original title, unless it is misleading or linkbait; don't editorialize."
[+] [-] cjbgkagh|3 years ago|reply
[+] [-] cjbgkagh|3 years ago|reply
To the people wondering where the control group is; most people don't test positive to GPCR-autoantibodies. I don't know where the threshold is set but the probability that all 76 long-covid patients test positive is otherwise rather low.
[+] [-] dpcan|3 years ago|reply
[+] [-] joshenders|3 years ago|reply
[+] [-] V__|3 years ago|reply
[+] [-] hijodelsol|3 years ago|reply
[+] [-] evandijk70|3 years ago|reply
[+] [-] deng|3 years ago|reply
https://www.frontiersin.org/articles/10.3389/fmed.2021.75466...
[+] [-] teilo|3 years ago|reply
[+] [-] pdar4123|3 years ago|reply
[+] [-] djmips|3 years ago|reply
"GPCRs are the largest superfamily of integral membrane proteins in humans10. GPCRs play an essential role in vertebrate physiology by sensing the external environment of a cell and responding to a variety of physiological stimuli11. For instance, GPCRs coordinate the cellular behavior involved in host immune responses."
" we suspect that the homeostasis of aab relationships, which are possibly a physiological part of our immune system, may break down, causing autoimmune disease."
https://www.nature.com/articles/s41467-018-07598-9
[+] [-] retrocryptid|3 years ago|reply
Interesting work, but this seems like only the first half of the experiment. Would love to see the data when the experiment is completed.
[+] [-] morninglight|3 years ago|reply
Should I start looking for a new ophthalmologist?
.
[+] [-] hollerith|3 years ago|reply
Some doctors are unwilling to admit when they don't know something. If he was like that, then maybe it would make sense to start looking for another ophthamologist.
[+] [-] delroth|3 years ago|reply
Granted, I have 0 experience in any medical field, but it doesn't immediately look like a red flag to me?
[+] [-] blkhp19|3 years ago|reply
[+] [-] AndrewUnmuted|3 years ago|reply
[+] [-] nicoburns|3 years ago|reply
[+] [-] bluehorseray|3 years ago|reply
[+] [-] dominotw|3 years ago|reply
[+] [-] unknown|3 years ago|reply
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