The Chimeric nature of SARS-CoV-2
Let me borrow some of your parts, bro.
Sometimes you draw plans, and life just smacks you in the face. This weekend was one of these, absolute chaos in the tech world, but it is not the focus here. One of the most significant papers was nonchalantly uploaded on the most used pre-print server by a group of clearly gifted researchers.
Unlike 99% of my articles, I will leave the conclusion at the start this one time. Why do the findings here matter ? The persistence of SARS-CoV-2 in the body of millions is real, regardless of their “immunity status”, and this persistence affects both the evolution of the chimeric virus itself, our immunity towards other pathogens, and the long-term health of many. The virus being able to recombine with bacteria and evolve new mutations is very impactful in the long-term.
As I wrote a couple of times this year, while researching with a friend…in retrospection, I could say we were both friends, but that person was also a sort of mentor, I often came up with “crazy” ideas, such as “Can the Spike interact with endotoxins ?”, “Can pieces of the Spike protein stick around for long, inducing damage ?”, “Can the Spike protein and the virus cause a level of immune amnesia ?”. Many of these propositions were later proved correct by amazing researchers, and some were proposed before me too, and I merely wasn’t aware of them at the time.
But one of my propositions was so “insane”, that I only voiced it publicly a couple of times, and privately to half a dozen people, including the mentor-friend, and at that point stated, “At this point, I learned to not just say no to whatever you propose, so I will say, yes, somehow”.
Which was the following “Assuming the Spike Protein can interact and break biofilms, and it can “pierce” organic membranes (cells, bacteria), could, theoretically, the virus leave pieces of itself in biofilms, and pick up “upgrades” ?
*At the time the potential interaction with the Spike/Virus with bacteria and biofilms was fringe, and unknown
Human microbiota is a reservoir of SARS-CoV-2 2 advantageous mutations
SARS-CoV-2 evolution has defied any sort of common sense for years now, even before Omicron surfaced. Using mathematical equations to attempt to understand the underlying mechanisms of this accelerated evolution, the math kinda doesn’t add up. As I recently wrote, SARS 2 evolutionary trajectory is 6 to 10 times faster than Influenza, which so far was the primary poster child of a pathogen that evolved and changed abnormally fast. Natural or vaccine-derived antibodies also can’t account for both the velocity and quantity of mutations.
As a Single-stranded (ss) RNA virus, SARS-CoV-2 requires RdRp for replication, but this enzyme is prone to error. RdRp stands for RNA-dependent RNA polymerase an enzyme that catalyzes the synthesis of RNA from an RNA template, and it is an essential part and function of the viral life cycle. Mutation alone can’t explain. Another possible explanation and one I covered in 2022 was recombination when different strains of coronaviruses “fuse” together, but the few observed recombination events also can’t account for the high numbers of mutations.
Most papers focus on a single amino acid mutation, but the authors decided to focus on the amino acids “around” the single mutation named here “Viral Mutation Fragments” (VMF), after testing different lengths (5, 7, and 9 amino acids), given the results after comparing to the largest protein database in the world, they settled for 7 amino acids, to attempt to find homologous fragment, meaning amino acids sequences that are identical to the VMFs.
A fictional example would be → SARS-CoV-2 amino acid sequence viral fragment HKKGGKK → it has a mutation becoming HXKGGKK → compare to the database → finding proteins almost identical → find JDHXKGG → HF is HXKGG
To the surprise of the authors they found that bacteria contributed to 60% of the HF, while other species such as fungi and plants contributed significantly less, they found that the number and proportion of bacterial HFs were not related to each other. For some mutations, both the number and proportion of bacterial HFs were very high, meaning that there were many similar sequences of amino acids in bacteria that had the same mutation as the spike protein.
By doing a complex analysis of the large groups of microbes (phyla) and looking for HF they found a startling correlation between the composition of the human microbiome and these identical fragments. Proteobacteria contributed more than 51 different types of HFs, meaning that they had the most similarities with the spike protein.
The last section of this incredible paper is where things get my type of crazy (in a good way for science). Unlike SARS-CoV-2, bacteria HFs are encoded by mRNAs, and comparing these to viral RNAs they found that the nucleotide sequences were not exactly the same but their percent identity (how much alike they are) ranged from 63% to 90% in the seven fragments examined.
The authors ran a series of very complex experiments and demonstrated in their paper that exogenous bacterial mRNA were effective templates for SARS-CoV-2 RdRP.
Although data errors cannot be ruled out due to different infection density data and variable persistence of gene surveillance for different variants, all the evidence provided above supports the idea that SARS-CoV-2 may acquire HFs from the human microbiota, as is summarized in a schematic graph (Fig. 5). In comparison with the original strain, SARS-CoV-2 VOCs have evolved into chimeras containing components from the human microbiota.
The authors propose scenarios on how what is described here may occur. First, the macrophages bear both bacteria and viruses at the same time, macrophages are first-responder and “eat up” invading pathogens and dissolve them. The persistence of the SARS-CoV-2 virus in macrophages has been described since 2021 (I still need to cover a recent 2023 paper that is quite good).
The second one is the presence of bacterial mRNA in other types of cells, during a SARS-CoV-2 infection in other types of cells, and when the cells are engulfed by the immune system, an exchange of the genetic material may occur.
The third is the “fringe” one (the one I am most prone to since I have proposed this since March 2020). In their own words, “Some bacteria might be potential hosts for the virus”. In the end, the authors went above and beyond my primary hypothesis which was SARS-CoV-2 itself “trading” single mutations, since there are many instances of multiple “variants” existing in one host.
Here the authors went further, and if further evidence by their team or other teams is published confirming their finding, we will finally understand the “chimeric” nature of SARS-CoV-2. One of my biggest criticisms since 2021 was always describing this virus as merely a bioweapon and not a chimera.
The following article has multiple other articles I wrote cited inside, and once again, it is somewhat required reading if you want to understand where things are going. I have no doubts in my mind that SARS-CoV-2 besides other regions in the body, this chimera can live inside biofilms, change genetic material, not with other coronaviruses, but with our own bacteria themselves.
And as a reminder what enables SARS-CoV-2 to interact with biofilms is, quite literally its NTD. Otherwise known as “Galectin-fold”. Dual-purpose amino acid sequence.
Tomorrow I start my house cleaning process unless something even more groundbreaking is published, otherwise, I must stick to my plan.
Defending ones self has become more difficult.
Is it possible that the government’s move to restrict antibiotic treatment was an attempt to diminish antibiotic resistant strains like C Diff from taking a stronghold in the microbiome and therefore being a fortified host for SC2?