Dean Koontz did not predict the coronavirus in a 1981 novel

In the 1981 print and onward the book mentioned “Gorki-400” and Gorki is a place in Soviet Russia where Biological Research Lab was available (do not know if Lab is still there). But after the breakage of Soviet Union in late 80’s, the book mentioned “Wuhan-400” from 1989 and onward edition to indicate Chinese Biological Research Lab as after the Cold War era, China became a factor for USA and NOT Soviet Union!

No, Dean Koontz did not predict the coronavirus in a 1981 novel
By Harmeet Kaur
CNN, March 13, 2020

The coronavirus is officially a global pandemic, so naturally, people are feeding their anxieties by voraciously consuming movies and books about other outbreaks.

Some of them bear eerie similarities to what's happening right now, prompting some people on the internet to claim that certain storytellers "predicted" the spread of coronavirus. One particularly striking example comes from a thriller novel by Dean Koontz called "The Eyes of Darkness."

In a tweet that has since been widely shared, someone said that Koontz had predicted the coronavirus outbreak based on a screenshot of a page in the book. But to say that Koontz saw all this coming is a bit of a stretch. A novel is a work of fiction, after all.

So let's break it down.

In the book, the virus is a man-made weapon

In the screenshot page from the novel, a character named Dombey narrates a story about a Chinese scientist who brought a biological weapon called "Wuhan-400" to the United States:

"To understand that," Dombey said, "you have to go back twenty months. It was around then that a Chinese scientist named Li Chen defected to the United States, carrying a diskette record of China's most important and dangerous new biological weapon in a decade. They call the stuff 'Wuhan-400' because it was developed at their RDNA labs outside the city of Wuhan, and it was the four-hundredth viable strain of man-made microorganisms created at that research center."

First, it's worth pointing out that in the original 1981 edition of "The Eyes of Darkness," this biological weapon was called "Gorki-400," in reference to a Russian locality. The name of the weapon was changed to "Wuhan-400" when the book was released again in 1989, according to the South China Morning Post.

It's true that the current coronavirus outbreak began in Wuhan, China. But the idea that the virus was created in a lab is actually a conspiracy theory that originated from unverified social media accounts and has since been widely dismissed by scientists from both China and the West.

Experts are still trying to figure out the exact source of the virus, but research indicates that it likely originated in bats and was transmitted to an intermediate host before jumping to people -- just like its cousin that caused the 2003 SARS epidemic.

In the book, the virus has a 100% mortality rate

In a later paragraph, the character Dombey goes on to say that no one infected with virus survives:

"And Wuhan-400 has other, equally important advantages over most biological agents. For one thing, you can become an infectious carrier only four hours after coming into contact with the virus. That's an incredibly short gestation period. Once infected, no one lives more than twenty-four hours. Most die in twelve. Wuhan-400's kill rate is one hundred percent."

That's not the case with the coronavirus.

First off, people infected by the coronavirus tend to develop symptoms about five days after exposure, and almost always within two weeks, according to a recent study.

Secondly, the mortality rate for coronavirus is not even close to 100%.

While the virus can be fatal, it's mostly the elderly and those with a weakened immune system or other health conditions who face more serious risks.

Officials estimate the death rate for the virus to be around 3% to 4% globally, based on the information they have, though they expect that number to fall.

So while Koontz may be a captivating writer, he's no psychic.

Coronavirus has been spreading in humans for decades!

Researchers from Australia, Britain and the US sought clues about the disease’s past and found it might have jumped from animal to humans long before the first detection in the central China city of Wuhan. In fact, these scientists have speculated that it could have been as long as a decade.

The proximal origin of SARS-CoV-2
Kristian G. Andersen, Andrew Rambaut, W. Ian Lipkin, Edward C. Holmes & Robert F. Garry
Nature, 17 March 2020

To the Editor — Since the first reports of novel pneumonia (COVID-19) in Wuhan, Hubei province, China1,2, there has been considerable discussion on the origin of the causative virus, SARS-CoV-23 (also referred to as HCoV-19)4. Infections with SARS-CoV-2 are now widespread, and as of 11 March 2020, 121,564 cases have been confirmed in more than 110 countries, with 4,373 deaths5.

