Sunday, March 29, 2020

Why are we locked inside our homes? - Several reasons!

Why are we locked inside our homes? - Several reasons!

  1. There is something in the skies they don’t want us to see. It could be a planet, an asteroid or extraterrestrials. Perhaps Nibiru!
  2. When the pack is divided it is much easier to subdue. A form of martial law could be invoked, and the shutdown of the WWW will likely follow. To contain networking efforts via the social media.
  3. A impending planetary cataclysm which cannot be prevented. A massive volcanic eruption or impending tectonic plate movement along one of the coastal areas of the Pacific region.
  4. That the initial impact of the virus, which is minimal and curable, is no longer controllable, and the mutation poses more of an existential threat than the original version of the virus. 

The main purpose of the virus has already been discussed, but the secondary scenario, which is much more relevant, has yet to present itself. Look to the skies every night. Don’t let your curiosity be a stranger to the question.

Thank you,
Joseph Pede

“We will do whatever it takes”

“We will do whatever it takes”

These anaesthetically intoxicating and occultic “magical words” have produced a complete or partial loss of perception for the convalescing public. When one becomes desensitized to the physical reality of a situation one becomes “defenceless, dependent and demoralized”.  

The “crown virus” is analogous to a terrorist attack. Rather than a perceptible and visual act of destruction, this unseen foe terrorizes the psyche. 

The empathetic resonance of these magical words, and their ongoing repetition, by political leaders, allows the masses to be subdued by their false sense of security. 

This elixir of words is not ambrosia, but rather arsenic. An apothecary filled only with intangible chaos.

This is your opportunity to break the chains that bind you and seek the truth. You, not them, must do whatever it takes to seek enlightenment. Your birth was an event planned by you. You chose to participate in these challenging times for a reason. 

Seek out that reason.

Thank you,
Joseph Pede

Saturday, March 28, 2020

Defiance of the Host

Defiance of the Host

The coronavirus, translated from Latin, means the “crown virus”. The crown is symbolic of ultimate rule. Here are a summary of the facts:

In 2016, the Covid-19 virus was created as a bioweapon by the Pilbright Institute, in conjunction with the Bill Gates Foundation, for which global patents were issued

In 2019, Dr Charles M Lieber, the Biology Chair at Harvard University sold a modified “crown virus" to Wuhan University and the Chinese government. Global casualties indicate that the virus is targeting Europeans, Persians and Asians. The jew obviously engineered the virus to target specific ethnic groups. jews are not Semites so casualties among jews will occur within European countries.

Dr Francis Boyle has unequivocally stated that a vaccine was created by the Pilbright Institute, and that it is available for use. This science is being withheld while the virus-simulation rages on. While already FDA approved quinine-based drugs have cured Covid-19, their global use has been withheld.

Because the virus was engineered to target specific ethnic groups, it has very likely mutated outside the bounds of who it was originally designed to infect - i.e. individuals with a high ACE2 receptor physiology - which would be Asians.

The main reasons why the jews unleashed the virus, was to fulfil the prophecy of the Red Heifer, and to construct the third temple in Jerusalem, while the remaining globalists (Vatican, monarchies, influential industrialists) wanted to implode the totally corrupt and fraudulent financial markets, which were riddled with unending debt and were completed manipulated, inaugurate the final phase of Agenda2030, employ artificial intelligence and the WWW to analyze global consciousness and human behaviour when a global workforce and/or society is idled and/or contained, test the impact of faltering global supply chains domestically and internationally, implant the virus for future control purposes (i.e. later introduce a nanotechnology based vaccine), create unlimited FIAT currency or debt to support an idle economy to eventually make the global debt unsustainable much sooner than anticipated (Agenda2030), introduce the concept of Global Collectivism (Fascism or Communism), remove God from the crisis by shutting down houses of worship and make national governments the saviours, by offering unlimited resources to its citizens (One World Religion led by the heretic Pope Francis), use the media to promote fear and promote restraint, reward public sector employees to sit on their asses at home so the prevailing government ideology will be guaranteed to carry on in the next election (remember ideology, not party), and last but not least, test the impact of 5G wave technology on the globally implanted virus. 

