I would feel better about the idea of the metaverse if it wasn’t currently dominated by companies and disaster capitalists trying to figure out a way to make more money as the real world’s resources are dwindling. The metaverse as envisioned by these people, by the tech giants, is not some promising new frontier for humanity. It is another place to spend money on things, except in this place the empty promise that buying stuff will make you happy is left even more exposed by the fact that the things in question do not physically exist.

As far as I can work out, the idea is to take the principle of artificial scarcity to an absurdist extreme – to make you want things you absolutely don’t need. The problem is not that I think this won’t work. The problem is that I think it will. The current NFT gold rush proves that people will pay tens of thousands of dollars for links to jpegs of monkeys generated by a computer, and honestly it is eroding my faith in humanity. What gaping deficiency are we living with that makes us feel the need to spend serious money on tokens that prove ownership of a procedurally generated image, just to feel part of something? This is all happening, of course, while the Earth continues to heat up, and at enormous environmental cost. I can’t help but wonder if these giant companies are so intent on selling us and the markets on the idea of a virtual future in order to distract us all from what they are doing to the real one..

I have seen what virtual worlds can do for people. I have spent my entire adult life reporting on them, and what people do in them and the meaning that they find there. So the fact that I’m now the one standing here saying that we don’t want this, feels significant. Meta has patented technology that could track what you look at and how your body moves in virtual reality in order to target ads at you. Is that the future of video games and all the other virtual places where we spend time – to have our attention continually tracked and monetised, even more so than it is in real life?

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.

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.

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.

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