To all aspiring young #WomenInSTEM: Mentee: Should I avoid being pregnant while trying to secure a faculty position? Me: Be pregnant & go on interviews. If they don’t welcome you with open arms and offer childcare options, they don’t deserve you. #KnowYourWorth

Such good work by @VirusesImmunity and team: "When they exposed the IgG antibodies from the long-COVID patients to nervous system tissues, they found that it attacked parts of the brain, thalamus, meninges, endocrine tissues, nervous system proteins ..." healthrising.org/blog/2026/0…

Today we had an incredible treat hosting Prof. Akiko Iwasaki @VirusesImmunity @BIG_CenterWashU @washumedicine! Thank you for visiting us and sharing your science! And thank you for your exceptional kindness! 🙏

Breaking: Funding from Vitalik Buterin’s Balvi Fund Expands Long COVID Rapamycin Trial PolyBio today announced new funding that is supporting an open-label extension phase in a clinical trial investigating low-dose Rapamycin as a potential treatment for Long COVID. All participants—including those initially randomized to placebo—will receive low-dose rapamycin during a defined follow-up period. 1/

IgG from Long COVID patients attacks nerves/brain tissue. Inject into mice --> real pain, fatigue, coordination loss, nerve damage ... Matches patients perfectly. Psychosomatic bros in shambles. Autoimmunity wins. Science > dismissal. 🧨 We need more research like this!

Ich freue mich sehr über die Kooperation mit Prof Akiko Iwasaki @VirusesImmunity bei dieser wichtigen Studie. Sie ist ein Meilenstein für unser Verständnis der Rolle von Autoantikörpern bei Long COVID. Link zum Artikel und der Thread von Akiko Iwasaki. sciencedirect.com/science/ar…

IgG von Menschen mit Long Covid führten bei Mäusen unteranderem zu Schmerz, Fatigue, Small Fiber Schäden. Generell waren Auto-AK gegen vaskuläre und neuronale Strukturen nachweisbar. Hoffentlich ein Schritt zu Diagnostik/Therapie, die Betroffenen Gaslighting zukünftig erspart.

A terrific study that sheds important insights into Long Covid

Wonderful day for a new #LongCOVID paper! Thanks to an incredible collaboration with @VirusesImmunity and brilliant work done by @keylas3, we studied the effects of injecting antibodies taken from people with LC into mice compared with what happened sciencedirect.com/science/ar… 1/

‼️‼️📄A new paper by Akiko Iwasaki and colleagues has just been published, and it goes exactly in the direction of what I commented on yesterday. Yesterday I posted that, in a relevant subgroup of Long COVID and ME/CFS, post-exertional autonomic dysfunction could fit very well with autoimmunity against GPCRs, especially muscarinic receptors. This new work takes an important step forward because it no longer stops at “there are autoantibodies”: it shows broad autoimmune reactivity against neural and vascular/peripheral tissues, includes profiling against GPCRs and ionotropic receptors, and also demonstrates that passive transfer of IgG from Long COVID patients into mice induces pain, fatigue-like behavior, loss of balance/coordination, small fiber nerve damage, and pain-related neuronal activation, recapitulating key symptoms of the donors. That strongly reinforces the idea that, in a subgroup of Long COVID, there is indeed functionally pathogenic autoimmunity, not just a nonspecific association. Another important point is that the paper does not reduce everything to a single autoantigen. On the contrary, it shows heterogeneity, with reactivity against the locus coeruleus, thalamus, sciatic nerve, meninges, and also against peripheral tissues such as the adrenal gland and thyroid. In other words, the message is not “there is only one antibody,” but rather that Long COVID probably contains several autoimmune subgroups, some more neurological, others more vascular, others more autonomic or glandular. For me, this paper strengthens an important transition: we move from suspecting autoimmunity to having much stronger evidence of pathogenic autoantibodies in a subgroup of Long COVID. The next step should be to demonstrate which ancestral HLA-II haplotypes / susceptible alleles are behind the development of that autoimmunity. Because if we are already starting to see more clearly that there are functional autoantibodies, and that some of them can target neural, vascular, and autonomic circuits, then the logical next question is: which patients are the ones who most easily lose tolerance after SARS-CoV-2 infection?

Crucial paper on #NeuroCovid just published! #LongCovid patients with neurocognitive symptoms showed increased antibodies against the nervous system that correlated with several neurological symptoms. Targeting these antibodies might offer therapeutic benefits for some patients

Important #LongCovid finding of auto-antibodies in patients directed to neural tissue, and then, by transferring the antibodies, recapitulated the disease symptoms in mice @CellCellPress @VirusesImmunity @putrinolab cell.com/cell/abstract/S0092…