In the background, this simulation is testing technology-based learning to do away with traditional classroom instruction, the prospects of digital currencies as replacements for paper money (as paper currency is unsanitary in pandemic situations), and indirectly implode the gas combustion engine so that electrification and autonomous vehicle solutions, especially for use in public transit, become something the public demands for safety/sanitary and environmental reasons, and not something the prevailing governments wishes to invoke. 

While digital currencies will at some point prevail, they cannot be devices controlled by individuals outside the circle of control. Any cryptocurrency which prevails will be one controlled by the BIS, IMF and World Bank, and very likely termed the SDR. An SDR backed by "gold and silver" and other important commodities. This will be the only means to measure a country's equity position in the global currency.

With youth defying public orders of restraint and containment, and with continued protests in Hong Kong, France and many other countries, the simulation has encountered many obstacles. The least of which is the growing skepticism about the honesty and integrity of our government officials, and why the planet is experiencing so much continued chaos. Many realize that most of chaos is centred about technology-based weather manipulation (ex floods, fires, earthquakes etc), Black Swan Events, Gladio Events, regional wars, advancement of the Yinon Plan to create an immigration and refugees crisis for European nations, and government policies which promote the complete breakdown of traditional family values, by promoting abortion, a homogenous society and gender confusion.

The virus is not the issue - it is simply another globalist device. The Egregore which prevails is all that matters. The defiance of the virus' host will set the path for the next decade. Our leaders, unfortunately, do not know how to orchestrate the next paradigm shift, and they certainly do not want our input. For any solution with public input, means a global government will fail.

Thank you,
Joseph Pede

Friday, March 27, 2020

Life and Time

Life and Time

When the simulation is complete
All that will remain is the balance of life and time
What once was can no longer be
The past has left us confused and bewildered

The smartphone was not as smart as it professed to be
The computer became mundane
Sitting and thinking became agonizing 
Talking with family rather than texting appeared odd

Many dreams have been shattered
Money has vanquished
The next purchase indefinitely delayed
The dream vacation has turned to nightmare

Kids are no longer distant
They too confused by the sudden circumstance
Mom and dad together for dinner
The family dog perplexed by the sudden change

Your hair is getting long
Your nails long for a manicure that is months away
The body lingers for a relaxing massage
The shopping mall begs for your return

The cars sits idle in the garage
Yet oil wars persist among nations
Economies experiencing devastation
While the stock market pokes at your sanity

The news can only communicate fear
Death and disease are edging closer
For some the virus is a monstrous quagmire
For the young a bewildering circumstance

The once empty churches have now secured their emptiness
Satan adventurously stirs among the masses
Angels have flocked to the heavens
Religion an uncertainty in these trying times

Colour has faded to black and white
Technology fully enslaved by the technocrats
Clarity has turned to confusion
Or is it vice versa

The virus has put the brakes on life
The road no longer offers as many possibilities
The path to reason has become far shorter
The ending is up to you

Thank you,
Joseph Pede

Thursday, March 26, 2020

Netanyahu Aide - ‘Hate is what unites our camp’

Netanyahu aide in leaked recording:

Hate is what unites our camp’

Natan Eshel heard saying negative campaigning works well with ‘non-Ashkenazi’ voters and that the ‘animal’ Miri Regev is particularly effective at it

Prime Minister Benjamin Netanyahu’s senior aide Natan Eshel said that “hate is what unites” the right-wing camp led by the Likud party and that negative campaigning works well on “non-Ashkenazi voters” in a leaked recording revealed by Channel 12 on Saturday.