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.

Notable features of the SARS-CoV-2 genome

Our comparison of alpha- and betacoronaviruses identifies two notable genomic features of SARS-CoV-2: (i) on the basis of structural studies7,8,9 and biochemical experiments1,9,10, SARS-CoV-2 appears to be optimized for binding to the human receptor ACE2; and (ii) the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides8, which additionally led to the predicted acquisition of three O-linked glycans around the site.

1. Mutations in the receptor-binding domain of SARS-CoV-2

The receptor-binding domain (RBD) in the spike protein is the most variable part of the coronavirus genome1,2. Six RBD amino acids have been shown to be critical for binding to ACE2 receptors and for determining the host range of SARS-CoV-like viruses7. With coordinates based on SARS-CoV, they are Y442, L472, N479, D480, T487 and Y4911, which correspond to L455, F486, Q493, S494, N501 and Y505 in SARS-CoV-27. Five of these six residues differ between SARS-CoV-2 and SARS-CoV (Fig. 1a). On the basis of structural studies7,8,9 and biochemical experiments1,9,10, SARS-CoV-2 seems to have an RBD that binds with high affinity to ACE2 from humans, ferrets, cats and other species with high receptor homology7.

While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal7 and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding7,11.

Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

2. Polybasic furin cleavage site and O-linked glycans

The second notable feature of SARS-CoV-2 is a polybasic cleavage site (RRAR) at the junction of S1 and S2, the two subunits of the spike8 (Fig. 1b). This allows effective cleavage by furin and other proteases and has a role in determining viral infectivity and host range12. In addition, a leading proline is also inserted at this site in SARS-CoV-2; thus, the inserted sequence is PRRA (Fig.

1b). The turn created by the proline is predicted to result in the addition of O-linked glycans to S673, T678 and S686, which flank the cleavage site and are unique to SARS-CoV-2 (Fig. 1b). Polybasic cleavage sites have not been observed in related ‘lineage B’ betacoronaviruses, although other human betacoronaviruses, including HKU1 (lineage A), have those sites and predicted O-linked glycans13. Given the level of genetic variation in the spike, it is likely that SARS-CoV-2-like viruses with partial or full polybasic cleavage sites will be discovered in other species.

The functional consequence of the polybasic cleavage site in SARS-CoV-2 is unknown, and it will be important to determine its impact on transmissibility and pathogenesis in animal models. Experiments with SARS-CoV have shown that insertion of a furin cleavage site at the S1–S2 junction enhances cell–cell fusion without affecting viral entry14. In addition, efficient cleavage of the MERS-CoV
spike enables MERS-like coronaviruses from bats to infect human cells15. In avian influenza viruses, rapid replication and transmission in highly dense chicken populations selects for the acquisition of polybasic cleavage sites in the hemagglutinin (HA) protein16, which serves a function similar to that of the coronavirus spike protein. Acquisition of polybasic cleavage sites in HA, by insertion or recombination, converts low-pathogenicity avian influenza viruses into highly pathogenic forms16. The acquisition of polybasic cleavage sites by HA has also been observed after repeated passage in cell culture or through animals17.

The function of the predicted O-linked glycans is unclear, but they could create a ‘mucin-like domain’ that shields epitopes or key residues on the SARS-CoV-2 spike protein18. Several viruses utilize mucin-like domains as glycan shields involved immunoevasion18.

Although prediction of O-linked glycosylation is robust, experimental studies are needed to determine if these sites are used in SARS-CoV-2.

Theories of SARS-CoV-2 origins

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 predicted7,11.

Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used19. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone20. Instead, we propose two scenarios that can plausibly explain the origin of SARS-CoV-2: (i) natural selection in an animal host before zoonotic transfer; and (ii) 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 Wuhan1,2, it is possible that an animal source was present at this location. Given the similarity of SARS-CoV-2 to bat SARS-CoV-like coronaviruses2, it is likely that bats serve as reservoir hosts for its progenitor. Although RaTG13, sampled from a Rhinolophus affinis bat1, 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 (Fig. 1a).

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 genome1, some pangolin coronaviruses exhibit strong similarity to SARS-CoV-2 in the RBD, including all six key RBD residues21 (Fig. 1). 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 coronaviruses22, 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 it1,2.

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 cases24. 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 transmission25.

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 China26. 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 world27, 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 (Fig. 1a) 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 mutation19.

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 vivo17. Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of
a progenitor virus with very high genetic similarity, which has not been described. Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described. Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred due to cell-culture passage, as such features suggest the involvement of an immune system18.

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. Obtaining related viral sequences from animal sources would be the most definitive way of revealing viral origins. For example, a future observation of an intermediate or fully formed polybasic cleavage site in a SARS-CoV-2-like virus from animals would lend even further support to the natural-selection hypotheses. It would also be helpful to obtain more genetic and functional data about SARS-CoV-2, including animal studies. The identification of a potential intermediate host of SARS-CoV-2, as well as sequencing of the virus from very early cases, would similarly be highly informative. Irrespective of the exact mechanisms by which SARS-CoV-2 originated via natural selection, the ongoing surveillance of pneumonia in humans and other animals is clearly of utmost importance.

References

    1. Zhou, P. et al. Nature https://doi.org/10.1038/s41586-020-2012-7 (2020).

    2. Wu, F. et al. Nature https://doi.org/10.1038/s41586-020-2008-3 (2020).

    3. Gorbalenya, A. E. et al. bioRxiv https://doi.org/10.1101/2020.02.07.937862 (2020).

    4. Jiang, S. et al. Lancet https://doi.org/10.1016/S0140-6736(20)30419-0 (2020).

    5. Dong, E., Du, H. & Gardner, L. Lancet Infect. Dis. https://doi.org/10.1016/S1473-3099(20)30120-1 (2020).

    6. Corman, V. M., Muth, D., Niemeyer, D. & Drosten, C. Adv. Virus Res. 100, 163–188 (2018).

    7. Wan, Y., Shang, J., Graham, R., Baric, R. S. & Li, F. J. Virol. https://doi.org/10.1128/JVI.00127-20 (2020).

    8. Walls, A. C. et al. bioRxiv https://doi.org/10.1101/2020.02.19.956581 (2020).

    9. Wrapp, D. et al. Science https://doi.org/10.1126/science.abb2507 (2020).

    10.Letko, M., Marzi, A. & Munster, V. Nat. Microbiol. https://doi.org/10.1038/s41564-020-0688-y (2020).

    11.Sheahan, T. et al. J. Virol. 82, 2274–2285 (2008).

    12.Nao, N. et al. MBio 8, e02298-16 (2017).

    13.Chan, C.-M. et al. Exp. Biol. Med. 233, 1527–1536 (2008).

    14.Follis, K. E., York, J. & Nunberg, J. H. Virology 350, 358–369 (2006).

    15.Menachery, V. D. et al. J. Virol. https://doi.org/10.1128/JVI.01774-19 (2019).

    16.Alexander, D. J. & Brown, I. H. Rev. Sci. Tech. 28, 19–38 (2009).

    17.Ito, T. et al. J. Virol. 75, 4439–4443 (2001).

    18.Bagdonaite, I. & Wandall, H. H. Glycobiology 28, 443–467 (2018).

    19.Cui, J., Li, F. & Shi, Z.-L. Nat. Rev. Microbiol. 17, 181–192 (2019).

    20.Almazán, F. et al. Virus Res. 189, 262–270 (2014).

    21.Zhang, T., Wu, Q. & Zhang, Z. bioRxiv https://doi.org/10.1101/2020.02.19.950253 (2020).

    22.Yamada, Y. & Liu, D. X. J. Virol. 83, 8744–8758 (2009).

