Response to Clare Craig

Dear Clare,

Thank you for your reply. 

The purpose of my letter was to better grasp your working hypothesis about what actually happened. I failed to specify a timeframe in the post title; I was referring to late 2019/early 2020.

In this response, I remain focused on verifying my understanding in relation to the questions I posed last week. There are points you raised that I do not address here; this should not be taken as agreement with or resistance to engaging with those points or any associated studies.

You responded to two of my questions by saying you can’t prove [X or Y]. That’s okay because I wasn’t asking for proof or challenging you to provide evidence for your beliefs. Rather, I was asking about what you personally believe, suspect, or think. Opinions, speculation, and conjecture are not illegal—at least not yet.😊

Lab Origin and Deployment

• Do you operate from the assumption that SARS-CoV-2 was “created” or tinkered with at WIV, irrespective of whether another lab may have been working on a version thereof? 

• You stated “anyone could have mimicked that work [at WIV] as a decoy.” By ‘anyone,’ do you mean ‘any other virus lab anywhere else'? What do you mean by 'decoy'? I’ve used 'decoy' to describe both SARS-CoV-2 and the COVID shot, so I’m comfortable with the term, but I don’t assume your meaning aligns with mine. 'Decoy' implies intent—do you mean to convey intent? If so, could you elaborate?

• You propose a mechanistic explanation for how the 'manmade' virus spread once it was 'out there.' However, like Matt Ridley, you haven't addressed how the Antagonist may have moved from its point(s) of origin to everywhere else and are instead asking the audience to simply accept that the virus 'got out there somehow.' In either a leaked/escaped or released scenario, what exactly are you envisioning could have occurred? What possibilities exist?¹ For example, is the idea that infected lab workers left the lab, expelled the virus into the air, and from there, 'it' took off? Given the conditions and timing you’ve suggested, it seems you would have to believe that something was either sprayed or released into the air at one or more locations—or delivered through a very direct method. Can you clarify your position?

• If you're reluctant to propose possible scenarios, perhaps you could instead share what you believe could not have happened?

• I don’t see a direct answer to my question about whether you believe Gain of Function is capable of producing agents can at least match nature. Based on your response about the virus causing a specific and unique disease, I assume your answer is yes. (Please let me know if I am mistaken.)

Spread/Transmission

• I currently believe that a newly-named coronavirus was not suddenly, quickly, or exponentially spreading from person to person or circulating in the air [in late 2019/early 2020]. When I say “spread” I am referring to the WHO’s (abrupt and unsubstantiated) claim in January 2020 that human-to-human transmission of the virus was occurring. Am I correct that you currently believe a newly-named manmade coronavirus was spreading in the air in late 2019/early 2020 - beginning on/around October 2019 - and (to a lesser extent) transmitting between humans?

• Here’s my layperson’s summary of your mechanistic proposition for spread once the virus was “out there” from the lab(s). Please let me know if this is correct.

  • The primary driver of SARS-CoV-2 spread, in your view, is aerosol transmission. This must be the case, you assert, because 'spread was too rapid, continued throughout lockdowns, reached remote places, and was unhindered by masking.' Aerosol transmission occurs when people exhale virus-containing particles into the air, where they can remain for 'very long periods of time.' 'Spread' is extremely fast, and the viruses and its variants 'traverse the world' independently of air travel. Most transmission occurs at night—when people are typically indoors or asleep.

• You believe SARS-CoV-2 was “spreading in a low-grade way” before March 2020. What does “spreading in a low-grade way” mean? In the air at a low prevalence/concentration and not being inhaled and expired at a high rate by many living things? Or, in the air, widely-”spread”, but not impacting surveillance, death, or any other kind of data for other reasons? Am I correct that your evidence for believing in this “low-grade spread” is the results of antibody testing/seroprevalence studies?

What Might’ve Been

• Your beliefs regarding October 2019 - May 2020 (and thereafter) seem almost entirely dependent on testing of one kind or another. That said, I’d like to pose questions that build off Footnote 7 in this article, which says:

  [Clare Craig] believes “covid” is a novel and characteristic disease caused by an engineered virus, albeit one the effects of which have been drastically exaggerated, such exaggeration in itself causing nearly all the associated harm; she believes that had we done nothing and not tested for anything, an out-of-season flu spike in influenza-like illness would have been noted.

  Put differently, you contend SARS-CoV-2 was “new”/newly-introduced to humans/their environment at some point in time and - had it gone ‘unfound’, unannounced, and “un-reacted to” - many places would’ve seen an out-of-season flu spike in outpatient and emergency department visits for influenza-like illness in spring 2020.

  • What is your rough estimate for this spike (% over normal for time of year)?

  • Do you believe the off-season ILI spike would have been accompanied by an increase in respiratory disease deaths? Why or why not? (If yes, what is your rough estimate for the rise? Would the rise have materialized in all-cause mortality for those weeks?)

  • UPDATE (post-pub): I didn’t initially ask about testing because the footnote quoted above says “and not tested for anything,” meaning SARS-CoV-2. Obviously, flu testing was happening; in the U.S. (and UK too, I think), the “surveillance season” is October through May. You are assuming more ILI in the form of visit data AND flu tests being given, but NOT in flu tests coming back positive, correct?

  • Which places (cities/regions) do you think would have seen such a spike - and why?

  • You believe COVID-19 is a “characteristic disease” caused by SARS-CoV-2.² Reviewing the long list of associated symptoms, is it your assumption that this “characteristic disease” would have been observed or characterized as such without a virus name, test, etc.? (Would it have been detected clinically?)³

This is my last set of questions.

I appreciate your time.

Regards,

Jessica

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Clare’s reply

Another reply to Jessica Hockett

My response to the above reply

Response to Clare Craig

1. This is something I’ve wondered about for a while (see January 2023 post). It seems key for lab origin proponents to be able to explain, unless they are proposing certain direct mechanisms.

2. I do not. See all articles here.

3. I haven’t spoken to any doctor or nurse in the U.S. who says they were seeing a new disease or difficult-to-treat pneumonia prior to the deployment of testing in their hospital.