Did a 2016 Wuhan virus cause COVID-19?

Actual Image of Corona Virus COVID-19
Actual Image of Corona Virus COVID-19

April 9, 2020

This forensic analysis compares a 2016 genetically synthesized rWIV1 virus in the Wuhan Institute of Virology that was spliced with a staphylococci gene (ORFX), and shares high homology with the SARS-CoV-2 virus which caused COVID-19 disease.

In 2016 doctors from the Wuhan Institute of Virology published the “Bat Severe Acute Respiratory Syndrom-Like Coronavirus W1V1 Encodes and Extra Accessory Protein, ORFX, Involved in Modulation of the Host Immune Response” paper in the American Society for Microbiology’s Journal of Virology.

In the 2016 paper, researchers Lei-Ping Zeng, Yu-Tao Gao, Xing-Yi Ge, Qian Zhang, Cheng Peng, Xing-Lou Yang, Bing Tan, Jing Chen, Aleksei A. Chmura, Peter Daszak, and Zheng-Li Shia identify their creation of “WIV1 mutant” viruses which were modified to “activate NF-KB” as a “strategy for construction of an infectious WIV1 BAC”. (BAC is a Bacterial Artificial Chromosome using bacteria to infect a virus with DNA in the laboratory.)

The researchers stated they knew “Bats harbor severe acute respiratory syndrome (SARS)-like coronaviruses (SL-CoVs) from which the causative agent of the 2002-2003 SARS pandemic is thought to have originated” and were focused upon two of those viruses (rWIV1 and rWIV1-deltaX), which showed promise for human infection.
(Note: rWIV1 means “recombinant Wuhan Institute of Virology: Virus #1” modified from a 2015 experiments by Zhen-Li Shia and Xing-Yi Ge)

This 2016 “mutant virus” synthesis was follow-up research to a 2015 research project (“A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence” by Zhengli-Li Shi (Zheng-Li Shia) and Xing-Yi Ge, et al.. The 2015 researchers obtained assays of “wild type SARS-CoV (Urbani), mouse-adapted SARS-CoV (MA15), and chimeric SARS-like CoVs” from the United States Army Medical Research Institute of Infectious Diseases. The 2015 experiments created a new chimeric virus CoV spike protein within RsWIV1-CoV. (Page 1508, “Rs” means “Research sample”)

Researchers from the 2015 experiments concluded “further adaptation is required for its replication to be equivalent to that of epidemic SARS-CoV in human respiratory cells…. mutations are both seldom and rare, reducing the likelihood of future emergence events in humans.” However, they speculated a trans-species viruses may already be “circulating within animal reservoirs” and raised ethical “research concerns [as] the potential to prepare for and mitigate future outbreaks must be weighed against the risk of creating more dangerous pathogens” since their findings proved the ease of building more harmful chimeric viruses using presently circulating strains. (Page 1512)

So, in 2016, the same researchers who in 2015 cautioned the world against more dangerous strains, decided to add a ORFX gene taken from highly infectious staphylococci and insert it between the ORF6 and ORF7 genes on the newly synthesized WIV1 (rWIV1) and WIV16 COVID mutant viruses.

Citing a difficulty in obtaining SARS-CoV viruses from international research facilities, the 2015 researchers Xing-Yi Ge & Zhengli-Li Shi at the Wuhan Institute or Virology “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.”

In follow-up to the 2015 research, the 2016 Wuhan researchers found the “WIV1 and WIV16 are two recently identified SL-CoV strains with high genomic similarity to human SARS-CoV“, with the WIV1 virus now containing a newly added “11-kDa accessory protein” at the ORFX gene.

The “novel” (new) 11-kDA protein is unique in that it induces unfolded protein response (UPR) and endoplasmic reticulum (ER) stress upon hemoglobin within red blood cells to cause a loss of protein folding homeostasis. In other words, it unwraps and opens up the protective hemoglobin molecule.

Meanwhile, the virus’ ORF6 and ORFX genes work to prevents infected cells from releasing interferon (IFN) proteins to alert surrounding cells about the infection. At the same time the virus’ ORF7 gene triggers a viral replication process by hijacking the body’s NF-KB pathways.

The virus’ ORF3 and ORF6 genes were already known to cause some suppression of interferon. But ORFX spiked the suppression, and this intentional increase in suppression of interferon by the virus’ ORFX gene explains why now 80.9% of persons who are infected with COVID-19 don’t know they have an infection, and don’t exhibit an immuno inflammatory response.

According to the 2016 researchers the “ORFX protein showed an inhibitory effect on IFN production“. Just to make sure, when the researchers then removed the ORFX gene from their “W1V1 mutant” viruses the “ORFX deletion… caused a significantly higher level of IFN“.