    23. Rambaut, A. Virological.org http://virological.org/t/356 (2020).

    24.Huang, C. et al. Lancet https://doi.org/10.1016/S0140-6736(20)30183-5 (2020).

    25.Dudas, G., Carvalho, L. M., Rambaut, A. & Bedford, T. eLife 7, e31257 (2018).

    26.Wang, N. et al. Virol. Sin. 33, 104–107 (2018).

    27.Ge, X.-Y. et al. Nature 503, 535–538 (2013).

    28.Lim, P. L. et al. N. Engl. J. Med. 350, 1740–1745 (2004).

    29.Wong, M. C., Javornik Cregeen, S. J., Ajami, N. J. & Petrosino, J. F. bioRxiv https://doi.org/10.1101/2020.02.07.939207

(2020).

    30.Liu, P., Chen, W. & Chen, J.-P. Viruses 11, 979 (2019).

Acknowledgements

We thank all those who have contributed sequences to the GISAID database (https://www.gisaid.org/) and analyses to Virological.org

(http://virological.org/). We thank M. Farzan for discussions, and the Wellcome Trust for support. K.G.A. is a Pew Biomedical Scholar

and is supported by NIH grant U19AI135995. A.R. is supported by the Wellcome Trust (Collaborators Award 206298/Z/17/Z?ARTIC network)

and the European Research Council (grant agreement no. 725422?ReservoirDOCS). E.C.H. is supported by an ARC Australian Laureate

Fellowship (FL170100022). R.F.G. is supported by NIH grants U19AI135995, U54 HG007480 and U19AI142790.

Author information

Affiliations

    Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA, USA
        Kristian G. Andersen
    Scripps Research Translational Institute, La Jolla, CA, USA
        Kristian G. Andersen
    Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK
        Andrew Rambaut
    Center for Infection and Immunity, Mailman School of Public Health of Columbia University, New York, NY, USA
        W. Ian Lipkin
    Marie Bashir Institute for Infectious Diseases and Biosecurity, School of Life and Environmental Sciences and School of Medical

Sciences, The University of Sydney, Sydney, Australia
        Edward C. Holmes
    Tulane University, School of Medicine, Department of Microbiology and Immunology, New Orleans, LA, USA
        Robert F. Garry
    Zalgen Labs, Germantown, MD, USA
        Robert F. Garry

Fatal Flaws : Coronavirus Exposed US

On Breitbart, Americans were gloating about how coronavirus was going to destroy China. Meanwhile half the US politicians are scrambling to cash in on the stock market using confidential information they received during briefings on the Covid-19 pandemic and the effects it would have on the markets and US economy. Basically "insider trading" worth tens of millions of dollars. Now they are cooking up excuses and more lies to cover their corruption. The "Trumpandemic" might have a lot more victims.

A catastrophic response to a pandemic
Ashfaque Swapan
Daily Star, March 15, 2020

"You only find out who is swimming naked when the tide goes out." — Warren Buffett, US investor and business magnate Coronavirus is beginning to scare the living daylights out of ordinary Americans.

The threat is two-fold. There's the actual threat from the virus itself, and then there's the godawful government screw-up in dealing with it. Like a fish that rots from the head, many critics point to US President Donald Trump.

At times like these, it is traditional for the US president to speak to the nation to provide reassurance. Trump addressed the nation from the Oval Office at the White House on March 11. His efforts left a lot to be desired, to put it mildly.

Former New York Times columnist Frank Rich lashed out in New York magazine: "The most urgent question is not whether the coronavirus is the crisis that will doom the Trump administration. It is whether the Trump administration is the crisis that will doom America."

Rich added, incredulously: "Has anyone ever heard of a televised presidential speech that had to be corrected within minutes after it ended by both the president who delivered it and officials in his own government?"

