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

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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."
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
American Journal of
Biomedical Science & Research
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
  
American Journal of Biomedical Science & Research
Am J Biomed Sci & Res
Copy@ Peter Borger
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
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-
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
American Journal of Biomedical Science & Research
Copy@ Peter Borger
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
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.
4. 
5.     
6. Hoffmann M, Kleine-WH, Schroeder S, Krüger N, Herrler T, et al. (2020)
   
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7. 
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There is plenty of pseudoscientific claims and conspiracy theory on Corona. One example is the text of Borger et al (Nov. 27th 2020), dealing with the first published qPCR test on SARS-CoV-2 (Corman et al. Jan 23rd 2020). This publication analyses the Borger Text showing that the criticism flawed, full of blemish including beginners errors.
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This extensive review report has been officially submitted to Eurosurveillance editorial board on 27th November 2020 via their submission-portal, enclosed to this review report is a retraction request letter, signed by all the main & co-authors. First and last listed names are the first and second main authors. All names in between are co-authors. More details can be found at
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The emergence of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome (MERS)-CoV underscores the threat of cross-species transmission events leading to outbreaks in humans. Here we examine the disease potential of a SARS-like virus, SHC014-CoV, which is currently circulating in Chinese horseshoe bat populations. Using the SARS-CoV reverse genetics system, we generated and characterized a chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone. The results indicate that group 2b viruses encoding the SHC014 spike in a wild-type backbone can efficiently use multiple orthologs of the SARS receptor human angiotensin converting enzyme II (ACE2), replicate efficiently in primary human airway cells and achieve in vitro titers equivalent to epidemic strains of SARS-CoV. Additionally, in vivo experiments demonstrate replication of the chimeric virus in mouse lung with notable pathogenesis. Evaluation of available SARS-based immune-therapeutic and prophylactic modalities revealed poor efficacy; both monoclonal antibody and vaccine approaches failed to neutralize and protect from infection with CoVs using the novel spike protein. On the basis of these findings, we synthetically re-derived an infectious full-length SHC014 recombinant virus and demonstrate robust viral replication both in vitro and in vivo. Our work suggests a potential risk of SARS-CoV re-emergence from viruses currently circulating in bat populations.
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The 2002-3 pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV) was one of the most significant public health events in recent history. An ongoing outbreak of Middle East respiratory syndrome coronavirus suggests that this group of viruses remains a key threat and that their distribution is wider than previously recognized. Although bats have been suggested to be the natural reservoirs of both viruses, attempts to isolate the progenitor virus of SARS-CoV from bats have been unsuccessful. Diverse SARS-like coronaviruses (SL-CoVs) have now been reported from bats in China, Europe and Africa, but none is considered a direct progenitor of SARS-CoV because of their phylogenetic disparity from this virus and the inability of their spike proteins to use the SARS-CoV cellular receptor molecule, the human angiotensin converting enzyme II (ACE2). Here we report whole-genome sequences of two novel bat coronaviruses from Chinese horseshoe bats (family: Rhinolophidae) in Yunnan, China: RsSHC014 and Rs3367. These viruses are far more closely related to SARS-CoV than any previously identified bat coronaviruses, particularly in the receptor binding domain of the spike protein. Most importantly, we report the first recorded isolation of a live SL-CoV (bat SL-CoV-WIV1) from bat faecal samples in Vero E6 cells, which has typical coronavirus morphology, 99.9% sequence identity to Rs3367 and uses ACE2 from humans, civets and Chinese horseshoe bats for cell entry. Preliminary in vitro testing indicates that WIV1 also has a broad species tropism. Our results provide the strongest evidence to date 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 SL-CoVs. They also highlight the importance of pathogen-discovery programs targeting high-risk wildlife groups in emerging disease hotspots as a strategy for pandemic preparedness.
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Background The H1N1 influenza A virus has been circulating in the human population for over 95 years, first manifesting itself in the pandemic of 1917–1918. Initial mortality was extremely high, but dropped exponentially over time. Influenza viruses have high mutation rates, and H1N1 has undergone significant genetic changes since 1918. The exact nature of H1N1 mutation accumulation over time has not been fully explored. Methods We have made a comprehensive historical analysis of mutational changes within H1N1 by examining over 4100 fully-sequenced H1N1 genomes. This has allowed us to examine the genetic changes arising within H1N1 from 1918 to the present. Results We document multiple extinction events, including the previously known extinction of the human H1N1 lineage in the 1950s, and an apparent second extinction of the human H1N1 lineage in 2009. These extinctions appear to be due to a continuous accumulation of mutations. At the time of its disappearance in 2009, the human H1N1 lineage had accumulated over 1400 point mutations (more than 10% of the genome), including approximately 330 non-synonymous changes (7.4% of all codons). The accumulation of both point mutations and non-synonymous amino acid changes occurred at constant rates (μ = 14.4 and 2.4 new mutations/year, respectively), and mutations accumulated uniformly across the entire influenza genome. We observed a continuous erosion over time of codon-specificity in H1N1, including a shift away from host (human, swine, and bird [duck]) codon preference patterns. Conclusions While there have been numerous adaptations within the H1N1 genome, most of the genetic changes we document here appear to be non-adaptive, and much of the change appears to be degenerative. We suggest H1N1 has been undergoing natural genetic attenuation, and that significant attenuation may even occur during a single pandemic. This process may play a role in natural pandemic cessation and has apparently contributed to the exponential decline in mortality rates over time, as seen in all major human influenza strains. These findings may be relevant to the development of strategies for managing influenza pandemics and strain evolution.
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During several months of 2003, a newly identified illness termed severe acute respiratory syndrome (SARS) spread rapidly through the world. A new coronavirus (SARS-CoV) was identified as the SARS pathogen, which triggered severe pneumonia and acute, often lethal, lung failure. Moreover, among infected individuals influenza such as the Spanish flu and the emergence of new respiratory disease viruses have caused high lethality resulting from acute lung failure. In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor. The high lethality of SARS-CoV infections, its enormous economic and social impact, fears of renewed outbreaks as well as the potential misuse of such viruses as biologic weapons make it paramount to understand the pathogenesis of SARS-CoV. Here we provide the first genetic proof that ACE2 is a crucial SARS-CoV receptor in vivo. SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway. These results provide a molecular explanation why SARS-CoV infections cause severe and often lethal lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses.
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Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available. We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations. Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds.
The recent emergence of the novel, pathogenic SARS-coronavirus 2 (SARS-CoV-2) in China and its rapid national and international spread pose a global health emergency. Cell entry of coronaviruses depends on binding of the viral spike (S) proteins to cellular receptors and on S protein priming by host cell proteases. Unravelling which cellular factors are used by SARS-CoV-2 for entry might provide insights into viral transmission and reveal therapeutic targets. Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. A TMPRSS2 inhibitor approved for clinical use blocked entry and might constitute a treatment option. Finally, we show that the sera from convalescent SARS patients cross-neutralized SARS-2-S-driven entry. Our results reveal important commonalities between SARS-CoV-2 and SARS-CoV infection and identify a potential target for antiviral intervention.