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

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.