It was approaching midnight when I finished almost 140 pages of testimony from Dr Ralph Baric, one of the world’s most experienced coronavirus researchers. I had intended to skim the document and return to it later. Instead I found myself needing to capture my thoughts immediately.
What concerned me was not a single dramatic admission. It was the pattern across the interview.
I saw a research community asking remarkably specific questions about SARS-related coronaviruses before the pandemic. Why did known sarbecoviruses lack furin cleavage sites? What would happen if an appropriate cleavage site were introduced? Would it alter entry, tissue tropism or disease? How could researchers show that such a change was causal?
These were not abstract questions. They formed part of a proposed experimental programme. That does not prove SARS-CoV-2 was created in a laboratory. But I cannot examine this record honestly and keep pretending a research-related origin is an irrational or scientifically illegitimate possibility.
What Baric Actually Acknowledged
The most important exchange concerned gain-of-function research.
Baric explained that removing a feature from a virus can show the feature is necessary for a particular effect. But to demonstrate causation more directly, a researcher may introduce that feature into another viral backbone and determine whether the virus acquires a new function.
His description was unambiguous: “That’s a gain-of-function experiment. There is no other way to think about it.”
This matters because the DEFUSE proposal involved searching for novel SARS-related coronaviruses and examining the importance of their cleavage sites. It also contemplated introducing human-compatible cleavage sites into selected viral backbones and evaluating the biological consequences.
The proposal was not funded by DARPA. That is an essential limitation. A rejected proposal is not evidence that the proposed experiments were performed elsewhere.
It remains evidence, however, that the work was being conceived, that the technical capability existed, and that the investigators regarded the absence of furin cleavage sites in known sarbecoviruses as an important scientific question before SARS-CoV-2 emerged.
I also have to correct an easy overstatement. Although the wider consortium included the Wuhan Institute of Virology, Baric testified that the proposed live-virus insertion component would have been performed by his laboratory. I therefore cannot claim DEFUSE proves a furin cleavage site was to be inserted at Wuhan.
What I can say is that a Wuhan-linked research collaboration was collecting and characterising SARS-related coronaviruses while the consortium proposed introducing cleavage sites into viral backbones. SARS-CoV-2 then emerged in Wuhan with the first recognised polybasic furin cleavage site among the sampled sarbecoviruses.
I consider that correspondence scientifically significant. I do not consider it proof.
Why the Furin Cleavage Site Matters
I think of the coronavirus spike as a folded entry mechanism on the surface of the virus. Before it can operate efficiently, parts of the spike must be cut by enzymes the host produces.
The furin cleavage site gives the virus access to a widely distributed human enzyme that can prepare the spike before it reaches the next cell. That can affect how efficiently the virus enters certain cells, which tissues it reaches and how readily it spreads.
Furin cleavage sites are not unique to SARS-CoV-2. MERS, HKU1 and OC43 also possess functional cleavage sites. The unusual point is narrower: before the pandemic, this feature had not been observed at the equivalent position in the known sarbecovirus lineage containing SARS-CoV-1 and SARS-CoV-2.
Baric believed natural sarbecoviruses with furin cleavage sites probably existed and had simply not yet been found. His testimony therefore does not support the claim that he considered natural acquisition impossible.
But this creates the central tension for me. Researchers considered the feature important enough to search for in nature and potentially introduce experimentally. When a virus then emerged carrying that very class of feature, the possibility of laboratory involvement was treated publicly as almost unthinkable.
I do not find that intellectually satisfactory.
The Origin Discussion Was Never as Settled as It Appeared
The public was told early in 2020 that genomic analysis strongly favoured natural emergence. The Proximal Origin paper played an enormous role in shaping that view.
Baric’s testimony reveals a more complicated position. He said natural origin was initially his leading explanation, and he regarded deliberate genetic engineering as unlikely. Yet he also stated that he never ruled out a laboratory leak and did not understand how anyone could conclusively exclude one.
I believe that distinction was largely lost in the public discussion.
A laboratory-associated origin does not require someone to have constructed SARS-CoV-2 nucleotide by nucleotide. A naturally collected virus could escape during research. A virus could change during laboratory passage. A modified virus could be involved. These are different hypotheses requiring different evidence.
