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Post-COVID / Long COVID mechanisms

COVID Immunology and immune dysregulation

Post-pandemic gut health and the microbiome

Nitric oxide and vascular biology

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Start with the research framework that predicted COVID autoimmunity before the consensus

Dr McMillan's research team — including Prof Anthony Turner, who co-discovered ACE2, and Prof Bruce Uhal, a leading pulmonary ACE2 researcher — published on COVID autoimmunity in May 2020, months before it entered mainstream scientific discourse.

That original hypothesis has since been validated by independent research groups. The page below brings together the core publications, the evolving framework, and the principles connecting ACE2 autoimmunity, gut-related viral persistence, and macrophage-driven long COVID.

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The immune disruption you are reading about has a deeper framework behind it

Much of the immune dysregulation seen after COVID-19 connects back to ACE2 — the receptor the virus exploits and the host may develop autoimmunity against.

Dr McMillan's published research explores this mechanism from the original 2020 hypothesis through to the 2026 macrophage-centred long COVID framework. If you are interested in how immune dysregulation, autoantibodies, and chronic macrophage activation fit together, the research page below is the most comprehensive starting point.

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The gut is not a bystander — it may be a central driver of long COVID

One of the key publications in Dr McMillan's research programme examines how the gut serves as a site of viral persistence after acute infection resolves. Published in 2024 with Prof Turner and Prof Uhal, the paper proposes that gut barrier disruption, microbiome changes, and localised immune activation contribute to the chronic symptoms that define long COVID.

The research page below puts this work in context alongside the broader ACE2 autoimmunity and macrophage frameworks.

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The intersection of virology and oncology is an emerging research area

Dr McMillan's research into ACE2 disruption, immune dysregulation, and viral persistence touches on mechanisms that are increasingly relevant to the cancer-virology intersection — including CD147-mediated pathways and chronic macrophage activation in tissue microenvironments.

While the primary research page focuses on COVID autoimmunity and long COVID, the mechanistic principles explored there are directly relevant to these broader questions.

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Viral persistence may be the key to understanding why symptoms do not resolve

Two of the five core publications in this research programme directly address viral persistence — one examining gut-related reservoirs, and one exploring how chronic macrophage activation sustains the inflammatory state long after acute infection clears.

The research page below brings these together alongside the original ACE2 autoimmunity framework and the independent evidence that validated it.

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Vascular biology connects directly to the ACE2 framework

ACE2 plays a central role in vascular regulation — it is a key enzyme in the pathway that maintains nitric oxide bioavailability and endothelial function. Dr McMillan's research proposes that autoimmune disruption of ACE2 helps explain the vascular and endothelial patterns seen in COVID-19 and long COVID.

The research page below covers the full framework, from the original 2020 hypothesis through to the 2026 macrophage model.

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