Part V - Getting closer to the truth behind the brain virus experiments

Are they the result of some bait and switch?

In Part 4 of this series on the brain virus, I highlighted numerous inconsistencies and gaps that could have influenced the studied outcome. Asking whether these could have resulted in lab mishaps suggested the possibility that the researchers may not have reported all their findings, that additional mutations could have taken place, and that there may be an intentional misnaming of the key viral variant in question. All this is speculative but follows rationally from the many disparities found in the study.

Even though it may indeed be that the researchers did additional lab work that was not explicitly spelled out and which may have resulted in undocumented mutations, it is still hard to believe that this would be enough to explain the emergence of a killer virus from a documented harmless progenitor.

Something else seems to be missing. In Part 4, I suggest another option: the inconsistencies and gaps may have contributed to the study outcome, yet additional factors that may have been just as important were overlooked

In this part, I will focus on a different type of contributors, not in terms of genetics or biological or evolutionary mechanisms, but funding.

And indeed, it may explain a lot I had not seen before - the possibility of a major bait and switch.

(Outlook: the next part of this series will look at the new preprint version that indicates bait and switch no. 2).

Previous work

As mentioned previously, in their prior work, Lu, Song, and colleagues (all members of Song’s lab) focused on, among others, vaccine development.

In their previous publication publication by Lu et al., the SARS-CoV-2-related pangolin variant GX_P2V(short_3UTR) was  investigated for two main reasons:

(1) To increase the understanding of CoV pathogenesis,

(2) As a basis of a new live attenuated vaccine for SARS-CoV-2.

Authors had high confidence in GX_P2V(short_3UTR) as a vaccine candidate

The idea that the GX_P2V(short_3UTR) variant could become a vaccine for SAR-CoV-2 was supported by Lu et al. by their following findings:

• Its attenuated nature, which was tested and confirmed in golden hamsters and BALB/c mice, and supplemented by various in vitro infection models.

• “Induction of significant neutralizing antibodies against SARS-CoV-2” (this was likely regarded as extremely important, seeing that this feature was particularly highlighted in the article title itself.) The authors found that golden hamsters, when infected intranasally with GX_P2V(short_3UTR), had a short duration of productive infection in pulmonary, not extrapulmonary, tissues. Of note, this infection induced neutralizing antibodies against pseudoviruses of both GX_P2V and SARS-CoV-2.

• High titer: In hamster sera, GX_P2V(short_3UTR) had a similar titre of neutralizing antibodies against SARS-CoV-2 when compared to sera from convalescent Covid patients.

• Substantial cross-neutralizing activity of the GX_P2V(short_3UTR) virus: the observation of the high neutralizing antibody titer against (pseudoviruses of) SARS-CoV-2 in the sera of hamsters was seen as highly promising. Now, the receptor binding domains of GX_P2V and SARS-CoV-2 share only 86.8% amino acid identity and only a single critical receptor-binding residue. Thus, the observed high titer indicated a great potential of this variant as a vaccine against SARS-CoV-2 variants or even related CoVs.

Note: NAb titer in test tube measurements has in recent years not only been regarded as a proxy for the efficacy of a vaccine in real life, but has been elevated to a de-facto gold standard; numerous studies and publications have followed this narrative, assuming that higher titer can be taken as a proof of better vaccine efficacy. However, this narrative is entirely flawed. That this measure is not only a poor proxy but often leads to seriously mistaken interpretations and results, has long been kept from the public. Please see also my book where I discuss some of the “inconvenient truths” in this regard.

Authors had a hypothetical explanation of what had caused the attenuated nature of GX_P2V(short_3UTR)

Lu et al. admit that the original wild-type GX_P2V virus was not isolated and thus was not available for comparative analysis. What they focus on is the attenuation of  GX_P2V(short_3UTR) in the tested animal models, asking specifically:

“How could GX_P2V produce these attenuating phenotypes while having growth capabilities similar to those of SARS-CoV-2?”

In their view, the attenuation can be explained and they offer two reasons. Importantly, one is the 104-nucleotide deletion in the hypervariable region (HVR) of the 3′-UTR of GX_P2V(short_3UTR). This is based on analogous findings obtained in a mouse hepatitis virus (MHV) model that revealed an association between HVR mutations and viral pathogenicity. 

(Note: Ironically, Lu et al. also postulate that the attenuation may be linked to the low virulence nature of the GX_P2V spike protein. I find this interesting as this suggests they were likely aware of the adverse potentials of the SARS-CoV-2 spike -- which has become the critical basic of most SARS-CoV-2 vaccines. The troubling and uniform vaccine design was rooted in, and enabled by, the official narrative that vehemently objects to spike’s intrinsic toxicity. I discussed all of this in my book.)

Authors suggested a novel attenuation strategy for making a live Covid vaccine based on the 104-ntd deletion

It may be interesting to note that in the earlier part of the pandemic, China was still actively using live attenuated vaccines. Lu and colleagues praise the effectiveness of these vaccines as they are able to stimulate both humoral and cellular immunity evoking a lasting immune response. In general, before the mRNA vaccine hype, most would have agreed with this assessment.

