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Member since: Sun Feb 14, 2016, 06:36 PM
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Journal Archives

Does your UVC wand actually do anything?

I've wondered about this, and figured many of you do also; very informative!

How to spot a fake UVC wand Scam

New podcast: "Finding Q"

Highly recommend to those interested in such matters. Similar to the HBO doc, but I found it more focused and cohesive. It's on Audible, but I don't know if one must be a member to listen. Eight parts, roughly 8 hours total.


Phylogeographic Mapping of Newly Discovered Coronaviruses

Phylogeographic Mapping of Newly Discovered Coronaviruses Pinpoints the Direct Progenitor of SARS-CoV-2 as Originating from Mojiang, China


In this article we reveal that the new coronavirus genomes from Asia contain sufficient information to narrow down the geographical source of the direct bat progenitor of SARS-CoV-2 to a quite small region, the south-central part of the Chinese province of Yunnan. In other words, this analysis identifies with good confidence and quite precisely the location where a bat virus that ultimately became SARS-CoV-2 left its bat reservoir host, initiating the chain of events that led to the COVID-19 pandemic.

The analysis does not specify the precise nature of this initiation event. The jump out of bats may have been into an intermediate host (that later went on to infect a human), or it may have been a jump directly into a human; or even the virus may have been procured as part of a research project.

Nevertheless, such a very substantial narrowing of the location of the jump from bats represents a major step forward. Its implications for understanding the origin of SARS-CoV-2 are profound because the requirement for a Yunnan connection markedly constrains origin theories. For example, advocates of the imported frozen food theory favoured in China now have to explain how imported food came to Wuhan carrying a virus from Yunnan (Zhou and Shi, 2021). Likewise, ideas that have circulated about possible European origins of the virus must now explain how a European patient zero could have acquired that virus from Yunnan. Also importantly, the bioweapon theory of Dr Li-Meng Yan is ruled out by the newly discovered viruses discussed here.

But perhaps the greatest significance of this finding will turn out to be that the region of Yunnan indicated as the likely geographic origin is centred on a place called the Mojiang mine. This mine is already well-known to COVID-19 origins investigators.

Much more at link. I tend to agree with their currently favored hypothesis: that the 2012 incident involving miners who contracted a respiratory disease from a bat guano-filled mineshaft represents the most parsimonious proximal origin story for Covid.

We favour this theory because it explains numerous otherwise puzzling features of SARS-CoV-2. These features are (1) the high improbability of a zoonotic appearance of a SARS-related coronavirus in Wuhan; (2) the apparently pre-adapted nature of the virus to humans (Piplani et al., 2021; van Dorp et al., 2020; Zhan et al, 2020); (3) a miner’s passage predicts a single zoonotic jump to humans [which fits the data on early human sequences (Bloom, 2021)] and which is inconsistent with most viral zoonoses, which typically feature multiple jumps into humans; (4) a miner-derived virus also explains the proclivity of SARS-CoV-2 for human lungs, which is a characteristic that many coronaviruses lack; (5) the theory can also explain the extensive attempts to deny or obscure research occurring at the WIV (see also the Zhou P. et al., 2020a addendum). The Mojiang miners hypothesis even has an evolutionary explanation for the infamous furin cleavage site. However, none of this precludes the possibility that the miner-derived virus was also lab-altered.

Since the theory specifically postulates that patient zero was a Mojiang miner who acquired one or more SARS-CoV-2-related viruses directly from the bats in the mine, the miners passaging theory matches perfectly the phylogeography of SARS-CoV-2 lineage revealed above. Indeed, it is an explicit prediction of the Mojiang miner passage theory that SARS-CoV-2 is composed of viruses originating there. Consequently, a miner passage origin is also consistent with SARS-CoV-2 being a mosaic of RmYN02, RpYN06, PrC31 and RaTG13 since, as the phylogeography shows, these viruses, or their close relatives, could have been present in the mine when the miners fell ill.

A miner passage is therefore not just compatible with but greatly strengthened by all the new evidence from wild viruses that has emerged since the pandemic began.

It's a long read, but worthwhile, IMHO. There are many more issues raised in the article that merit discussion.

Shall we discuss?

Nature: How the coronavirus infects cells--and why Delta is so dangerous

The virus that causes SARS, SARS-CoV, uses either of two host protease enzymes to break in: TMPRSS2 (pronounced ‘tempress two’) or cathepsin L. TMPRSS2 is the faster route in, but SARS-CoV often enters instead through an endosome — a lipid-surrounded bubble — which relies on cathepsin L. When virions enter cells by this route, however, antiviral proteins can trap them.