The researchers determined their virus successfully “subverted” and antagonized the antiviral interferon response by infected cells.

To add the ORFX gene from staphylococci, the 2016 Chinese researchers first grew cloned staphylococci ORFX genes and spliced them into their new WIV1 and WIVdeltaX SARS-CoV2 strains from the 2015 experiments. According to their publication, “The coding region of ORFX was amplified by reverse transcription-PCR (RT-PCR) from viral RNA using the Superscript one-step RT-PCR kit (Invitrogen). The amplified gene was cloned into plasmid pCAGGS with a C-terminal hemagglutinin (HA) tag (pCAGGS-ORFX) for eukaryotic expression.”

That is the evolution of a 2015 Wuhan Institute of Virology research project which purchased SARS-CoV samples from a U.S. Army research facility, concluded their 2015 research with a caution against creating more dangerous viral strains. From there, a new 2016 Wuhan Institute of Virology research project proceeded with creating those dangerous strain which is nearly identical to the COVID-19 pandemic virus that originated in Wuhan, China.

What is the difference between COVID-19 and the r-WIF1 virus from 2016? In COVID-19 the ORFX gene is missing, but the new ORF8 gene on COVID-19 is 57% different from previous strains and behaves the same as the ORFX gene did on rWIV1. Amazing coincidence?

So now what?

It is well established that Vitamin C serves as a “sacrificial antioxidant” within the epithelial surface in the lungs, and acts as a first level of defense to destroy pathogens (bacteria, fungi, and some viruses) in the lungs and prevent them from entering the blood stream.

Normally, the lungs’ Respiratory Tract Lining Fluid (RTLF) acts as a sort of ‘reserve’ to store Vitamin C in higher levels than is normally found in the blood stream. But lower intake of dietary Vitamin C means lower levels of epithelial Vitamin C, and easier potential for passage of some pathogens to enter into the blood. Where Vitamin C levels are also particularly important are with dehydroascorbic acid (DHA) which is carried by GLUT-1 along with 3-OMG.

A red blood cell protein called GLUT1 is a transporter of DHA, but GLUT1 also has a high affinity for glucose.  A sub-population of GLUT1 is capable of binding to a d-glucose called 3-O-methylglucose (3-OMG), which is not subject to being metabolized by the body.  Without sufficient DHA levels to competitively suppress binding the 3-OMG readily attaches to the sub-population of GLUT1.   This results in uninhibited 3-OMG transport. 

Subsequently, 3-OMG is used by the COVID-19 virus to disable oxygen-carrying and carbon dioxide removing hemoglobin by what’s called “non-enzymatic glycation” of hemoglobin. Hemoglobin is responsible for carrying oxygen throughout the body to nourish major organs and other tissue and removing harmful CO2 from the blood.

COVID-19, in the absence of sufficient DHA, uses the 3-OMG to destabilize hemoglobin beginning with non-enzymatic glycation of oxyhemoglobin via structural surface glycoproteins (ORF3a and ORF8) at the 1-beta chain of hemoglobin.  The resultant methemoglobin and hemichromes are cleaved into small fragments as free iron is released from its usual position within the porphyrin ring and acts as a harmful oxidizer. (Figure 1)

Different stages of hemoglobin. The illustration shows the bond susceptibility identified in patent pending composition of medicines and therapeutic treatments for COVID-19, SARS-CoV, SARS-CoV-2, and MERS-CoV viruses against non-enzymatic glycation at the 1-beta chain of hemoglobin.

As it is being circulated throughout the body, COVID-19 also possesses the ORF8 gene (and parts of 11kDA protein), which silences infected cells from alerting other cells about the infection (releasing interferon).

The newly released iron free radicals tear up major organs and other tissue, because Vitamin C levels were low, and dietary absorption levels of iron is also low.

This contributes to why infected patients experience low levels of VO2, high levels of CO2, toxins in the blood, and organ failure from sepsis as COVID-19 spreads throughout the body and continues to bind to ACE-2 receptors on major organs.

Boost your Health. Always follow the advice of your doctor. For many people, one of the best things they might consider doing (in addition to not being exposed) is increasing Vitamin C intake to at least 3000 mg per day (broken down into 1000 mg dosages with a full glass of water, once in the morning, once midday, and once in early evening).

Hot water poured over sliced lemons is also a natural source of dietary Vitamin C. Most people can handle up to 5,000 mg. of Vitamin C per day if they drink enough water and don’t have other underlying health issues. Check with your doctor if you have any questions specific to your particular health needs.