Trump and his aides hastily backtracked as they scrambled to clean up after his mess. No, Trump's travel ban did not mean cutting off trade with Europe. No, his ban did not include US citizens and permanent residents, either. As for his promises of health insurance companies waiving charges for coronavirus treatment? Here Trump (and his speechwriters) were being economical with the truth. It's
not the treatment, just the testing, silly!

The speech spooked the markets. The Dow Jones stock market index went down 10 percent, its sharpest drop since its 1987 crash.

In a bit of gallows humour, Wall Street strategist Luca Paolini was quoted by the Financial Times as saying, "This was the most expensive speech in history."

Right from the get go, the Trump administration treated the pandemic as a public relations challenge rather than a public health crisis. The administration's stand—now exposed as disastrously fanciful—was that it was just a few cases, and soon it would be gone.

All February, the administration sat on the information while crucial weeks went by.

From a public health standpoint, the country lost crucial time to track the spread of the virus. The biggest challenge in the US now is that we have no idea how badly the population is affected or where the hotspots are. Epidemiologists are essentially flying blind.

It's an outrage how few people have been tested. According to the Atlanta-based Centers for Disease Control and Prevention, so far only 15,000 people have been tested in the US, a nation of 350 million people.

South Korea has the capacity to test as many people per day. Testing is free, takes less than 10 minutes, and results are texted by the next day. "A nation of 51 million, South Korea has tested about 250,000 people since its outbreak began on Jan. 20. It has conducted 3,600 tests per million people compared to five per million in the US," the National Public Radio reports.

On top of the incompetence, there are broader socio-economic public health challenges to which there are no satisfactory answers. A huge part of the US population are hourly workers, who live paycheque-to-paycheque. Will they agree to quarantine themselves without pay in the event of symptoms when that could mean going out without food or missing the rent payment? How to identify, monitor and treat the tens of millions of people without medical insurance who cannot afford to see a doctor?

Instead of dealing with these critical challenges head-on, the administration and its right-wing supporters continue going down the rabbit hole with bizarre conspiracy theories, including one that considered it a Democratic "deep state" plot to undermine Trump before facts overtook them. There is an absurd xenophobic edge in Trump's reference to a "foreign virus". What other kinds will they
come up with? "Undocumented virus"? "H1B virus"? The mind boggles.

There's nothing like a real crisis to expose the shortcomings in an administration and a policy. But will the right lessons be drawn?

Peter Wehner, a Republican who was a writer in the administrations of US presidents Ronald Reagan, George H.W. Bush and George W. Bush, is confident that it will.

"The coronavirus is quite likely to be the Trump presidency's inflection point, when everything changed, when the bluster and ignorance and shallowness of America's 45th president became undeniable, an empirical reality, as indisputable as the laws of science or a mathematical equation," Wehner writes in The Atlantic magazine.

"It has taken a good deal longer than it should have, but Americans have now seen the con man behind the curtain. The president, enraged for having been unmasked, will become more desperate, more embittered, more unhinged. He knows nothing will be the same. His administration may stagger on, but it will be only a hollow shell. The Trump presidency is over."

I'm a bit more sceptical, I'm afraid. My caution springs from H.L. Mencken's 1926 observation in the Chicago Daily Tribune: "No one in this world, so far as I know… has ever lost money by underestimating the intelligence of the great masses of the plain people. Nor has anyone ever lost public office thereby."

Ashfaque Swapan is a contributing editor for Siliconeer, a digital daily for South Asians in the United States.

‘US wasted precious time China has bought!’ Beijing shreds Washington over ‘racist’ coronavirus rhetoric
RT : 21 Mar, 2020
Washington has passed off blame to Beijing for its own failures in addressing the Covid-19 outbreak, China’s Foreign Ministry said, hitting back at the ‘Chinese virus’ rhetoric with the ironic term ‘Trumpandemic.’

“Some people in the United States attempt to stigmatize China's fight against the epidemic and shirk its responsibility to China,”

Foreign Ministry spokesperson Geng Shuang told reporters on Friday, referring to the finger-pointing adopted by President Trump and other top officials (after weeks of US media outlets calling it the 'Chinese' and 'Wuhan' virus).