Never forget the jew, Dr. Charles M. Lieber who took bribes for selling the coronavirus to Chinese officials. I'm sure the jews will erase as much as possible from the internet to hide this fact. The jews brought us Covid-19 and it is programmed to attack Asians, Europeans and Persians. Never forget what the jew has done to humanity. They continue to commit genocides and atrocities under the fiction of the hollow-cast.

Thank you,
Joseph Pede

Wednesday, March 25, 2020

"Corona" meaning in Latin


Corona in Latin means "Crown"

The coronavirus is the "Crown Virus"

Thank you,
Joseph Pede

Sunday, March 22, 2020

Of Whine and Roses


Of Whine and Roses

Let us mourn this new morn
For current events have created panic in the hearts of humanity
What was once a normal day
Has transformed into a sacrilegious holiday

Fear has pricked our maddened calm 
Sidewalks are empty of shadows
Roads are empty of fumes
Empty malls no different than the already deserted pews

These are the days of whine and roses
Days of reflection and foreboding
When biblehub becomes more relevant than pornhub
When the confused seek out their forgotten novenas

Find the fierceness you once stowed away
Let your anger shake the legislature walls
Condemn those who make jolly our demise
Let your clenched fists replace the silent hands of prayer

Thank you,
Joseph Pede

It should be obvious by the findings that there are at least two strains of Covid-19, perhaps more. The virus has been designed to target specific ethnic groups. One attacking the Chinese and the other attacking Europeans. A previous study of the ACE2 receptor is shown below. How can Europeans who have the "least" ACE2 receptor be so greatly impacted?

The jew, Dr. Charles Lieber, who developed this strain of Covid-19 and his satanic cult of jews have specifically targeted Chinese and Europeans with this bio-weapon.

I am Italian, and what is happening to Italians is unacceptable. I urge all Italians in Italy to do what must be done. An eye for an eye. Rid Italy and Europe of all jews and destroy their synagogues, for this is what they are doing to you. 

Historically, jews have committed never-ending genocides and atrocities. Now their rabbis openly declare war and curse our Christian faith via Covid-19. These demons must not be allowed to murder any more.

Thank you,
Joseph Pede

ACE2 is also "abundantly present in humans in the epithelia of the lung and small intestine, which might provide possible routes of entry for the SARS-CoV," while it was also observed "in arterial and venous endothelial cells and arterial smooth muscle cells" - which would include the heart.
This has led some to speculate that Asians, who have higher concentrations of ACE2 (per the 1000 genome project) may be affected to a greater degree than those of European ancestry, who produce the least of it - and have largely been the asymptomatic 'super spreaders' such as Diamond Princess coronavirus victim Rebecca Frasure.

Covid-19 and why not D-Wave Systems

By now everyone should have realized that Covid-19 is a dangerous "Black Swan Event", and that the vaccine for Covid-19 was in place prior to the outbreak. Why Covid-19 was created is the bigger question?

Canada is at the forefront of "quantum computing" yet we have failed to seek solutions from one of most technologically advanced companies in the world. It is known as D-Wave Systems. Why has their intervention not been solicited?

People everywhere should try and understand the true implications of Covid-19 - Financial Resets, Totalitarian Technocracies, Viruses as a key 21st century bio-weapons (others weapons include weather manipulation, A.I. control of global consciousness, abortion, gender neutrality etc), Depopulation Agendas, Global Collectivism, and most importantly the battle between Good and Evil, or God and Satan, and the DESTRUCTION of the FAMILY.

Please read the following article.