SARS-CoV-2 differs from SARS-CoV because it efficiently uses TMPRSS2, an enzyme found in high amounts on the outside of respiratory cells. First, TMPRSS2 cuts a site on the spike’s S2 subunit8. That cut exposes a run of hydrophobic amino acids that rapidly buries itself in the closest membrane — that of the host cell. Next, the extended spike folds back onto itself, like a zipper, forcing the viral and cell membranes to fuse.

The virus then ejects its genome directly into the cell. By invading in this spring-loaded manner, SARS-CoV-2 infects faster than SARS-CoV and avoids being trapped in endosomes, according to work published in April by Barclay and her colleagues at Imperial College London9.

The virus’s speedy entry using TMPRSS2 explains why the malaria drug chloroquine didn’t work in clinical trials as a COVID-19 treatment, despite early promising studies in the lab10. Those turned out to have used cells that rely exclusively on cathepsins for endosomal entry. “When the virus transmits and replicates in the human airway, it doesn’t use endosomes, so chloroquine, which is an endosomal disrupting drug, is not effective in real life,” says Barclay.

Much more at https://www.nature.com/articles/d41586-021-02039-y

The covid-19 lab leak hypothesis: did the media fall victim to a misinformation campaign?


The theory that SARS-CoV-2 may have originated in a lab was considered a debunked conspiracy theory, but some experts are revisiting it amid calls for a new, more thorough investigation. Paul Thacker explains the dramatic U turn and the role of contemporary science journalism

Those who are interested should read the whole article at the link. Excerpting a few paragraphs won't really help much.

My question is: what role did DU play?

Science: "SARS-CoV-2 immune evasion by the B.1.427/B.1.429 VOC" (California "epsilon")

So I guess the question is how significant a 2-3 fold reduction in neutralizing antibodies is, clinically.

(Pfizer and Moderna)


A novel variant of concern (VOC) named CAL.20C (B.1.427/B.1.429), originally detected in California, carries spike glycoprotein mutations S13I in the signal peptide, W152C in the N-terminal domain (NTD), and L452R in the receptor-binding domain (RBD). Plasma from individuals vaccinated with a Wuhan-1 isolate-based mRNA vaccine or convalescent individuals exhibited neutralizing titers, which were reduced 2-3.5 fold against the B.1.427/B.1.429 variant relative to wildtype pseudoviruses. The L452R mutation reduced neutralizing activity of 14 out of 34 RBD-specific monoclonal antibodies (mAbs). The S13I and W152C mutations resulted in total loss of neutralization for 10 out of 10 NTD-specific mAbs since the NTD antigenic supersite was remodeled by a shift of the signal peptide cleavage site and formation of a new disulphide bond, as revealed by mass spectrometry and structural studies.

The incidence of the B.1.427/B.1.429 lineages is increasing rapidly
The SARS-CoV-2 B.1.427/B.1.429 variant was reported for the first time at the beginning of 2021 in California and as of May 2021 has been detected in 34 additional countries (41, 42). The two lineages B.1.427 and B.1.429 (belonging to clade 20C according to Nextstrain designation) share the same S mutations (S13I, and W152C in the NTD and L452R in the RBD), but harbor different mutations in other SARS-CoV-2 genes (42). Molecular clock analysis suggest that the progenitor of both lineages emerged in May 2020, diverging to give rise to the B.1.427 and B.1.429 lineages in June-July 2020 (42). The fast rise in the number of cases associated with the B.1.427/B.1.429 lineages led to their classification as a VOC by the US Center for Disease Control

These findings show that the three mutations present in the B1.427/B.1.429 S glycoprotein decrease the neutralizing activity of vaccine-elicited and infection-elicited Abs, suggesting that these lineage-defining residue substitutions are associated with immune evasion. However, these data also underscore the higher quality of Ab responses induced by vaccination compared to infection and their enhanced resilience to mutations found in VOC.

