Summary: Amidst the tsunami of misinformation about COVID-19, there are those working to provide us with clear and useful information. For those few who seek such information, here are two articles from Nature Medicine.
“In the fight against the new coronavirus outbreak,
we must also struggle with human bias.“
By Joana Gonçalves-Sá, Assoc. Professor at Nova Business School (bio).
Excerpt from Nature Medicine, March 2020.
For the past 10 years, I have been working with large datasets that might be relevant to public health and epidemiology, from Google searches and social-media sentiment to weather conditions. More recently, I started to study a different type of contagion: how cognitive biases can be exploited by online platforms to make us even more susceptible to ‘misinformation viruses’. The current outbreak enables us to bring them together.
There is a staggering amount of misinformation propagating online. During the first 4 weeks of January 2020, there were over 15 million Twitter posts on this topic and, to date, the most concerning conspiracy theory circulating online related to the factitious claim that the virus was engineered by the Chinese, with political or economic goals.
As is often the case with misinformation, ‘science’ is used to support conspiracy theories. What seems like scientific evidence is even used to support the idea that scientists cannot be trusted. In this particular situation, an article published online on the bioRxiv platform had reportedly found “uncanny” similarities between the new coronavirus and human immunodeficiency virus. The article has now been retracted, but the suggestion that the virus was indeed lab-created is harder to withdraw.
In parallel, a photo of a bottle of bleach has been widely shared. Its label states its effectiveness against several bacteria and viruses, including coronavirus. This was used as further evidence of the conspiracy: how did this bleach brand know that there would be an outbreak of a new virus called corona?
It is likely that people sharing this article online had never heard of the BLAST algorithm or P values before. They may not have understood that the bioRxiv article had not yet been vetted by the wider scientific community. They may not have known that ‘coronavirus’ is a thousand-year-old type of virus, rather than this novel strain (SARS-CoV-2), which causes a disease whose official name is now COVID-19 …The naming deliberately avoids using geographical location, to minimize stigmatization, or mention of the likely animal host. However, this is unlikely to reduce all false videos and posts blaming the Chinese and their eating habits for the outbreak.
Overall, it is possible that people sharing such misinformation overestimate their ability to understand very complex problems and might be experiencing a form of the Dunning-Kruger effect, which states that people are often more confident than they are knowledgeable. This may be exacerbated by a lack of trust in institutions, be they governments, the pharmaceutical industry, or the traditional media.
For decades, scientists, medical doctors, science communicators, and journalists have been trying to promote the democratization of knowledge, the participation of citizens, and a more critical society. Social networks could be expected to facilitate and even amplify these efforts. It now seems that we might have gotten more than we asked for: a society that is over-critical and over-informed but, unfortunately, not very knowledgeable. …
—————- See the full article. —————-
“The proximal origin of SARS-CoV-2.”
By Kristian G. Andersen, Andrew Rambaut, W. Ian Lipkin, Edward C. Holmes & Robert F. Garry,
Nature Medicine, in press, published 17 March.
This is correspondence, and so probably not peer-reviewed.
This is an excerpt. Footnotes and graphics are omitted. Images added.
Since the first reports of novel pneumonia (COVID-19) in Wuhan, Hubei province, China, there has been considerable discussion on the origin of the causative virus, SARS-CoV-23 (also referred to as HCoV-19). …SARS-CoV-2 is the seventh coronavirus known to infect humans; SARS-CoV, MERS-CoV and SARS-CoV-2 can cause severe disease, whereas HKU1, NL63, OC43 and 229E are associated with mild symptoms6. Here we review what can be deduced about the origin of SARS-CoV-2 from comparative analysis of genomic data. We offer a perspective on the notable features of the SARS-CoV-2 genome and discuss scenarios by which they could have arisen. Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus.
It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus. As noted above, the RBD of SARS-CoV-2 is optimized for binding to human ACE2 with an efficient solution different from those previously predicted. Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone. Instead, we propose two scenarios that can plausibly explain the origin of SARS-CoV-2 …
- natural selection in an animal host before zoonotic transfer; and
- natural selection in humans following zoonotic transfer. We also discuss whether selection during passage could have given rise to SARS-CoV-2.
