On a related note, did Altmann say anything else interesting about his studies in his talk?
It was more an overview, history and call to arms talk. He showed QoL and employment data for their 1000 adult cohort (terrible as you'd expect). He emphasised not becoming siloed with our pet hypotheses and to keep options open and work together.
"During the last four or five years, evidence has appeared of variable quality for all of these. And so they all have some evidence base, some stronger than others. I guess my plea to all of us as a community is not to become tribal or siloed about them, to try and just pull together to try and work out what on Earth is going on. […] Four or five years later and 50,000 publications plus on PubMed later on long Covid, as a group we've learnt a lot and published a lot — we haven't done terrifically well at helping those 400 million people with long Covid."
He talked about the induction of autoimmunity and as a potential driver for symptoms. (Looking at
HuProt arrays) —
"When we look at those, we do see clusters of auto-antibody specificities coming up together in a proportion of our patients. They're sometimes extracellular targets, often intracellular targets. Some of our referees have given us a hard time about that. So how can an antigen
possibly be involved in an autoimmune disease if it's intracellular? Um, they're going to be horrified when they learn about diseases like lupus and Sjogren's and myositis and the targets in those."
"… often leads you to study T cell auto-antigen targets as well. […] Some of these auto-antigens with really good credentials in potential perturbations of immune responses. We're trying to follow up at the moment."
He did cover it not being "airborne-AIDS" —
"Clearly we sign up to [LC] being a disease of immune subversion […] I certainly feel that on social media and in my email in-box I'm confronted by a lot of people […] who feel that to explain the symptoms the immune system must be shot to pieces and SARS-CoV-2 must have destroyed the immune system. And unless I agree that long Covid is AIDS-like that I've somehow let people down. […] I do think there are immune subset differences, but I don't think it's remotely AIDS-like, I think these are quite nuanced disturbances."
On the things we need —
"In my life I've been involved in two of these, even harder than long COVID. […] This was moving from a complete dog's dinner to a situation where now we have 220 loci, some of them like HLA-B with 10584 alleles where we know them to the nearest nucleotide in any given population, for all their disease associations. […] And that started out in conferences like this […] And ditto all those CD antigens […] Could Sante Fe be known as the transformative moment when we all put our heads together and really did this job and showed that we can do as well for long COVID as we did for the HLA workshops and CD antigen workshops. And just get it sorted to open up the flood gates for all of those biomarkers that we need for the trials."