Admittedly, one of the main challenges with such vaccines is to ensure their (lasting!) attenuated nature.

In this regard, Lu and collaborators propose that their findings may also be utilized as a novel attenuation strategy, emphasizing

“[S]hortening the 3′-UTR is a novel strategy for making a live attenuated SARS-CoV-2 variant that warrants further investigations.”

In summarizing the expected benefits of GX_P2V(short_3UTR), the published paper by Lu et al. is very optimistic about this pangolin CoV variant, as follows:

• GX_P2V(short_3UTR) itself could serve as a live attenuated vaccine against SARS-CoV-2.

• Its attenuated nature has also the potential as a vaccine vector for the expression of protective antigens like SARS-CoV-2 RBDs.

• Shortening the 3′-UTR is a novel strategy for making a live attenuated SARS-CoV-2 variant.

A Shift of Research Goals - From Vaccines to Spillovers: Is This an Intentional Bait and Switch?

Based on their confidence in developing a new Covid-19 vaccine, it would not be surprising that the group around Song and Lu further investigated GX_P2V(short_3UTR)  for its expected potential.

Apparently they tested this vaccine candidate on different animal models, including the specific humanized mice model mentioned in the preprint. And this is when the big oops may have happened.

In this context, their conclusion that the high mortality of the virus was “surprising,” is now beginning to make sense. It indeed is the opposite of what they had predicted in their previous work.

Rumor has it that the publish-or-perish directive is as merciless in China as elsewhere, or worse.

So, what might all of this have looked like from the perspective of these researchers?

• It seemed they had a strong model for a novel live attenuated vaccine candidate, including a mechanism to facilitate this attenuation.  

• “Surprisingly” however, this idea backfired - their own experiments on humanized mice seemed to suggest the opposite.

• Some may say they had done a lot of work on those viruses, in vain.

• Some may even say that researchers follow the hype (or the money).

• The article by Lu et al. was published in 2022 at the tail end of China’s utilization of live attenuated vaccines for Covid. But then the narrative changed, with the claim that inactivated vaccines  elicit lower levels of antibody response compared to ones using mRNA technology (there is more to this assertion, please see my book). The new hype seems to have reached China sometime in 2023, and by the spring of 2023, China had its own mRNA Covid vaccine. 

• When the hype about the superiority of mRNA vaccines became the mainstream narrative, Lu, Song, and their colleagues would still have been working on their live vaccine candidate. Wouldn’t it be a shame if all the work on GX_P2V(short_3UTR) had been wasted on an outdated vaccine technology?

• At the same time, the enormous push by the WHO/WEF and other 3-letter agencies to detect novel viruses with pathogenic potential, could indeed have provided a way out of the dilemma.

I let the reader come up with their own conclusion of what could have been driving the publication of the new preprint by Song et al.

Whichever may have been the case, a few things are certain:

• The work on GX_P2V(short_3UTR) has attracted a lot of attention -- not for their potential as vaccines, but, as emphasized by Song et al., because of the unexplored spillover risk of these viruses.

• Fact is that neither the attenuated nature of a virus, nor its purported high lethality can be rigorously proven unless demonstrated on appropriate in vitro and in vivo models, via statistically powered tests, and in a repeatable way, confirmed by several independent labs and institutions.

• However, research funding these days does not seem to require the existence of a real virus or the actuality of a real pandemic. All that is needed is the belief that something may have the potential to turn into something. (Nonetheless, a seemingly perfect killer would certainly attract much more attention than one known to be harmless).

Conclusion

In conclusion, in their preprint, Song and collaborators report that most basic lab experiments quickly changed the pathogenicity of a pangolin CoVs variant. The small sample size (n=4) as well as other inconsistencies raise some questions.

However, when analyzing the context in which the work had been done, including their previous findings and goals, the genesis of the purported killer virus may indeed be explained as summarized in the lower part of the figure below.

This figure extends the analysis of Part 4 of this series, considering the context in which the experiments seem to have happened. It would have made sense that the “unexpected” findings - contradicting reason and expectations - would have needed to be whitewashed and crafted differently.

Yet, it seems premature to blame researchers who might be forced to employ some bait and switch, just to save their skin.

If anything is to blame then it is the system - but it’s about much more than feeding scientists a single narrative and putting them under enormous pressure to produce.

I spent decades as a professional, among others, in cryptography and data security. One of the most serious concerns of early internet security was originally described as “the thief masquerading as the police officer.” Back then, it seemed merely hypothetical, and “police” and “thief” did not only refer to such specific categories of individuals but were also be a placeholder for other entities.

The reader may draw their own conclusion if we now have reached the state where this foul trick has become reality, e.g. in terms of research agendas, experimental results, but also regulatory agencies and organizations that are supposed to investigate and test in an unbiased manner and to actually facilitate true and real science.