Thank you,
Joseph Pede



Scientists recently tasked the world’s fastest supercomputer with running thousands of simulations to find drug compounds that could fight the coronavirus.
IBM supercomputer — called “Summit”, housed at the Oak Ridge National Laboratory in Tennessee — has identified 77 treatments that may be able to stop COVID-19 dead in its tracks.
The research, detailed a paper uploaded to the preprint server ChemRxiv, could even help researchers develop a vaccine for the deadly virus — but so far, it’s only an important first step.
“Our results don’t mean that we have found a cure or treatment for the coronavirus,” said Jeremy Smith, director of the Oak Ridge National Laboratory Center for Molecular Biophysics, in a statement.
“We are very hopeful, though, that our computational findings will both inform future studies and provide a framework that experimentalists will use to further investigate these compounds,” he added.
The massive supercomputer was tasked with finding compounds that could bind to the “spike protein” or “S-protein” of the virus that it uses to infect host cells. By rendering the protein ineffective, the virus would be inhibited from spreading.
Using previously-created models of the coronavirus spike, the researchers simulated how particles in the viral protein would react to different drug compounds.
The team cut down the list from 77 to the top seven most promising candidates to treat the SARS-CoV-2 virus.
“Given the results from both sets of docking calculations, our work suggests that at least the seven compounds identified here would be reasonable initial compounds for experimental investigations in limiting SARS-CoV-2’s virus-host interactions,” reads the paper.
Next, the team is planning to run another simulation using a highly accurate spike protein model first identified in a study published last week by a different team of researchers.

Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation

 See all authors and affiliations

Science  13 Mar 2020:
Vol. 367, Issue 6483, pp. 1260-1263
DOI: 10.1126/science.abb2507

Structure of the nCoV trimeric spike

The World Health Organization has declared the outbreak of a novel coronavirus (2019-nCoV) to be a public health emergency of international concern. The virus binds to host cells through its trimeric spike glycoprotein, making this protein a key target for potential therapies and diagnostics. Wrapp et al. determined a 3.5-angstrom-resolution structure of the 2019-nCoV trimeric spike protein by cryo–electron microscopy. Using biophysical assays, the authors show that this protein binds at least 10 times more tightly than the corresponding spike protein of severe acute respiratory syndrome (SARS)–CoV to their common host cell receptor. They also tested three antibodies known to bind to the SARS-CoV spike protein but did not detect binding to the 2019-nCoV spike protein. These studies provide valuable information to guide the development of medical counter-measures for 2019-nCoV.
Science, this issue p. 1260


The outbreak of a novel coronavirus (2019-nCoV) represents a pandemic threat that has been declared a public health emergency of international concern. The CoV spike (S) glycoprotein is a key target for vaccines, therapeutic antibodies, and diagnostics. To facilitate medical countermeasure development, we determined a 3.5-angstrom-resolution cryo–electron microscopy structure of the 2019-nCoV S trimer in the prefusion conformation. The predominant state of the trimer has one of the three receptor-binding domains (RBDs) rotated up in a receptor-accessible conformation. We also provide biophysical and structural evidence that the 2019-nCoV S protein binds angiotensin-converting enzyme 2 (ACE2) with higher affinity than does severe acute respiratory syndrome (SARS)-CoV S. Additionally, we tested several published SARS-CoV RBD-specific monoclonal antibodies and found that they do not have appreciable binding to 2019-nCoV S, suggesting that antibody cross-reactivity may be limited between the two RBDs. The structure of 2019-nCoV S should enable the rapid development and evaluation of medical countermeasures to address the ongoing public health crisis

