Dr. Philp McMillan,  John McMillan

The World Health Organization declared the pandemic over. Governments moved on. Life returned to a semblance of normalcy. Yet five years after SARS-CoV-2 first emerged, the virus continues its relentless march through human populations, spawning variant after variant with no signs of slowing. The original SARS coronavirus from 2003 disappeared completely within two years, exhausting its mutation capacity. This one? Still going strong. “The reality is that I know some stuff that very few people know,” says Dr. Philip McMillan, a physician who has spent years tracking the virus’s unusual behavior. “The question is, suppose it is not just another virus.” What if treating SARS-CoV-2 like any other coronavirus is the fundamental mistake we’ve been making all along? Understanding where this virus came from isn’t just historical curiosity. It’s about grasping what we’re fighting and whether our current strategies have any chance of working.

The Internet Detective Who Cracked the Code

In May 2020, while most of the world was locked down and scientists were dismissing the lab leak theory as conspiracy nonsense, a 30-year-old man in Bhubaneswar, India, was doing something unusual. He was systematically combing through Chinese government databases in the middle of the night. The man, known only by his Twitter handle @TheSeeker268, had no virology degree or formal training in epidemiology. What he had was a photographic memory, fluency in advanced Google search protocols, and an unshakeable conviction that something didn’t add up about the official story. What he found would reignite the entire debate about COVID’s origins.

First came the biowaste contract. In December 2019, the Wuhan CDC issued a tender for disposing of two tons of biowaste. Along with it came a heat map showing a disease spread pattern across Wuhan, weeks before the official outbreak began. The location? The lab closest to the Huanan seafood market. Then came the timeline that made no sense. In September 2019, three months before the world knew anything about a novel coronavirus, Chinese authorities ordered RT-PCR testing kits specifically for coronaviruses. Why would you order specialized testing equipment for a virus that didn’t officially exist yet? The most damning evidence was what wasn’t there. After five years of intensive searching, no one has found an intermediate animal host that could have carried the virus from bats to humans. If SARS-CoV-2 had originated in the wet market as initially claimed, there should be a clear infection trail, from the person who caught or transported the infected animal, through every stop on their journey, leading directly to the market. That trail doesn’t exist. “Lab leak theory assumes someone was doing legitimate research and an accidental exposure occurred,” @TheSeeker268 noted. “That’s actually less biased than assuming ‘unsanitary wet market practices.'”

The Genetic Fingerprint That Shouldn’t Exist

What makes SARS-CoV-2 truly unique among coronaviruses is a 12-nucleotide insertion at the junction of its spike protein, a sequence completely foreign to all beta-coronaviruses. This insertion creates what’s called a furin cleavage site, changing everything about how the virus functions. Nobel laureate David Baltimore initially called the furin cleavage site “the smoking gun for the origin of the virus,” noting that the 12-nucleotide insertion “is entirely foreign to the beta-coronavirus class of virus that SARS-CoV-2 is in.” While Baltimore later clarified he remained uncertain about the virus’s origins, the furin cleavage site remains the subject of intense scientific scrutiny. Research published in Frontiers in Virology found that a 19-nucleotide portion of the SARS-CoV-2 genome encompassing the furin cleavage site is a 100% complementary match to a proprietary sequence found in US patent 9,587,003, filed in 2016. The patent? Titled “Modified polynucleotides for the production of oncology-related proteins and peptides.” Research focused on making viruses more infectious to cells for potential cancer therapy applications. The furin cleavage site isn’t just an academic curiosity. It’s the mechanism that allows SARS-CoV-2 to attack the human body in ways no other coronavirus can. While most coronaviruses optimize for one or two efficient entry pathways into cells, SARS-CoV-2 can use multiple receptor types, including ACE2, TMPRSS2, furin, neuropilin-1, CD209, TLR4, and GRP78, giving it unprecedented access to human tissue. Studies have demonstrated that the furin cleavage site is key to SARS-CoV-2 pathogenesis, with research showing that removal of the site reduces the virus’s ability to cause disease, confirming its central role in the virus’s enhanced capabilities.

Why a Lab-Enhanced Virus Behaves Differently

Natural viral evolution follows predictable patterns. Viruses gradually mutate over time, typically optimizing for a single efficient entry pathway. They adapt to their hosts, eventually reaching equilibrium. The original SARS-CoV mutated roughly six times per year before burning out completely within two years. SARS-CoV-2 has shown no such restraint. It continues mutating at rates far exceeding typical coronavirus evolution, showing no signs of stabilizing even after five years. More troubling is its unprecedented multi-system infection capability. The virus can infect the lungs, heart, kidneys, intestines, blood vessels, brain, and immune cells, an achievement no other coronavirus has managed. This isn’t how natural viruses typically behave. Natural selection usually drives specialization, not this kind of broad-spectrum capability. Early in the pandemic, the virus seemed almost perfectly designed to target populations with specific vulnerabilities: the elderly, those with diabetes, hypertension, and cardiovascular disease. People with elevated serum ACE2, a marker for cardiometabolic risk, showed the highest disease severity. Children were largely spared in the early waves, which is unusual for natural respiratory viruses that typically devastate both the very young and the very old. The virus’s ability to efficiently infect cells is enhanced by the furin cleavage site, which “makes the virus more efficiently infectious,” exactly the kind of enhancement gain-of-function research aims to achieve.

The Treatment Strategy Fork in the Road

Here’s where origin matters most: if SARS-CoV-2 evolved naturally, standard antiviral approaches should eventually work, and the virus should stabilize into an endemic pattern like seasonal flu. Vaccination should create stable, lasting immunity. But if the virus carries engineered enhancements, specifically the furin cleavage site and its multi-receptor entry mechanisms, then treatment strategies must target these specific features. Furin cleavage site inhibitors, multi-receptor blocking strategies, and approaches that account for the virus’s enhanced capabilities become essential. You can’t fight an engineered pathogen with tools designed for natural evolution. The stakes extend beyond current treatment. Understanding the virus’s origin shapes how we predict future variants. Natural viruses follow evolutionary selection pressures. Lab-enhanced viruses may retain their engineered features across multiple variant generations, recombining in unexpected ways. The Omicron variants now affecting children differently than early strains may be exhibiting exactly this kind of unpredictable behavior.

The Cost of Not Asking

The pattern is familiar and frustrating. The lab leak theory was dismissed as conspiracy nonsense, until it became mainstream scientific discussion. Early treatment protocols were suppressed, potentially costing lives. Questions were censored, ensuring research wasn’t conducted. “There can be no evidence if the research is not being done,” Dr. McMillan emphasizes. “The research has not been done.” Five years later, variants continue emerging. The virus continues its unprecedented behavior. And we continue treating it as if it’s just another cold. The origin question isn’t about assigning blame. It’s about understanding capabilities. A natural origin means we treat it like a normal coronavirus and wait for endemicity. A lab origin, whether accidental or intentional, means we need strategies specifically targeting engineered features. After five years without finding an animal host, watching unprecedented multi-system infection patterns, and observing continuous evolution with no plateau in sight, the evidence suggests we may be fighting with the wrong weapons. The question isn’t whether we’re brave enough to ask where COVID came from. It’s whether we can afford not to find out.

References:

@TheSeeker268, world’s foremost virus origins hunter, on how he began combing internet

MSH3 Homology and Potential Recombination Link to SARS-CoV-2 Furin Cleavage Site

Furin Cleavage Site Is Key to SARS-CoV-2 Pathogenesis

The Debate over Origins of SARS-CoV-2