The correct conclusion is not that laboratory origin has been proved. It is that it was pushed outside acceptable scientific discussion before the necessary evidence had been obtained.
Why I Am Not Treating This as Ancient History
For me the most important question is no longer simply where the virus came from. I want to know what kind of biological problem I am dealing with.
If SARS-CoV-2 acquired unusual properties through laboratory manipulation or adaptation, I would want to know precisely which properties were enhanced. Was the change limited to respiratory transmission? Did it alter tissue distribution? Did it change how spike is processed? Did it increase access to vascular, immune or neurological compartments?
I cannot assume an engineered origin would automatically explain Long COVID. That would be another leap beyond the evidence. Natural evolution can also produce viruses with complex and damaging properties.
Even so, origin and pathogenesis cannot be completely separated. If the virus was selected or modified according to particular experimental objectives, those objectives could point me towards biological functions that deserve closer investigation.
That is why I think the gain-of-function question remains medically relevant.
From Acute Infection to Immune Pathology
Since 2020 I have argued that the most serious effects of COVID cannot be understood by counting infected cells. I have been particularly concerned about the immune response triggered by spike: vascular inflammation, macrophage activation and autoimmune phenomena.
Baric’s testimony also revisited an older coronavirus-vaccine concern. In animal work with alum-adjuvanted SARS vaccines, researchers had observed a strong T-helper-2 response and potentially dangerous inflammatory pathology after viral exposure. Baric said this was why he had warned the WHO and others to look carefully for vaccine-associated immune pathology.
He also explained that the subsequent mRNA-vaccine studies he participated in did not show the same signal in their experimental systems. I therefore cannot use the earlier alum findings as proof that current mRNA vaccination produces the same pathology.
What the history does show is that re-exposure has long been recognised as an important immunological question in coronavirus research.
That is the part I believe is now being neglected.
A person may experience an apparently mild reinfection and then develop cardiovascular, neurological, gastrointestinal or inflammatory problems weeks later. Without longitudinal studies, tissue analysis and autopsy work, I cannot confidently determine whether these events are connected.
Absence of immediate respiratory collapse is not evidence of biological harmlessness.
The Claim I Think We Can Defend
I cannot honestly say Baric’s testimony proves SARS-CoV-2 was engineered. I also cannot say DEFUSE proves the proposed furin-cleavage-site work was performed.
What I can say is that, before the pandemic, scientists connected to a Wuhan-centred coronavirus research programme had identified the absence of furin cleavage sites in known sarbecoviruses as a major research question. They proposed searching for such viruses and experimentally introducing suitable cleavage sites to test their effects. Baric himself classified the causal insertion experiment as gain-of-function research.
SARS-CoV-2 then appeared with precisely the kind of previously unobserved feature the proposal had highlighted.
I believe that coincidence is too important to dismiss, but still insufficient to establish causation.
The missing evidence is not technical plausibility. It is provenance: the original samples, complete sequence databases, experimental records, laboratory notebooks and incident documentation.
I Believe the Medical Question Is Still Open
I understand why people want to move on from the pandemic. But I do not believe the biology has agreed to move on with us.
I am seeing signals of persistent ill health and changing patterns of inflammatory disease that require serious investigation. I must be careful not to assign all of those changes to SARS-CoV-2 without appropriate controls, age-standardised data and mechanistic evidence. Temporal association alone is not causation.
But refusing to investigate the association is not scientific caution either.
I need to keep three questions separate but connected: where SARS-CoV-2 came from, which biological functions made it unusual, and whether repeated exposure is contributing to cumulative immune-mediated disease.
I do not yet have final answers. What I have is enough evidence to reject complacency.
If this virus was enhanced, adapted or selected in a research setting, understanding that history may help me identify the functions that continue to matter clinically. If it arose entirely through nature, its unusual biology still demands the same attention.
Either way, the greatest mistake now would be to confuse a milder acute presentation with a harmless virus. The origin debate matters, but the deeper responsibility is to understand what SARS-CoV-2 continues to do after the visible infection has passed.
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