The novel coronavirus 2019-nCoV has recently emerged as a human pathogen in the city of Wuhan in China’s Hubei province, causing fever, severe respiratory illness, and pneumonia—a disease recently named COVID-19 (12). According to the World Health Organization (WHO), as of 16 February 2020, there had been >51,000 confirmed cases globally, leading to at least 1600 deaths. The emerging pathogen was rapidly characterized as a new member of the betacoronavirus genus, closely related to several bat coronaviruses and to severe acute respiratory syndrome coronavirus (SARS-CoV) (34). Compared with SARS-CoV, 2019-nCoV appears to be more readily transmitted from human to human, spreading to multiple continents and leading to the WHO’s declaration of a Public Health Emergency of International Concern (PHEIC) on 30 January 2020 (156).
2019-nCoV makes use of a densely glycosylated spike (S) protein to gain entry into host cells. The S protein is a trimeric class I fusion protein that exists in a metastable prefusion conformation that undergoes a substantial structural rearrangement to fuse the viral membrane with the host cell membrane (78). This process is triggered when the S1 subunit binds to a host cell receptor. Receptor binding destabilizes the prefusion trimer, resulting in shedding of the S1 subunit and transition of the S2 subunit to a stable postfusion conformation (9). To engage a host cell receptor, the receptor-binding domain (RBD) of S1 undergoes hinge-like conformational movements that transiently hide or expose the determinants of receptor binding. These two states are referred to as the “down” conformation and the “up” conformation, where down corresponds to the receptor-inaccessible state and up corresponds to the receptor-accessible state, which is thought to be less stable (1013). Because of the indispensable function of the S protein, it represents a target for antibody-mediated neutralization, and characterization of the prefusion S structure would provide atomic-level information to guide vaccine design and development.
Based on the first reported genome sequence of 2019-nCoV (4), we expressed ectodomain residues 1 to 1208 of 2019-nCoV S, adding two stabilizing proline mutations in the C-terminal S2 fusion machinery using a previous stabilization strategy that proved effective for other betacoronavirus S proteins (1114). Figure 1A shows the domain organization of the expression construct, and figure S1 shows the purification process. We obtained ~0.5 mg/liter of the recombinant prefusion-stabilized S ectodomain from FreeStyle 293 cells and purified the protein to homogeneity by affinity chromatography and size-exclusion chromatography (fig. S1). Cryo–electron microscopy (cryo-EM) grids were prepared using this purified, fully glycosylated S protein, and preliminary screening revealed a high particle density with little aggregation near the edges of the holes.

Fig. 1 Structure of 2019-nCoV S in the prefusion conformation.
(A) Schematic of 2019-nCoV S primary structure colored by domain. Domains that were excluded from the ectodomain expression construct or could not be visualized in the final map are colored white. SS, signal sequence; S2′, S2′ protease cleavage site; FP, fusion peptide; HR1, heptad repeat 1; CH, central helix; CD, connector domain; HR2, heptad repeat 2; TM, transmembrane domain; CT, cytoplasmic tail. Arrows denote protease cleavage sites. (B) Side and top views of the prefusion structure of the 2019-nCoV S protein with a single RBD in the up conformation. The two RBD down protomers are shown as cryo-EM density in either white or gray and the RBD up protomer is shown in ribbons colored corresponding to the schematic in (A).

