Lecturer Life Sciences: HU University of Applied Sciences | PhD in Neuroscience | Exotic animal keeper | Dancer | Runner | Tries to play guitar • He/Him ⬛🌫️⬜🟪

Joined November 2019
Back at the @ISLCPAIS , bit too late because of traffic issues. First talk is on the creation, goals and aims of the ilsc-PAIS working group
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What about noninfectious cases? Chemical exposure, extreme psychological distress leading to ME?
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This was an audience question. The organization stated that knowledge on these etiologies is also valuable, it is not the focus of the organization since they want to have the infection associated angle at the forefront. Though the welcome collaboration with associated themes
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Time for the last talk by @DavidPutrino. But first some explanations about award tht are in the works by ILSC-PAIS. Proposal request will open somewhere in October.
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A crash leads to increased blood lactate - and putrino is suggesting continuous blood lactate monitoring as possible pacing support
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Q: from Q fever advocacy - is there a way of measuring effects of Mito related symptoms? - no, not conventional. But putrino measures resting metabolic rate. Seems people with Mito dysfunction have higher BMR, through burning carbs
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Takeaways: 1: treat drivers, not symptoms 2: complexity isn't mysterious 3: run towards complexity, not away from it. For me this all boils down to wicked problems, interdisciplinary approaches and daring to take steps into the unknown. Hope the @ISLCPAIS makes that happen!
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What do we need next: testing for large arrays of autoantibody activity. We now only have set specific tests. Interventions: IVIG, FcRn inhibitors - make these more available Next big step: personalized medicine eg. CAR-T
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Autoimmunity: study: expose human IgG from controls and LC to human brain tissue. Antibodies are reacting to human brain tissue. Injecting mice with the AABs from pwLC with pain as symptom showed pain.
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Mitochondrial transplantation following optic crush injury - autologous from a healthy muscle. Could this be an avenue. David Putrino is exploring this
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mitochondrial dysfunction: many papers that show that this is happening in LC. But trying things in patients is trial and error. Know what exactly is wrong in the Krebs cycle would be a nice next step. But probably very individual
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We are not adequately evaluating what happens in our bodies after SARS-CoV-2 (regarding viral/bacterial reactivation)
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Viral reactivation: sustained reactivation in pwLC is possible. Also bacterial reactivation, bartonella henselae. Think broad about viral persistence, what else has SARS-CoV-2 riled up?
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What do we need next: subtyping with viral persistence as a basis. Medications that can penetrate immune privileged sites if the virus is still there. Intracellular targeting of SARS-COV-2
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Learning from successes and failures. Eg. The LC-PAX trial. Ideas of why it failed can also help inform future research.
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There are many others, but David skips to mystery 3
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Mystery 2- exploration of LC along 10 key symptoms 1: viral persistence. Lots of evidence for virus in some way sticking around. Eg antigen persistence in people with LC more frequent.
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Good point: should treatment approaches change depending on cause. Eg. Diabetes following COVID?
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Mystery 1: we don't know how to diagnose LC Mystery 2: we don't know why they are so sick Mystery 3: we don't know how to treat LC
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Main theme will be on 'mythbusting' - 3 mysteries on LC
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Time of the last parallel session at @ISLCPAIS. First on the PIPASC study on neuroinflammation after SARS-CoV-2 infection.
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Q: fiber type specific effects and other waste products? - no separation of fiber types yet. No look into other waste products yet.
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Data suggests impaired autophagy and some aspects of increased muscle aging
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