Collectively, these findings demonstrate that the S13I and W152C mutations found in the B.1.427/B.1.429 S variant are jointly responsible for escape from NTD-specific mAbs, due to deletion of the SARS-CoV-2 S two N-terminal residues and overall rearrangement of the NTD antigenic supersite. Our data support that the SARS-CoV-2 NTD evolved a compensatory mechanism to form an alternative disulfide bond and that mutations of the S signal peptide occur in vivo in a clinical setting to promote immune evasion. The SARS-CoV-2 B.1.427/B.1.429 S variant therefore relies on an indirect and unusual neutralization-escape strategy.

Substantial Differences in SARS-CoV-2 Ab Responses Elicited by Natural Infection and mRNA Vaccine

This is really, really good news. It was difficult choosing only a few paragraphs to quote, so I encourage you to follow the link to read more, if only the "Discussion" section.

What it says, though, is that mRNA vaccine immunity appears to be superior to natural immunity--for various reasons they describe (some included below).


In this study, we compared antibody responses induced by SARS-CoV-2 natural exposure with the responses induced by the mRNA vaccines.


mRNA vaccines induce higher Ab levels and greater Ab breadth than natural exposure to infection and differences were particularly notable against the RBD domain. ... (snip) ...The virus uses the spike RBD domain that binds to the ACE2 receptor on respiratory cells to enter and infect them. Vaccinated individuals had significantly elevated Ab levels against RBD domain segments, supporting the protective immunity induced by this vaccine as previously published. To account for this difference between natural exposure and the vaccine, the virus may have evolved to conceal the RBD epitope to evade immune recognition. The mRNA vaccine produces a protein conformation that better exposes the RBD epitope to the immune system.

In addition to inducing increased Ab levels again SARS-CoV-2 RBD, the mRNA vaccine induced cross-reactive responses against SARS spike and SARS RBD. Conversely, natural exposure did not induce a cross-reactive response against the SARS spike and SARS RBD. The weak anti-RBD response induced by natural exposure may provide a mechanism for new variants to enter the population. This result can be interpreted based on immune selection pressure. Importantly, the mRNA vaccine induces a marked cross-reactive response against SARS spike, indicating that the mRNA vaccine adopts a conformation that presents cross-reactive epitopes to the immune system. This effect of the mRNA vaccine to induce cross-reactivity against diverse CoV strains is encouraging, providing further evidence that it may be effective against emerging virus variants.


These results may also have relevance for both the dose response hypothesis and with regard to herd immunity. Several authors have suggested that disease outcomes may be related to the dose inoculum, with individuals being exposed to inocula with higher virus loads potentially having more severe disease outcomes. [9] While the currently used vaccines in this setting do not rely on viral materials, they do offer a glimpse into controlled high level exposure to proteins that are specific to SARS-CoV-2. Our results show that individuals who have been vaccinated mount higher across-the-board antibody responses than those who have been exposed to variable viral inocula (i.e. through natural exposure). Second, the variable antibody responses among the pre-vaccine population may also indicate that immune responses to natural infections are not as strong as those among individuals who have been vaccinated. This could also indicate that immunity from naturally acquired infections is not as strong as that acquired from vaccination, with potential relevance for reaching and maintaining herd immunity. We should not assume that previously infected individuals are immune or that they cannot transmit the virus.

ETA: adding the standard disclaimer for all pre-print articles posted on bioRxiv
bioRxiv is receiving many new papers on coronavirus SARS-CoV-2. A reminder: these are preliminary reports that have not been peer-reviewed. They should not be regarded as conclusive, guide clinical practice/health-related behavior, or be reported in news media as established information.

Nature: Engineered bat virus stirs debate over risky research

Engineered bat virus stirs debate over risky research

Lab-made coronavirus related to SARS can infect human cells.


An experiment that created a hybrid version of a bat coronavirus — one related to the virus that causes SARS (severe acute respiratory syndrome) — has triggered renewed debate over whether engineering lab variants of viruses with possible pandemic potential is worth the risks.

In an article published in Nature Medicine1 on 9 November, scientists investigated a virus called SHC014, which is found in horseshoe bats in China. The researchers created a chimaeric virus, made up of a surface protein of SHC014 and the backbone of a SARS virus that had been adapted to grow in mice and to mimic human disease. The chimaera infected human airway cells — proving that the surface protein of SHC014 has the necessary structure to bind to a key receptor on the cells and to infect them. It also caused disease in mice, but did not kill them.

Although almost all coronaviruses isolated from bats have not been able to bind to the key human receptor, SHC014 is not the first that can do so. In 2013, researchers reported this ability for the first time in a different coronavirus isolated from the same bat population2.

