It has been three years since the COVID-19 outbreak started, yet the CDC and WHO have not acknowledged that the virus escaped from the Wuhan Institute of Virology.
Due to the repeated instances of lying by our institutions, 72% of the public now distrusts them. While concerning, this lack of trust may indicate a potential for positive change.
The evidence supporting the theory of a lab leak is extremely strong, while there is no evidence to support the theory that the virus originated from animals. Anyone with knowledge in biology who denies the possibility of a lab origin is either deceitful or willfully ignorant.
I will discuss three facts that collectively indicate that SARS-CoV-2 was created in a lab. It is worth noting that one of these facts is that the creators themselves stated their intentions beforehand.
Viruses, which consist of genetic material or codons that specify amino acids, are parasites that must live inside of host cells. There are 20 amino acids used for building proteins, which are utilized by viruses to replicate themselves using the cell's machinery.
It is a difficult task for viruses to adapt to a new host as they are highly specialized and specific to their current host. Although viruses can randomly mutate, it is rare for these mutations to give them an advantage in another host. Nevertheless, if a virus is able to infect a new host, it will continue to evolve through natural selection to become better adapted for reproduction in the new host.
Having a highly tuned receptor binding domain (RBD) is crucial for a virus to successfully infect a new host. The RBD helps the virus recognize and bind to the host cell, allowing it to enter. In the case of SARS, the RBD is 201 codons in length. Jesse Bloom from Caltech examined the codon sequence of RBD in order to identify the sequence that would optimize its binding to human cells. On the first day, out of the 4000 possible combinations, SARS-CoV-2 had an optimization rate of over 99% and was only 21 codons away from being perfect. This confirms the effectiveness of Bloom's work. Later, in the more infectious Omicron variant, one of the 21 codons identified by Bloom was found to have mutated as he had predicted.
To provide background information, when SARS-CoV-1 first infected humans, only 15% of its RBD (Receptor Binding Domain) was optimized. However, over time, there were mutations in its RBD documented, which eventually allowed it to spread from one human to another. The question is, how is it possible that SARS-CoV-2 was able to be so well adapted from the start, without requiring as many mutations?
As early as 2005, Ralph Baric from UNC, who was a co-author of multiple papers with the WIV on bat coronavirus, conducted experiments on transgenic mice. Dr. Steven Quay testified before Congress that genetically modified mice with human-like lung tissue were infected with human coronaviruses to demonstrate their susceptibility. The WIV has reportedly collaborated with Dr. Ralph Baric's laboratory for years on the development of humanized mice.
Researchers use humanized mice to create viruses that can efficiently infect humans. This is achieved through a gain-of-function method, where the virus is repeatedly passed through humanized, genetically modified mice that develop symptoms similar to human pneumonia. Through multiple repetitions, the virus evolves and becomes lethal to the humanized mice, creating a virus optimized for human infectivity.
The virus needs to perform a complex process even after attaching itself to the host cell. This includes the cleavage of the spike protein to initiate viral fusion with the cell membrane. Some viruses like Ebola have furin cleavage sites (FCS) in their spike proteins to aid in cleavage. However, until recently, Sarbecoviruses, the clade of viruses that SARS-CoV-2 belongs to, did not have FCS.
Using the FCS (Furin Cleavage Site) to enhance infectivity by incorporating it into viruses has been a common practice among gain-of-function researchers ever since a 2004 paper demonstrated its effectiveness. In 2006, modifications to FCS were implemented to demonstrate that furin cleavage at position R667 produces separate S1 and S2 subunits, which enhances the ability of the virus to fuse with host cell membranes. Baric collaborated with WIV and proposed a funding request to DARPA for the continuation of FCS work. The proposal aims to examine all SARS-CoV gene sequences and identify potential furin cleavage sites.
There are numerous papers and proposals stating that FCS (furin cleavage site) has been added, and a molecular fingerprint confirms this. Creating an FCS involves adding the amino acid arginine at a specific site, and there are six different codons to specify it. However, in Sarbecoviruses, Nature prefers some codons over others. The codon CGG used in SARS-CoV-2 is very rare as it represents only 1.5% of the total Arg codons. However, there are two consecutive CGG codons present in the virus. It is not surprising because the codon CGG has been widely used in labs as a representation of Arg for more than a decade.
According to virologist and Nobel Prize winner David Baltimore, the fact that FCS was inserted in SARS-CoV-2 is evidence that the virus might have originated from a lab. It should be noted that despite facing strong criticism from his superiors, his subsequent statement cannot be considered a complete retraction:
について fact check pages that claim the FCS insertion is “factually inaccurate” by using half-truths can be comical to read. It is noteworthy that the CGG CGG genetic sequence and furin cleavage sites are also found in naturally-occurring viruses.
While the CGG codon pair has been found in some coronaviruses, it is important to note that it is not present in the Sarbecovirus clade, which includes both the coronavirus strain responsible for COVID-19 and the pangolin viruses often cited as a possible source. Additionally, even in the coronaviruses with a CGG codon pair, it is not located in the FCS. And although some coronaviruses do have FCS, none in the Sarbecovirus clade possess this feature due to the significant evolutionary distance between them and earlier coronaviruses that do.
Lab codon optimization leaves a stronger molecular fingerprint than RBD optimization and FCS insertion in the lab. Different codons can code for the same amino acid, and labs tend to prefer some codons over others, just like nature. The structure of RNA can sometimes create loops that impede the translation of certain codons into proteins. Labs prefer to use codons that do not have this problem but still code for the same amino acid.
To ensure accuracy, researchers typically select the most suitable codons when creating genetic material. In this case, the virus RaTg13 is the most genetically similar to SARS-CoV-2. RaTg13 was discovered in 2012 after six miners were killed by a disease with symptoms very similar to Covid after being exposed to bat guano in Yunnan Province, China. The analysis of the coding regions for the spike protein in both viruses discovered 200 mutations that were all synonymous. This means that although the codon was modified, it still resulted in the same amino acid.
It is unlikely for a codon to undergo mutation and retain its original meaning, with only a 15% chance of being synonymous. The chance of 200 synonymous mutations occurring by chance is extremely low and it would not likely occur in the expected lifetime of the universe. This suggests that the WIV may have utilized codon optimization during the creation of SARS-CoV-2.
There is sufficient evidence, including the changes made to SARS-CoV-2's ORF8 which allow it to be transmitted without symptoms, but further investigation at this time is unnecessary.
It is believed that researchers in Wuhan, who were conducting gain-of-function experiments and were funded and aided by the U.S. government, created a new virus that accidentally spread and caused a world-wide pandemic. This has resulted in a devastating impact on the world economy, with six million people dead and widespread loss of trust in our institutions. It is a tragic reminder of the potential harm that can result from reckless scientific research.