Does this make any sense? The endothelial damage is likely due to direct damage by the virus yet the evidence is mixed as to whether the virus actually infects endothelial cells?
Discussion about the B cell compartment states that is confusing why patients with deficiencies in antibody production don’t seem to get very sick. But then no real mention of autoimmunity?
I’ll describe the clinical course in simple terms. Here’s what your typical COVID-19 patient looks like who is going to end up in the hospital with severe COVID-19. The first week is a URI that might actually get better. Then 6 to 12 days later the respiratory distress begins.
Everyone (even our top immunologists) draws the viral load like this. But this is completely wrong! This is what they want to see but this only happens in rare instances. This is not what typically happens to viral load even in patients with severe COVID-19 who are hospitalized.
This is a more accurate depiction of viral load based on actual data from hospitalized COVID-19 patients. Even if you believe there is a viral reservoir (which there could be) the viral load is much lower with the onset of severe symptoms. Please challenge me on this with data.
So then what happens with immune response? The innate system always responds first and there is the suggestion that it is ineffectual. So then in comes the adaptive immune response. You tell me who is the bad actor here. The virus or the host response? We have to get this right.
Please I really want to see some data to the contrary here. If I’m wrong then make sure that I know! Otherwise look at this study and any of the mAb trials. nejm.org/doi/full/10.10…
• • •
Missing some Tweet in this thread? You can try to
force a refresh
There are two patterns to identify among doctors (and other health professionals) which signal evidence they might not be getting the diagnosis right. Both types are very prevalent in discussions of acute and long COVID.
Premature closure is a cognitive error where the physician fails to consider the reasonable alternatives and settles on a diagnosis that does not match the clinical characteristics of the disease. This faulty decision making process often leads to delayed diagnosis.
At the other extreme is labeling disease processes as multifactorial. While every health problem has many contributing factors, this attribution is cognitive cover for the fact that the physician just doesn’t know. It can provide false justification for not investigating further.
I’m realizing that in modern medicine there are these conditions that are viewed as unpopular siblings in certain disciplines. For instance in rheumatology it might be Sjogrens and in neurology it might be POTS.
Those who study more well defined and understood conditions scoff at the poor research in these areas, question the clinical practices, and often label patients with those conditions as difficult or likely falsely attributing symptoms that might not be real.
I wonder if it was the same many years ago when there were other conditions that weren’t well understood. If doctors had the same gall and presumptions. Or maybe back then there was a much more prevalent acceptance that knowledge was limited.
Aptamers. Oligonucleotide or peptide molecules that bind to a specific target molecule. I’m almost certain that this is the one big medical advances that is going to come out of this pandemic.
You already see companies including BioNTech doing something similar by deploying mRNA to treat early MS which is an autoimmune disease. These short segments of mRNA get coded into what are the equivalent of aptamers.
These aptamers can then bind to specific target molecules with a certain degree of specificity depending on the proteins encoded. That could include autoimmune antibodies or other disease causing molecules.