1. Natural selection in an animal host before zoonotic transfer.
As many early cases of COVID-19 were linked to the Huanan market in Wuhan, it is possible that an animal source was present at this location. Given the similarity of SARS-CoV-2 to bat SARS-CoV-like coronaviruses, it is likely that bats serve as reservoir hosts for its progenitor. Although RaTG13, sampled from a Rhinolophus affinis bat, is ~96% identical overall to SARS-CoV-2, its spike diverges in the RBD, which suggests that it may not bind efficiently to human ACE27.
Malayan pangolins (Manis javanica) illegally imported into Guangdong province contain coronaviruses similar to SARS-CoV-221. Although the RaTG13 bat virus remains the closest to SARS-CoV-2 across the genome, some pangolin coronaviruses exhibit strong similarity to SARS-CoV-2 in the RBD, including all six key RBD residues. This clearly shows that the SARS-CoV-2 spike protein optimized for binding to human-like ACE2 is the result of natural selection.
Neither the bat betacoronaviruses nor the pangolin betacoronaviruses sampled thus far have polybasic cleavage sites. Although no animal coronavirus has been identified that is sufficiently similar to have served as the direct progenitor of SARS-CoV-2, the diversity of coronaviruses in bats and other species is massively undersampled. Mutations, insertions and deletions can occur near the S1–S2 junction of coronaviruses, which shows that the polybasic cleavage site can arise by a natural evolutionary process. For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog.
2. Natural selection in humans following zoonotic transfer.
It is possible that a progenitor of SARS-CoV-2 jumped into humans, acquiring the genomic features described above through adaptation during undetected human-to-human transmission. Once acquired, these adaptations would enable the pandemic to take off and produce a sufficiently large cluster of cases to trigger the surveillance system that detected it.
All SARS-CoV-2 genomes sequenced so far have the genomic features described above and are thus derived from a common ancestor that had them too. The presence in pangolins of an RBD very similar to that of SARS-CoV-2 means that we can infer this was also probably in the virus that jumped to humans. This leaves the insertion of polybasic cleavage site to occur during human-to-human transmission.
Estimates of the timing of the most recent common ancestor of SARS-CoV-2 made with current sequence data point to emergence of the virus in late November 2019 to early December 201923, compatible with the earliest retrospectively confirmed cases. Hence, this scenario presumes a period of unrecognized transmission in humans between the initial zoonotic event and the acquisition of the polybasic cleavage site. Sufficient opportunity could have arisen if there had been many prior zoonotic events that produced short chains of human-to-human transmission over an extended period. This is essentially the situation for MERS-CoV, for which all human cases are the result of repeated jumps of the virus from dromedary camels, producing single infections or short transmission chains that eventually resolve, with no adaptation to sustained transmission.
Studies of banked human samples could provide information on whether such cryptic spread has occurred. Retrospective serological studies could also be informative, and a few such studies have been conducted showing low-level exposures to SARS-CoV-like coronaviruses in certain areas of China. Critically, however, these studies could not have distinguished whether exposures were due to prior infections with SARS-CoV, SARS-CoV-2 or other SARS-CoV-like coronaviruses. Further serological studies should be conducted to determine the extent of prior human exposure to SARS-CoV-2.
3. Selection during passage.
Basic research involving passage of bat SARS-CoV-like coronaviruses in cell culture and/or animal models has been ongoing for many years in biosafety level 2 laboratories across the world, and there are documented instances of laboratory escapes of SARS-CoV28. We must therefore examine the possibility of an inadvertent laboratory release of SARS-CoV-2.
In theory, it is possible that SARS-CoV-2 acquired RBD mutations during adaptation to passage in cell culture, as has been observed in studies of SARS-CoV11. The finding of SARS-CoV-like coronaviruses from pangolins with nearly identical RBDs, however, provides a much stronger and more parsimonious explanation of how SARS-CoV-2 acquired these via recombination or mutation.
