Dr. Phlip McMillan,  John McMillan

Four years ago, Belgian virologist Geert Vanden Bossche argued that mass vaccination could drive the evolution of SARS-CoV-2 variants capable of evading our immune defences. The idea sounded remote in 2021, but the continuous emergence of new viral lineages has validated his concerns. Omicron sub-lineages such as LP8.1.1 alone account for more than one-tenth of recent global isolates, LF.7.7.2 follows close behind, and an Alberta sample sporting “fifty spike mutations” forced laboratories to re-verify every step of their testing to rule out error. If the World Health Organization had to name every distinct COVID offshoot with a Greek letter, the alphabet would have been exhausted twice over.

Critically, most of this diversification has been observed in countries with extensive vaccination or hybrid immunity (exactly the landscape Vanden Bossche claimed would propel viral drift). While the timing initially seems off, the sheer proliferation of SARS-CoV-2 variants lends credence to his theory: repeated immune encounters apply underlying evolutionary pressure that selects for change. Geert forecasts that a variant potentially capable of widespread immune escape will eventually emerge. Yet, four years on, such a mass-casualty variant has not been observed.

Dr Philip McMillan, a clinician and researcher, posits that the disconnect lies in the presentation. Unlike the acute, severe respiratory illness characteristic of Alpha or Delta, current COVID variants often cause less dramatic initial symptoms. This leads to the question: has the danger truly lessened, or has it merely shifted, becoming delayed and harder to recognise?

The paradox is clinical. Unlike Alpha or Delta, many current infections begin and end with no more than a runny nose. This gap between relentless genomic churn and apparently “mild” disease has fostered a shrug among policy-makers and the public alike. Yet hospital statistics show continous excess deaths from stroke, cardiac arrhythmia and kidney failure. Something is not adding up.

The Quiet Mechanics of a “COVID STORM”

Early COVID killed mainly by an excessive inflammatory response causing blood vessels in the lungs to be blocked by microclots and preventing oxygen reaching tissues. Today the virus circulates in hosts who have been primed by vaccines, prior infections, or both. Airway defences such as mucosal immunity blunt the initial hit, but viral fragments can still slip into the bloodstream. Once in the circulation, those spike protein fragments are carried through networks of blood vessels throughout the body (brain, heart, kidneys, skin, everywhere).

Dr McMillan describes a significant shift in the disease’s typical progression, a concept he terms the “COVID STORM (Spike Triggered autOimmune Response Mechanism)”. This hypothesis moves away from the familiar picture of acute respiratory distress and can be outlined as a three-step sequence:

1. Mild upper-airway illness – often dismissed as a seasonal bug.
2. Persistent viraemia – viable virus or spike-protein debris circulates in the bloodstream for weeks.
3. Organ-specific fallout – endothelial irritation, micro-clotting or local inflammation, particularly affecting the vascular system, causes vulnerable tissues to fail.

This view reframes COVID-19, emphasising its nature not just as a respiratory illness but fundamentally as a vascular disease. Early in the pandemic, the virus was novel; it could reach the lungs unimpeded, sometimes provoking an over-zealous immune response or cytokine storm. Now, with widespread prior exposure through infection or vaccination, the dynamic appears different: while less likely to cause overwhelming lung damage, the virus may circulate more freely throughout the body.

Autopsy research backs this idea. Studies from 2022 onward have identified viral RNA or protein in heart muscle, kidney glomeruli and cerebral vessels long after nasal swabs turned negative. Spike-protein persistence appears most pronounced in patients who received multiple vaccine doses plus breakthrough infection, hinting at immune modulation (a shift in antibody and cellular response).

Data from clinical registries also reinforce this theory: Denmark reports a 12 percent thirty-day mortality among hospitalised COVID patients aged over 65, driven largely by vascular events rather than pneumonia. Similar trends emerge from England’s stroke audits and U.S. renal-replacement tallies. The critical challenge lies in the time lag. If serious health events occur weeks after a mild “cold”, the connection back to the initial SARS-CoV-2 infection can easily be missed, fostering a dangerous sense of complacency.

Stroke at the Vatican: A Case That Fits the Pattern

When Pope Benedict XVII (88, hypertension, diabetes) died of a sudden brain bleed on 30 March, official statements cited “irreversible cardiocirculatory collapse”. Weeks earlier he had battled bronchitis and bilateral pneumonia but appeared to recover. No PCR test confirmed SARS-CoV-2 infection, yet the timeline mirrors thousands of elderly cases where modest respiratory symptoms precede vascular tragedy.

Dr McMillan proposes a specific, though speculative, biological pathway linking the initial infection to the fatal stroke. This hypothesis involves the SARS-CoV-2 spike protein circulating in the bloodstream. Spike-protein fragments carry regions prone to misfolding in a prion-like manner. If circulating long enough, these fragments may disturb the blood-brain barrier. In brains already weakened by cerebral amyloid angiopathy (amyloid deposits lining small arteries), a final inflammatory kick can turn a silent weakness into a fatal haemorrhage. The hypothesis remains unproven, but it aligns with neuropathology reports that identify spike antigen in cerebral vessels months post-infection.

Importantly, the same logic extends beyond the brain. Similar “COVID STORM” effects could potentially impact the heart, kidneys or other organs susceptible to microvascular damage and inflammation. Kidneys filter 150 litres of blood daily; persistent micro-thrombi can erode function quietly. Cardiac muscle relies on tiny capillaries; endothelial swelling and clot fragments can cause arrhythmias without warning. None of these outcomes looks like “COVID” in isolation, which is why they risk being missed unless patient histories and datasets are examined side by side.

Mounting a Robust Defense

Robust mucosal immunity remains the first line of defence, whether through early natural infection, favourable genetics or an optimal vaccine response. This protects some individuals regardless of their vaccination status. Yet mucosal barriers wane with time, age and chronic disease. The remainder of the population sits on a spectrum of vulnerability shaped by exposure history, comorbidities and antibody phenotype.

The most significant danger, perhaps, is the prevailing narrative shift: reducing a virus that caused global upheaval to “just a cold”. Dr McMillan draws a parallel with HIV, which often presents with mild, flu-like symptoms initially but leads to devastating long-term consequences if untreated. “People are assuming that it is mild,” he warns, “and because it is mild, it’s irrelevant… It is not a cold.” Downplaying the risk ignores the potential for insidious, delayed damage, invites late diagnosis and contributes to missed research opportunities.

Geert’s Hidden Monster

Geert Vanden Bossche’s predicted “monster” may never appear as a single, instantly lethal variant that causes rapid, widespread respiratory failure like the earliest waves. Instead, the real danger might lie in the cumulative toll of continued viral circulation, which could drive delayed yet serious vascular, neurological, and immune-mediated complications through mechanisms such as the hypothesised “COVID storm”.

Steps to validate and mitigate these effects

• Clinicians should ask about recent respiratory illness when assessing unexplained stroke, kidney injury, or sudden arrhythmia, even if PCR tests are negative.
• Researchers should prioritise longitudinal tissue studies that map viral persistence, antibody-class shifts, and endothelial biomarkers.
• General readers should take lingering fatigue, chest flutter, or unusual neurological symptoms after “just a sniffle” seriously and seek follow-up rather than soldier on.

Recognising that apparently mild infections can trigger serious downstream problems is essential. The virus that shut down the world in 2020 is still with us, evolving and circulating. Geert’s “monster variant” may be playing a long game, weakening our vascular integrity through repeated, seemingly harmless encounters. Staying alert to subtle signals, logging data, and funding research on delayed complications offer the best chance of countering COVID-19’s next move.