The whole article is worth reading at the link, but this is the paragraph I'd like to discuss:

Studies testing hybrid viruses in human cell culture and animal models are limited in what they can say about the threat posed by a wild virus, Daszak agrees. But he argues that they can help indicate which pathogens should be prioritized for further research attention.

The general topic is gain-of-function (GOF) research, which is controversial, and about which I, personally, remain ambivalent.

But this article highlights and clearly illustrates what one viewpoint postulates: that GOF research is mostly academic (while being highly risky).

The proof is that the paper being referenced (A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence https://www.nature.com/articles/nm.3985) is a study of a group of viruses collected at the same time, and from the same location as the virus RaTG13, which is the bat coronavirus that, to date, is the closest known relative to SARS-CoV-2, causative agent of Covid-19.

To be clear: RaTG13 was (at least partially in 2016; fully by 2018) sequenced at the same time, so was known about and published (in 2016, as sample "4991" in Coexistence of multiple coronaviruses in several bat colonies in an abandoned mineshaft https://link.springer.com/article/10.1007/s12250-016-3713-9 ).

If it sounds like a detective case where the serial killer is apprehended by police, taken in for questioning, and is then released (:cough:Ted Bundy:cough: ), it's because it is the scientific equivalent.

After the current pandemic outbreak, when queried about why RaTG13 did not undergo further analysis and experimentation, the researchers said that RaTG13 (basically, paraphrasing) "wasn't interesting enough." Here's what that paper says about RaTG13 aka RaBtCoV/4991:

Only two sequences detected in this study were homologous to betacoronaviruses. One of them (RaBtCoV/4991) was detected in a R. affinis sample and was related to SL-CoV. The conserved 440-bp RdRp fragment of RaBt-CoV/4991 had 89% nt identity and 95% aa identity with SL-CoV Rs672 (Yuan et al., 2010). In the phylogenetic tree, RaBtCoV/4991 showed more divergence from human SARS-CoV than other bat SL-CoVs and could be considered as a new strain of this virus lineage (Figure 2).

RaTG13 was in the sights, the crosshairs, but then shelved as being "not interesting enough." That they characterized it as a potential "new strain" and also failed to pursue studying it, strikes me as odd.

Yes, hindsight is 20/20. But the whole point of GOF research is the be able to predict and prepare for that unforeseen future pandemic. If it fails--and let's be honest, short of them having had the actual SARS-CoV-2 virus in their sampling population, this was damned close!--then we must question the value of such research vis a vis risk vs. reward.

Of course, another view could be that this research failed to predict this pandemic because there wasn't enough being invested in GOF work. I suspect that will be the prevailing conclusion, and that tons more money will be spent expanding that focus, with hundreds more BSL3/4 labs being built worldwide.

Are we prepared for that?

BTW, the article in the title of this OP is from 2015.

No, I am not certain of that at all

In fact, I am fairly confident that the virus has a natural evolution and that transmission was zoonotic.

But what intrigues me is the cover-up. When someone goes to great lengths to obscure something, there's a reason.

When I received my scientific training, one of the most valuable tips I learned was to design experiments as though you were trying to *disprove* your favored hypothesis. To approach your studies as a contrarian--because your peer reviewers will most certainly be doing so. It's the best way to try to ensure a balanced perspective, to fight against our natural inclination towards confirmation bias.

So that partly explains my approach to this. The other part, as I described above, is my observation of odd behaviors on the part of the CCP regarding this question on origins. That set off major alarms for me.

In terms of the Nature citation issue: nobody will ever convince me that it was trivial. Even for a "rushed" paper. Especially because of the surrounding circumstances: it was Shi's own prior work that deserved the cite. One thing I can absolutely guarantee you: no scientist, especially when writing a paper for Nature, omits an opportunity to cite their own published work. Go ahead and ask any/every scientist you know if that is a fair statement. Not to mention that the piece of data in question (RaTG13 sequence) was the central, pivotal piece of data proving the paper's thesis: that the newly discovered infectious agent was a bat coronavirus. Why not mention that you know this because your lab collected that specimin back in 2013 inside of a mineshaft where, just months prior, six workers contracted a mysterious respiratory disease--that would kill three of them--and that you partially sequenced that specimin and published about it in 2016? I mean, that is the normal way for a scientist to report a finding.