The acquisition of both the polybasic cleavage site and predicted O-linked glycans also argues against culture-based scenarios. New polybasic cleavage sites have been observed only after prolonged passage of low-pathogenicity avian influenza virus in vitro or in Vivo. …
Conclusions.
In the midst of the global COVID-19 public-health emergency, it is reasonable to wonder why the origins of the pandemic matter. Detailed understanding of how an animal virus jumped species boundaries to infect humans so productively will help in the prevention of future zoonotic events. For example, if SARS-CoV-2 pre-adapted in another animal species, then there is the risk of future re-emergence events. In contrast, if the adaptive process occurred in humans, then even if repeated zoonotic transfers occur, they are unlikely to take off without the same series of mutations. In addition, identifying the closest viral relatives of SARS-CoV-2 circulating in animals will greatly assist studies of viral function. Indeed, the availability of the RaTG13 bat sequence helped reveal key RBD mutations and the polybasic cleavage site.
The genomic features described here may explain in part the infectiousness and transmissibility of SARS-CoV-2 in humans. Although the evidence shows that SARS-CoV-2 is not a purposefully manipulated virus, it is currently impossible to prove or disprove the other theories of its origin described here. However, since we observed all notable SARS-CoV-2 features, including the optimized RBD and polybasic cleavage site, in related coronaviruses in nature, we do not believe that any type of laboratory-based scenario is plausible.
More scientific data could swing the balance of evidence to favor one hypothesis over another. …
—————- See the full article. —————-
See all the articles about COVID-19 at Nature Medicine.
Posts about effects of COVID-19
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- Lessons from the coronavirus about climate change.
- A devastating epidemic spreads across America – An epidemic of panic and ignorance.
- Soon we’ll see if the US can defend itself again COVID-19.
- COVID-19 will hit world economy hard. Here’s how.
- Seeing what went wrong can help us beat COVID-19.
- COVID-19 shows the new center of the world.
- Prepare now in case they close the stock market.
- The key to surviving the COVID-19 pandemic.
It’s easy to follow the COVID-19 story
The World Health Organization provides daily information, from highly technical information to news for the general public. These are the best sources of information.
- There is their daily situation report, with detailed numbers.
- The Director-General of WHO gives frequent briefings, which are quite insightful.
- Their daily press briefings have more information. An audio goes up quickly afterwards. A transcript is posted the next day.
Also, see the wealth of information at the CDC website, especially their situation reports.
For More Information
Ideas! For some shopping ideas, see my recommended books and films at Amazon. Also, see a powerful and disturbing story about “Birth of a Man of Steel …for the Soviet Union.”
Please like us on Facebook and follow us on Twitter. Also, see these posts about epidemics…
- See the ugly cost of the next big flu pandemic. We can do more to prepare.
- Stratfor: The superbugs are coming. We have time to prepare.
- Posts debunking the hysteria about the 2009 swine flu in America.
- Posts debunking the hysteria about the 2015 ebola epidemic in America.
- Important: A vaccine against the fears that make us weak.
He predicted 9/11 and COVID-19
In his 1994 novel Debt of Honor
“Therefore containment is the only option,” General Pickett went on.
“How do you contain a whole country?” said Cliff Rutledge, Assistant Secretary of State for Policy.
“That’s the problem we face,” President Ryan said. “The only way to contain the epidemic is to shut down all places of assembly – theaters, shopping malls, sports stadia, business offices, everything – and interstate travel. To the best of our information, at least 30 states are so far untouched by this disease. We would do well to keep it that way. We can accomplish that by preventing all interstate travel until such time as we have a handle on the severity of the disease we are facing, and then we can come up with less severe countermeasures.”
“Mr Presdient, that’s unconstitutional,” Pat Martin (representing DoJ) sid at once. Travel is a constitutionally protect right. … {But} Mr. President, I do not see that we have much of a choice here. …The Constitution is not a suicide pact.” …
“Thank you” Ryan said, checking his watch. “I am calling the issue on the table.”
Defense, Treasury, Justice, and Commerce voted aye. All the rest voted no. Ryan looked at them for a long few seconds. “The ayes have it,” the President said coldly. …This has absolute nad unconditional priority over any other matter.”