After collecting and processing 3207 micrograph movies, we obtained a 3.5-Å-resolution three-dimensional (3D) reconstruction of an asymmetrical trimer in which a single RBD was observed in the up conformation. (Fig. 1B, fig. S2, and table S1). Because of the small size of the RBD (~21 kDa), the asymmetry of this conformation was not readily apparent until ab initio 3D reconstruction and classification were performed (Fig. 1B and fig. S3). By using the 3D variability feature in cryoSPARC v2 (15), we observed breathing of the S1 subunits as the RBD underwent a hinge-like movement, which likely contributed to the relatively poor local resolution of S1 compared with the more stable S2 subunit (movies S1 and S2). This seemingly stochastic RBD movement has been captured during structural characterization of the closely related betacoronaviruses SARS-CoV and MERS-CoV, as well as the more distantly related alphacoronavirus porcine epidemic diarrhea virus (PEDV) (10111316). The observation of this phenomenon in 2019-nCoV S suggests that it shares the same mechanism of triggering that is thought to be conserved among the Coronaviridae, wherein receptor binding to exposed RBDs leads to an unstable three-RBD up conformation that results in shedding of S1 and refolding of S2 (1112).
Because the S2 subunit appeared to be a symmetric trimer, we performed a 3D refinement imposing C3 symmetry, resulting in a 3.2-Å-resolution map with excellent density for the S2 subunit. Using both maps, we built most of the 2019-nCoV S ectodomain, including glycans at 44 of the 66 N-linked glycosylation sites per trimer (fig. S4). Our final model spans S residues 27 to 1146, with several flexible loops omitted. Like all previously reported coronavirus S ectodomain structures, the density for 2019-nCoV S begins to fade after the connector domain, reflecting the flexibility of the heptad repeat 2 domain in the prefusion conformation (fig. S4A) (131618).
The overall structure of 2019-nCoV S resembles that of SARS-CoV S, with a root mean square deviation (RMSD) of 3.8 Å over 959 Cα atoms (Fig. 2A). One of the larger differences between these two structures (although still relatively minor) is the position of the RBDs in their respective down conformations. Whereas the SARS-CoV RBD in the down conformation packs tightly against the N-terminal domain (NTD) of the neighboring protomer, the 2019-nCoV RBD in the down conformation is angled closer to the central cavity of the trimer (Fig. 2B). Despite this observed conformational difference, when the individual structural domains of 2019-nCoV S are aligned to their counterparts from SARS-CoV S, they reflect the high degree of structural homology between the two proteins, with the NTDs, RBDs, subdomains 1 and 2 (SD1 and SD2), and S2 subunits yielding individual RMSD values of 2.6 Å, 3.0 Å, 2.7 Å, and 2.0 Å, respectively (Fig. 2C).

Fig. 2 Structural comparison between 2019-nCoV S and SARS-CoV S.
(A) Single protomer of 2019-nCoV S with the RBD in the down conformation (left) is shown in ribbons colored according to Fig. 1. A protomer of 2019-nCoV S in the RBD up conformation is shown (center) next to a protomer of SARS-CoV S in the RBD up conformation (right), displayed as ribbons and colored white (PDB ID: 6CRZ). (B) RBDs of 2019-nCoV and SARS-CoV aligned based on the position of the adjacent NTD from the neighboring protomer. The 2019-nCoV RBD is colored green and the SARS-CoV RBD is colored white. The 2019-nCoV NTD is colored blue. (C) Structural domains from 2019-nCoV S have been aligned to their counterparts from SARS-CoV S as follows: NTD (top left), RBD (top right), SD1 and SD2 (bottom left), and S2 (bottom right).

2019-nCoV S shares 98% sequence identity with the S protein from the bat coronavirus RaTG13, with the most notable variation arising from an insertion in the S1/S2 protease cleavage site that results in an “RRAR” furin recognition site in 2019-nCoV (19) rather than the single arginine in SARS-CoV (fig. S5) (2023). Notably, amino acid insertions that create a polybasic furin site in a related position in hemagglutinin proteins are often found in highly virulent avian and human influenza viruses (24). In the structure reported here, the S1/S2 junction is in a disordered, solvent-exposed loop. In addition to this insertion of residues in the S1/S2 junction, 29 variant residues exist between 2019-nCoV S and RaTG13 S, with 17 of these positions mapping to the RBD (figs. S5 and S6). We also analyzed the 61 available 2019-nCoV S sequences in the Global Initiative on Sharing All Influenza Data database ( and found that there were only nine amino acid substitutions among all deposited sequences. Most of these substitutions are relatively conservative and are not expected to have a substantial effect on the structure or function of the 2019-nCoV S protein (fig. S6).
Recent reports demonstrating that 2019-nCoV S and SARS-CoV S share the same functional host cell receptor, angiotensin-converting enzyme 2 (ACE2) (222527), prompted us to quantify the kinetics of this interaction by surface plasmon resonance. ACE2 bound to the 2019-nCoV S ectodomain with ~15 nM affinity, which is ~10- to 20-fold higher than ACE2 binding to SARS-CoV S (Fig. 3A and fig. S7) (14). We also formed a complex of ACE2 bound to the 2019-nCoV S ectodomain and observed it by negative-stain EM, which showed that it strongly resembled the complex formed between SARS-CoV S and ACE2 that has been observed at high resolution by cryo-EM (Fig. 3B) (1428). The high affinity of 2019-nCoV S for human ACE2 may contribute to the apparent ease with which 2019-nCoV can spread from human to human (1); however, additional studies are needed to investigate this possibility.

