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A SARS-like Coronavirus was Expected, but nothing was done to be Prepared

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Abstract

It was common knowledge that some strain of coronavirus-sooner or later-was going to cause a pandemic. It was known since the SARS-CoV-outbreak in 2003. In 2013 and 2015, the world was informed that a variant of SARS-CoV in bats was emerging as a threat for humans. Why was no action taken by our governments and the World Health Organization (WHO)? The Corona crisis was not only conceivable and foreseeable, but the world could have been prepared. We could have had medication and we could have had a vaccine long ago. That is, when there had been visionary medical-political global leadership." Unlike the other coronaviruses, both the SARS-CoV strain of 2003 and SARS-CoV2 (COVID19-virus) do not contain the HE protein [9,10]. Further, a short lysine-rich region (KTFPPTEPKKDKKKKTDEAQ) in the N-protein was reported to be unique to SARS-CoV [10]. Intriguingly, an almost identical sequence (KTFPPTEPKKDKKKKADETQ) is found in the N-protein of SARS-CoV2 [11]. Both characteristics prove that we are dealing with a variant of the same virus of 2003."
425
A SARS-like Coronavirus was Expected, but nothing
was done to be Prepared
Copy Right@ Peter Borger
This work is licensed under Creative Commons Attribution 4.0 License
AJBSR.MS.ID.001312.
American Journal of
Biomedical Science & Research
www.biomedgrid.com
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ISSN: 2642-1747
Mini Review
Peter Borger*
The Independent Research Initiative on Information & Origins, Studiengemeinschaft “Wort und Wissen”, Germany
*Corresponding author: Peter Borger, The Independent Research Initiative on Information & Origins, Studiengemeinschaft “Wort und
Wissen”, Germany.
To Cite This Article: Peter Borger. A SARS-like Coronavirus was Expected, but nothing was done to be Prepared. 2020 - 8(5). AJBSR.
MS.ID.001312. DOI: 10.34297/AJBSR.2020.08.001312.
Received: April 13, 2020; Published: April 29, 2020
It was common knowledge that some strain of coronavirus-
sooner or later-was going to cause a pandemic. It was known since
the SARS-CoV-outbreak in 2003. In 2013 and 2015, the world was
informed that a variant of SARS-CoV in bats was emerging as a
threat for humans. Why was no action taken by our governments
and the World Health Organization (WHO)? The Corona crisis was
not only conceivable and foreseeable, but the world could have been
prepared. We could have had medication and we could have had a
vaccine long ago. That is, when there had been visionary medical-
political global leadership.
Corona and SARS
Coronaviruses are well-known respiratory viruses. The
name coronavirus (latin, corona: crown) was given to the virus,
since the proteins that protrude from the virus envelope, seen
through an electron microscope, are reminiscent of a crown.
They predominantly infect humans, birds and bats, but also
other animals. Coronaviruses are positive sense, single stranded
RNA viruses. This means that instead of DNA they have a single-
stranded RNA molecule as genetic material. They originate in the
genomes of higher organisms and new strains emerge frequently
through recombination. At present, we know of seven types of
coronaviruses that can infect humans. Infected with these viruses,
humans develop respiratory symptoms of various severities. It is
estimated that approximately 10% of common colds are caused by
 
coronaviruses, in particular the SARS-strains, can lead to more
severe respiratory tract infections and can be potentially lethal [1].
A lethal strain of coronaviruses, now known as SARS-CoV, was
 
congress of lung specialists in Adelaide, Australia in 2003, I clearly
recall the special attention given to SARS-CoV. This was because
this Coronavirus caused severe acute respiratory syndrome (SARS)
with a mortality rate of 9-10%. With outbreaks in 32 countries,
SARS-CoV was considered a serious threat to Western society.
Fortunately, SARS-CoV was not as contagious as feared and due
to the appropriate measures the threat faded within months. But
we all knew this was not going to be the last corona challenge.
  
of over 30% of infected persons, it is the most lethal coronavirus to
   
causing a pandemic. Nevertheless, virologists and lung scientists
anticipated another deadly coronavirus strain-it would only be
a matter of time. Now it is there: SARS-CoV2. This virus causes
COVID-19. And it already went pandemic. With a mortality of 3-4%
SARS-CoV2 is not as deadly as the earlier corona viruses but is far
more contagious. Therefore, COVID-19 can be-and will be as we are
currently witnessing-lethal for the weakest part of our society.
The genome of the coronavirus is the largest of all RNA
viruses that infect humans and they all have a very similar
molecular structure (Figure 1). The N-protein is currently used as
a diagnostic marker. This means that if this protein is detected in
patients, it is an aggressive, i.e. highly infectious, form of corona.
Further, coronaviruses contain three major envelope proteins.
        