    This practice ignores the huge sacrifices made by the Chinese people to safeguard human health and safety, and denigrates China's major public health security contributions.

Over the last two months, Beijing has helped the US buy time in its efforts to combat the coronavirus by providing “timely information” and other aid, the spokesman said, noting that the US president himself acknowledged as much during a press briefing last week. But most of that assistance has gone to waste, he lamented.

    It is a pity, as many US media and specialists have noted, that the US has wasted the precious time China has bought.

Despite being the only country that has managed to contain the outbreak, China has been accused of suppressing information in the early stages of the Covid-19 outbreak – which began in the city of Wuhan late last year. The spokesman insisted the country has taken “the most comprehensive, strictest and most thorough prevention and control measures,” and has been “open” and “transparent” about the virus.

Geng went on to list the numerous joint meetings between American and Chinese health officials in recent weeks, arguing Beijing was doing its part to assist the US response to the lethal illness, but implored Washington to take responsibility for its own shortcomings.

“We hope that the United States will respect objective facts, respect international public opinion, do its own thing... stop slandering other countries, passing on responsibilities, and play a constructive role in fighting the epidemic,” he said.

While President Trump argues that the phrase "Chinese virus" is “not racist at all,” stating that he uses the term simply because the pathogen “comes from China,” his insistence on the label has piqued the ire of Beijing. In a string of tweets earlier on Friday, Chinese state media outlet Xinhua slammed the moniker as bigoted, and fired back with its own Trumpian term of derision, renaming the outbreak the “Trumpandemic.”

Where did the Novel Coronavirus Come From?

The article is an edited version of an article which was first published on a WeChat official account named Gong Yi Kan Shi Jie. The article reflects the author’s opinions and not necessarily the views of CGTN.

.

Given that some major U.S. media and politicians made groundless claims that the novel coronavirus originates in China, blamed and slandered China, even asked for an apology from China, then I have every reason to ask 10 questions for the United States about its origin too. Better still, unlike the U.S., I did a lot homework and will base my questions on international media coverage of COVID-19.

Ten Questions for the U.S.: Where did the Novel Coronavirus Come From?

By Wang Fuhua

Global Research, March 21, 2020

CGN by Wang Fuhua

Question 1

Since the director of the U.S. Centers of Disease Control, Robert Redfield admitted that some Americans seemingly dying from flu were tested positive for the novel coronavirus, can I conclude that those people actually died from the novel coronavirus? Among the 34 million influenza patients, with a death toll of 20,000, how many were misdiagnosed?

When did the misdiagnoses start? And did it actually start from August 2019? These questions are so vital that the world is waiting for an explanation from the United States.

Question 2

When there were some misdiagnoses admitted by U.S. CDC, I’m scratching my head – isn’t the U.S. that owns the best medical technologies in the world? Why did that happen?

As the ground glass opacity (white patches) can be easily seen in CT scans of the lungs of patients with the novel coronavirus-infected pneumonia, it should have been an easy thing to separate the cases of COVID-19 and H1N1 flu. But why were there so many misdiagnoses?

Well, that reminds me of the U.S. Vice President Mike Pence’s request of controlling all messaging regard to the coronavirus. Why does the White House call for messaging control? Does the U.S. need to hide something? Are they plotting some conspiracy?

Question 3

Why did the U.S. withdraw from the 1972 Biological and Toxin Weapons Convention (BTWC) in 2001? Why did it try to prevent a monitoring mechanism for the execution of the Convention? Is it standing in the way of developing biological weapon for the U.S.?

If not, why are there new biological laboratories in Georgia, Ukraine, Moldova, Armenia, Azerbaijan, Uzbekistan and Kazakhstan? Are those labs for biochemical warfare? It’s impossible that they are keeping viruses as pets. If the U.S. is aiming at provoking a biochemical war, who would be the first target then?