Fig. 3 2019-nCoV S binds human ACE2 with high affinity.
(A) Surface plasmon resonance sensorgram showing the binding kinetics for human ACE2 and immobilized 2019-nCoV S. Data are shown as black lines, and the best fit of the data to a 1:1 binding model is shown in red. (B) Negative-stain EM 2D class averages of 2019-nCoV S bound by ACE2. Averages have been rotated so that ACE2 is positioned above the 2019-nCoV S protein with respect to the viral membrane. A diagram depicting the ACE2-bound 2019-nCoV S protein is shown (right) with ACE2 in blue and S protein protomers colored tan, pink, and green.

The overall structural homology and shared receptor usage between SARS-CoV S and 2019-nCoV S prompted us to test published SARS-CoV RBD-directed monoclonal antibodies (mAbs) for cross-reactivity to the 2019-nCoV RBD (Fig. 4A). A 2019-nCoV RBD-SD1 fragment (S residues 319 to 591) was recombinantly expressed, and appropriate folding of this construct was validated by measuring ACE2 binding using biolayer interferometry (BLI) (Fig. 4B). Cross-reactivity of the SARS-CoV RBD-directed mAbs S230, m396, and 80R was then evaluated by BLI (122931). Despite the relatively high degree of structural homology between the 2019-nCoV RBD and the SARS-CoV RBD, no binding to the 2019-nCoV RBD could be detected for any of the three mAbs at the concentration tested (1 μM) (Fig. 4C), in contrast to the strong binding that we observed to the SARS-CoV RBD (fig. S8). Although the epitopes of these three antibodies represent a relatively small percentage of the surface area of the 2019-nCoV RBD, the lack of observed binding suggests that SARS-directed mAbs will not necessarily be cross-reactive and that future antibody isolation and therapeutic design efforts will benefit from using 2019-nCoV S proteins as probes.

Fig. 4 Antigenicity of the 2019-nCoV RBD.
(A) SARS-CoV RBD shown as a white molecular surface (PDB ID: 2AJF), with residues that vary in the 2019-nCoV RBD colored red. The ACE2-binding site is outlined with a black dashed line. (B) Biolayer interferometry sensorgram showing binding to ACE2 by the 2019-nCoV RBD-SD1. Binding data are shown as a black line, and the best fit of the data to a 1:1 binding model is shown in red. (C) Biolayer interferometry to measure cross-reactivity of the SARS-CoV RBD-directed antibodies S230, m396, and 80R. Sensor tips with immobilized antibodies were dipped into wells containing 2019-nCoV RBD-SD1, and the resulting data are shown as a black line.

The rapid global spread of 2019-nCoV, which prompted the PHEIC declaration by WHO, signals the urgent need for coronavirus vaccines and therapeutics. Knowing the atomic-level structure of the 2019-nCoV spike will allow for additional protein-engineering efforts that could improve antigenicity and protein expression for vaccine development. The structural data will also facilitate the evaluation of 2019-nCoV spike mutations that will occur as the virus undergoes genetic drift and help to define whether those residues have surface exposure and map to sites of known antibody epitopes for other coronavirus spike proteins. In addition, the structure provides assurance that the protein produced by this construct is homogeneous and in the prefusion conformation, which should maintain the most neutralization-sensitive epitopes when used as candidate vaccine antigens or B cell probes for isolating neutralizing human mAbs. Furthermore, the atomic-level detail will enable the design and screening of small molecules with fusion-inhibiting potential. This information will support precision vaccine design and the discovery of antiviral therapeutics, accelerating medical countermeasure development.