      
has hemagglutinin and esterase activities, and ensures the virus’
cellular exit. The third protein, which forms the crown of the virus,
is the S-protein. It is responsible for receptor binding. The S-protein

in regulating the blood pressure and located mainly on cells of
  

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Am J Biomed Sci & Res
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Mice lacking this receptor are resistant to the SARS-CoV virus
and do not develop SARS symptoms [2]. The S protein is the most
attractive target for the development of vaccines and antibodies
because the protease activity of the S protein allows it to enter the
cells of the human body. Interestingly, the S-protein of SARS-CoV2
differs genetically from SARS-CoV by four small insertions.
Figure 1: Coronavirus genome and main encoded proteins. Spike protein (S), membrane protein (M), nucleoprotein (N) and the two replicase
proteins (R1 and R2), poly-A tail (AAA). Hemagglutinin-esterase (HE) is not present in SARS-CoV [10] and SARS-CoV2 [11].
COVID-19 is a SARS-like virus that can be treated with
chloroquine
In February 2020, the coronavirus currently causing the disease
COVID-19 was named SARS-CoV2 by an international consortium of
virus experts. They gave it his name because it is very similar to the
coronavirus SARS-CoV that spread SARS in 2003. On 11 February
       
would be COVID-19, a shortened version of coronavirus disease
   
causes COVID-19 and the one that caused the outbreak of SARS in
2003 are related to each other genetically, but the diseases they
cause are quite different. SARS was more deadly but much less
infectious than COVID-19. There have been no outbreaks of SARS
anywhere in the world since 2003.” [4].
The fact of the matter is that the symptoms associated with
SARS-CoV1 and SARS-CoV2, the syndromes of SARS and Covid-19,
can hardly be distinguished from each other. Based on symptoms
only, a pulmonologist would not be able to tell whether a patient is
infected with SARS-CoV1 or with SARS-CoV2. Laboratory scientists
can only determine the difference between the two infections by
performing tests at the molecular level, such as polymerase chain
reaction (PCR) assays or antibody-based test kits. The genetics of
the COVID-19 virus show that it is very likely a variant of the old
SARS-CoV1 virus from 2003. A study from March 2020 shows that
the genetic material of the SARS-CoV2 virus is 96.11% identical
to the SARS virus strain RaTG13 [5]. If the same method would
be used as evolutionary biologists do to compare the genes of
humans and chimpanzees (i.e. the insertions are not counted as
differences), the genomes of both viruses would be about 99%
identical. Furthermore, the group led by virologist Markus Hoffman
at the Leibniz Institute for Primate Research in Göttingen, Germany,
   
infect human cells as SARS-CoV [6]. The fact that COVID-19 (SARS-
         
dealing with an old SARS-like virus. As early as 2005, it was shown
that this drug reduced the virus-receptor binding and abrogated
infection and spread of SARS-CoV and virus spread was mitigated
when the cells were either treated with chloroquine prior to or after

      
most probably is a duck!” In other words, it is almost certain that
Covid-19 is SARS. We are dealing with a new-but weakened-SARS-
outbreak!
We can only call ourselves fortunate that SARS-CoV2 virus is less
mortal that the strain of 2003. Over time, a random accumulation
of mutations cause viruses to become weaker [8]. RNA viruses
mutate very rapidly and the relentless accumulation of mutations
reduces lethality. At the same time they may become more
infectious, however. The virus variants that are highly pathogenic
and mortal are becoming scarcer. Ultimately, an arrangement
of “peaceful coexistence” with their hosts can be expected. For
           
pandemic in summer 2009 but had calmed down and behaved
          
insertions in the S protein, the now spreading SARS-CoV2 virus
is more infectious than SARS-CoV from 2003, but fortunately also
less dangerous-just as one would expect from an ageing mutant
virus. Together, these studies strongly suggest that the coronavirus
causing COVID-19 is very closely related to the SARS-CoV virus of
2003-if not a predecessor. Genetic analyses indicated that the virus
of 2003 was not a recombination of known viruses, but a novel virus
that emerged suddenly from a mammalian reservoir in China. But
unlike most other coronaviruses, the SARS-CoV strain of 2003 did


unique to SARS-CoV [10]. Intriguingly, an almost identical sequence
   
Am J Biomed Sci & Res
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CoV2 [11]. Both characteristics prove that we are dealing with a
variant of the same virus of 2003.
SARS-CoV research was discontinued after 2008
One of the most disturbing discoveries of my investigations
into SARS-Viruses, is the observation that SARS-CoV research was
discontinued in 2008. If you enter the terms “sars cov” or “sars-
  
more than 4800 research articles about SARS-CoV were published
between 2003 and 2008. After 2008, no studies addressing SARS-
        