Also, how about the swine flu outbreak in China last year? The odd thing is that it broke out in different places simultaneously instead of breaking out separately. Why were drones used to poison the pigs? Was the U.S. behind all that? I heard that it was the pork speculators. But that theory makes no sense – since the swine flu killed millions of pigs in China during the same period of time, pork speculators would suffer great loss instead of profits.

The best possible answer to that was foreign meddling. I was among those who wondered if the U.S. had anything to do with that and hoped for an explanation.

Question 4

The U.S. Army Medical Research Institute of Infectious Diseases, located on Fort Detrick, Maryland, was shut down in July 2019. Was it because there was a virus leakage incident?

Just one month later, there was an influenza outbreak across the country. Were those two things related in any way?

Were the misdiagnoses simply cooked up to cover up such secrets? Did that also become a motive for the U.S. to shift the blame to other countries by labeling them as the origin of the novel coronavirus?

Was that an epic coincidence or a dirty secret in disguise? Why did the U.S. erase huge number of English news reports on the internet covering the shutdown in March 2020? Is there anything to hide, or is there anything to worry about?

Question 5

At the 7th Military World Games (October 18-27, 2019) held in Wuhan, why did the U.S. team (369 members) win ZERO gold medal? Did that even look like a reasonable record for the world’s leading military power? Did your government do it on purpose?

Was anyone among the 369 participants ever (mis)diagnosed with influenza? Was it possible they were carriers of the novel coronavirus?

The best thing for the U.S. now is to stop burying its head in the sand and give the 369 people PCT tests to see if they are infected.

Question 6

Why did the U.S. hold Event 201, a global pandemic exercise in October 2019? Why was the CIA deputy director participating it? Is it because the U.S. has foreseen a highly-infectious virus is about to cause a pandemic? One month later, cases of pneumonia of unknown cause were detected in China and there was a pandemic three months later. Probably, it’s not just a coincidence.

Question 7

Japan, South Korea, Italy and Iran all reported that many of their first COVID-19 confirmed cases had no exposure history with China but showed connection with the United States. How come?

Genetic research shows that the type of novel coronavirus found in China belongs to Group C, but Group A and Group B viruses – Group C’s parental and grand parental viruses – are both found in the United States. Why? A Japanese patient was diagnosed with influenza in Hawaii but was tested positive for COVID-19 when he returned to Japan. How to explain that?

Some COVID-19 cases in the U.S. had no connection with China whatsoever. So where does it come from?

Question 8

You’ve got no reason to deny that the 1918 Pandemic originated within your territory. But you let Spain bear the blame for as long as a century. Don’t you feel shame on that?

History seems to repeat itself. So, is the U.S. playing the trick again and attempting to label the novel coronavirus as the “Chinese Virus”?

Question 9

The 1918 Pandemic, causing 1 billion infections, with a death toll “estimated to have been anywhere from 17 million to 50 million, and possibly as high as 100 million… one of the deadliest epidemics in human history,” according to wikipedia, was proven originating in the U.S., but the U.S. has never apologized to the world.

So far, the origin of the novel coronavirus is still unknown, but the United States is requiring China for an apology, how ridiculous is that! Just to remind the 2009 H1N1 influenza pandemic killing 300,000 people also originated in the U.S., and also the same for HIV AIDS. So why not confess to the world?

Question 10

In movies, the U.S. is fond of playing the role of the world savior. The image of Captain America is one of its most popular symbols. However, in reality, in the face of a disaster like COVID-19, where is Captain America?

The U.S. is not doing enough to protect its citizens at home or on the Diamond Princess cruise ship. It even attempted to make Japan responsible for Americans on Diamond Princess. How does the U.S. have the brass to do all these and accuse China of being irresponsible?

While China bought the world valuable time to battle COVID-19, the U.S. accused China of being passive and lacking transparency. Well, when the White House instructed the CDC to stop tallying the people tested for novel coronavirus, did that count as transparency?

When the U.S. government advised its people not to wear masks, was it not being passive? Just too many questions call for the U.S.’s explanations.