Clinical reasoning · Post-viral immune dysregulation
A postgraduate-level course for clinicians who want a structured, evidence-calibrated way to reason through Long COVID — organ damage versus immune dysregulation, phenotype recognition, and diagnostic safety. Built on peer-reviewed immunology, and honest about what remains hypothesis.
The clinical problem
Years into the pandemic's aftermath, post-COVID illness still doesn't behave like the conditions most of us trained on. Patients present unwell with normal investigations. Symptoms cross organ systems and resist a single label. Post-exertional malaise, dysautonomia and persistent immune activation sit largely outside the frameworks we were taught — and the evidence base is moving quickly enough that some of last year's certainties are this year's open questions.
This course is an invitation to reason through that gap deliberately, rather than around it.
If your framework for the post-viral patient feels incomplete, that isn't a gap in your competence. It's a gap in the field — and it's worth closing.
Fit
This is a reasoning course, not a treatment protocol. Being clear about that up front respects your time.
Proposed structure
A draft outline of the clinical-reasoning arc. Content is in development and may change; module tags show where the underlying science is hypothesis, contested or novel.
Why single-diagnosis thinking stalls when several processes overlap in one patient, and what replaces it.
The central differential — different mechanisms, investigations and safety nets — and how the distinction reorganises the work-up.
A proposed unifying driver — persistent macrophage and innate-immune activation — presented as a testable model, with its supporting evidence and its gaps.
Why the gut–immune interface may amplify persistent activation, and why sequence can matter more than symptom loudness.
Recognising autonomic and exertional phenotypes — and the safety point on why graded exertion can backfire.
Endothelial and coagulation findings as a phenotype domain — with the microclot question presented as genuinely unresolved, not a basis for practice.
Cognitive symptoms as a neuroimmune phenomenon — including original, explicitly-flagged proposals held as tentative until tested.
The discipline of holding “immune dysregulation” and “serious alternative diagnosis” in mind at once — and treating normal results as information, not reassurance.
Draft outline · subject to change before enrolment
How we handle evidence
The labels aren't decoration — they run through every module. This is the part designed for the sceptic in the room, and it's deliberate.
Supported by peer-reviewed evidence we can point to directly.
A biologically reasoned model that is not yet settled. The macrophage-centred hub sits here — proposed, testable, not proven.
Findings under genuine scientific dispute — such as microclots — presented as open questions, not resolved ones.
Original proposals from this work, flagged as tentative and unproven, and kept clearly separate from established evidence.
Fair questions
If you're weighing whether this is worth your attention or your name, these are the right things to ask.
Continuing professional development
The course is being designed to meet CPD standards, and we are working toward formal accreditation so that your time can count toward your professional development.
No obligation
Registering simply means you'll hear first when the structure is finalised, when enrolment opens, and where CPD accreditation stands. There's no automated sequence and nothing to buy.
Your message reaches the McMillan Research team directly. We'll reply personally — clinician to clinician.