        
CoV publication was not published until December 2019, after the
SARS-COV2 outbreak in China. Nevertheless, a handful of scientists
carried on the SARS-research. In 2013, a Chinese group reported
in Nature that Chinese horseshoe bats are natural reservoirs of
SARS-CoV, and that intermediate hosts may not be necessary for
direct human infection by some bat viruses. They also emphasized
the importance of pathogen-discovery programs targeting high-
risk wildlife groups in emerging disease hotspots as a strategy
for pandemic preparedness [13]. Two years later, an international
group of virologists reported in Nature Medicine that a SARS-like
cluster of circulating bat coronaviruses shows potential for human
emergence [14]. So by 2015, the world had been warned twice that
another SARS-CoV outbreak, or that of a very similar SARS-like
virus, could be imminent.
No action taken by global governments and WHO
Despite two warnings in high-ranked journals the world was
unprepared for another SARS-CoV outbreak. Why was no action
taken by our governments and the WHO? Thousands of people
died during the epidemics of 2003 and 2012, while surprisingly
no vaccine, treatment, or diagnostic had been established. In 2019,
another deadly coronavirus kills thousands and thousands of
people-and there will be many more. Yes, today there are diagnostic
kits available, but a vaccine or treatment was not developed after
the last SARS-CoV outbreak. By 2015 at the latest, after the warnings
published in Nature and Nature Medicine, measures should have
 
We may really ask ourselves why our governments led by the WHO,
did not install a research and development program to be prepared

challenge, and not very costly either, to be properly prepared. In
2012, under the supervision of the Robert-Koch Institute (Berlin,
Gemany) the advisors of the German government anticipated a
novel SARS-outbreak and presented a detailed risk analysis of a
       
SARS-virus was made partly because the natural variant in 2003
quickly pushed the different health systems to their limits [15]. The
German government did not take action, however.
Between the outbreak of SARS in 2003 and the outbreak of
COVID-19 in 2019 lie 16 years. Was a treatment for SARS developed
in these 16 years? Was a vaccine developed? Was a blocking
antibody developed? All knowledge to do so was available. The
shocking fact is that the decisive actions to be prepared for the
next outbreak of a deadly SARS-virus were not taken. Despite
being warned twice in 2013 and 2015 that a SARS- virus outbreak
might be looming in China, the global governments and the
WHO did not demonstrate the slightest proactivity. There was
ample opportunity to develop cures and vaccines to prevent the
current corona crisis, which de facto began 16 years ago. If the
governments and the WHO had listened to the experts, if they had
taken the warnings seriously, the world would have been prepared
in 2019. There would have been blocking antibodies, vaccines and
treatments. With visionary leadership during the past decade,
SARS-CoV2 would have been stopped in China. The corona crisis
is a particularly clear demonstration of how far-reaching medico-
economic policy decisions can be. Considering the victims and the

responsibilities.
References
1. https://www.sinobiological.com/research/virus/human-coronavirus
2. Kuba K, Imai Y, Rao S, Gao H, Guo F, et al. (2005) A crucial role of

lung injury. Nature Medicine 11(8): 875-879.
3. https://www.newscientist.com/term/covid-19/.
4. 
5.     


6. Hoffmann M, Kleine-WH, Schroeder S, Krüger N, Herrler T, et al. (2020)
   
by a Clinically Proven Protease Inhibitor. Cell 18(12): 271-280.
7. 
Chloroquine is a potent inhibitor of SARS coronavirus infection and
spread. Virol J 2: 69.
8. Carter RW, Sanford JC (2012) A new look at an old virus: patterns of
  
Theor Biol Med Model 9: 42.
9. Collier L, Oxford J (2006) Human Virology, Oxford University Press :75.
10. Marra MA, Steven JMJ, Caroline RA, Robert AH, Angela BW et al. (2003)
Science. The Genome sequence of the SARS-associated coronavirus.
Science 300(5624): 1399-1404.
11. https://www.ncbi.nlm.nih.gov/nuccore/MN908947
12. https://www.ncbi.nlm.nih.gov/pubmed/
13. Ge XY, Li JL, Yang XL, Chmura AA, Zhu G, et al. (2013) Isolation and
         
receptor. Nature. 503(7477): 535-538.
14.     
SARS-like cluster of circulating bat coronaviruses shows potential for
human emergence. Nature Med 21(12): 1508-1513.
15. Deutscher Bundestag (2012) Bericht zur Risikoanalyse im
Bevölkerungsschutz 2012.
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