Below is the Addendum, published a full nine months later. See for yourself. There's nothing relevent in there that wasn't known in Feb 2020, and the critical citation I'm so concerned with is right there, too--Ge et al (2016). Why the nine month delay? Aren't you even a little bit curious?

Published: 17 November 2020

Addendum: A pneumonia outbreak associated with a new coronavirus of probable bat origin

Peng Zhou, Xing-Lou Yang, […]Zheng-Li Shi
Nature volume 588, pageE6(2020)

Here we provide further information about the bat SARS-related coronavirus (SARSr-CoV) strain RaTG13 reported in our Article. Between 1 July and 1 October 2012, we received 13 serum samples collected from 4 patients (one of whom was deceased) who showed severe respiratory disease. These patients had visited a mine cave in Tongguan town, Mojiang County, Yunnan Province, China, to clean bat faeces in order to mine copper before being admitted to the First Affiliated Hospital of Kunming Medical University on 26–27 April 2012. The samples we received were collected by the hospital staff in June, July, August and September 2012. To investigate the cause of the respiratory disease, we tested the samples using PCR methods developed in our laboratory targeting the RNA-dependent RNA polymerases (RdRp) of Ebola virus, Nipah virus and bat SARSr-CoV Rp3, and all of the samples were negative for the presence of these viruses. We also tested the serum samples for the presence of antibodies against the nucleocapsid proteins of these three viruses, and none of the samples gave a positive result. Recently, we retested the samples with our validated enzyme-linked immunosorbent assay (ELISA) against the SARS coronavirus 2 (SARS-CoV-2) nucleocapsid protein—which has greater than 90% amino acid sequence identity with bat SARSr-CoV Rp3—and confirmed that these patients were not infected by SARS-CoV-2.

We suspected that the patients had been infected by an unknown virus. Therefore, we and other groups sampled animals including bats, rats and musk shrews in or around the cave, and found some alphacoronaviruses1 and paramyxoviruses2. Between 2012 and 2015, our group sampled bats once or twice a year in this cave and collected a total of 1,322 samples. From these samples, we detected 293 highly diverse coronaviruses, of which 284 were designated alphacoronaviruses and 9 were designated betacoronaviruses on the basis of partial RdRp sequences. All of the nine betacoronaviruses are SARSr-CoVs, one of which (sample ID4991; renamed RaTG13 in our Article to reflect the bat species, the location and the sampling year) was described in a 2016 publication1. The partial RdRp sequence (370 bp) of ID4991 was deposited in GenBank in 2016 under accession number KP876546. All of the identified bat SARSr-CoVs are distantly related to SARS-CoV based on partial RdRp sequences. In 2018, as the next-generation sequencing technology and capability in our laboratory had improved, we performed further sequencing of these bat viruses and obtained almost the full-length genome sequence (without the 5′ and 3′ ends) of RaTG13. In 2020, we compared the sequence of SARS-CoV-2 with our unpublished bat coronavirus sequences and found that it shared a 96.2% identity with RaTG13.

Ge, X. Y. et al. Coexistence of multiple coronaviruses in several bat colonies in an abandoned mineshaft. Virol. Sin. 31, 31–40 (2016).

Cnet: How the coronavirus origin story is being rewritten by a guerrilla Twitter group

This isn't going away. Please read the full article.


After a lot of trial and error, the Seeker stumbled upon exactly what he was looking for: a master's thesis written by a Chinese doctor. The document contained an account of six cases of "severe pneumonia caused by unknown viruses" in workers who had been cleaning an abandoned copper mine in Yunnan, China, in 2012. The patients' symptoms seemed eerily similar to those of COVID-19. Three of the patients, it said, died from the mystery illness.

The Yunnan mine and its resident bats, the Seeker knew, had been sampled by researchers at the Wuhan Institute of Virology. He'd uncovered a missing puzzle piece: an association between the closest known relative of the coronavirus and research conducted at the institute in Wuhan, China.


Part of the problem is that the origins story has become entangled in geopolitics and conspiracy. Bad actors have seized upon the lab leak theory for political gain, sometimes attempting to shift the blame for catastrophic failures in managing the pandemic. Instead of remaining a scientific debate, the origin story morphed into a political one. For instance, in March 2020, US President Donald Trump and Secretary of State Mike Pompeo began propagating the idea that SARS-CoV-2 may have leaked from a Wuhan lab. The lab leak became intertwined with Trump, foreign policy and the right. Deigin says Trump weighing in "poisoned" the discussion.
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