Earlier when Monkeypox started spreading unlikely fast, and some scientists started looking into the genetic sequences being uploaded to public databases, I shared their analyses and my own opinions. That there was a high likelihood that this virus didn’t evolve naturally.
Monkeypox may have undergone 'accelerated evolution,' scientists say
The virus is mutating up to 12 times faster than expected.
The virus, which has infected more than 3,500 people in 48 countries since its detection outside Africa in May, may be more infectious due to dozens of new mutations. In all, the virus carries 50 new mutations not seen in previous strains detected from 2018 to 2019, according to a new study published June 24 in the journal Nature Medicine. Scientists usually don't expect viruses like monkeypox to gain more than one or two mutations each year, the study authors noted.
As a large double-stranded DNA virus, monkeypox is much more able to correct replication errors than an RNA virus such as HIV, meaning that the current monkeypox strain should have really only accumulated a handful of mutations since it first started circulating in 2018. But, after collecting DNA from 15 monkeypox viral samples and reconstructing their genetic information, the researchers found that the real mutation rate was six to 12 times higher than they expected.
The massive jump in the monkey virus's rate of mutation "is far more than one would expect considering previous estimates of the substitution rate for Orthopoxviruses," the researchers wrote in the paper. "Our data reveals additional clues of ongoing viral evolution and potential human adaptation."
Historically, monkeypox is transmitted from person to person by close skin contact with open skin lesions, bodily fluids, contaminated material or respiratory droplets coughed into the air. But the unprecedented speed of new infections could suggest that something may have changed about how the virus infects its hosts — and the new mutations could be a possible cause.
Many of the mutations identified by the researchers also carry telltale clues that they may have emerged due to the virus's contact with the human immune system, specifically a family of the virus-fighting enzymes called APOBEC3. These enzymes attack viruses by forcing them to make mistakes when they copy their genetic code, an act which usually causes the virus to break apart. However, sometimes, the virus survives the encounter and simply picks up a few mutations in its genetic code, according to STAT. It may be that these sorts of battles happened repeatedly and caused the virus to pick up many mutations in a short span of time, the researchers theorized.
The virus's mutation rate ramped up in 2018, and there's a few explanations as to why it did so. It's possible that the virus has been circulating in humans, at low levels, since then, picking up a slew of new mutations through its battles with enzymes. Alternatively, the virus may have been spreading among animals in non-endemic countries without us noticing for quite some time, and then this year, it suddenly leapt back over to humans.
Or it's possible that, after a monkeypox outbreak hit Nigeria in 2017, the virus mostly spread in African countries — rapidly evolving as it moved between smaller communities before mounting a resurgence in non-endemic countries this year.
“Accelerated Evolution” can have quite a few meanings, but under the current circumstances, it has only two. Only two real possibilities.
1. Gain of Function
2. Global immune shift from both a highly transmissible virus with hyper glycolysis, and the use of a certain IMMUNE SUPPRESSIVE, NON-NEUTRALIZING therapy.
Here is a tweet from one of the very few scientists I trust on the entire planet.
John Paul @ThingsHiddenn
@TheInsiderPaper Not Africa where all cases were imported from 🤣🤣🤣🤣🤣🤣The likelihood is that both are true. Now we should look a little deeper into the paper, to see if we can find clues about what is going on.
Given the dynamics in relation to APOBEC3 (a class of proteins that has a direct relation to viral infections, your resistance towards them), authors say it is uncertain the origins or introductions of this virus in the human population. Before we delve into the APOBEC3 question, let us go further into the paper.
The second highlighted test already has evidence. Recombination isn’t solely a “coronavirus” thing, all viruses can go through recombination, SARS class viruses are just better at it than most of the others, one could argue they are chimeric by nature.
Monkeypox virus genome sequences from multiple lesions indicates co-infection of a UK returning traveller
Co-infection = viral population diversity, in an oversimplified way. The third highlight is one that jumped to my eyes pretty fast. First, is a tweet from weeks ago.
I find it fascinating that not only the virus has its own tools to inhibit your immune response, it now has a very complementary response to co-exist and spread better existing along SARS-CoV-2, I am sure it is merely a coincidence. I am going to make an argument for the point Daoyu raised.
The image above comes from a paper referring to the Nigerian MonkeyPox outbreak of 2017–18, and the authors argue one of the explanations for that outbreak would be loss of immune and viral latency… am I alone in seeing a trend here ? Malnourishment, which is endemic in the whole African continent, can lead to immune dysfunction, and a faster loss of immunity granted by vaccination, and so do other endemic diseases to the region (HIV being one of the biggest ones).
SARS-CoV-2 is also known to interact with APOBEC.
Different APOBECs will have different effects on you, in this particular case Apobec2 deficiency causes mitochondrial defects and mitophagy in skeletal muscle leading to myopathy and atrophy.
So my argument so far (very opinionated to be clear) is the following. Both the viral infection of SARS-CoV-2, and the pandemic measures (lockdowns literally work in reverse, help spread diseases, and hinder your immune response to other viruses) help drive the evolution of the current strain of MonkeyPox a little by causing enough subclinical immune shift in the infected.
In the global vaccination campaigns, with a vaccine that has extensive literature on its immunosuppressive effects, the constant reinfection causes a shift (drastic change in immunology) of immunological landscape (population-wide immune system and their response), which gave the proper and perfect landscape for certain latent viral infections to go rampant and evolve in months what would take, perhaps, decades.
The accelerated evolution they can’t explain has a clear cause…
Will leave this tweet without further commentary too.
FYI I will be changing the name of my Reverse AIDS posts to what I meant to be because I don’t want any correlation with the “VAIDS” crowd. Paradoxical Acquired Immune Dysfunction. This is what the mountain of direct and interdisciplinary evidence points to.
I might also send two e-mails today, even though trying my best not to…
Who didn't see this coming?
"The virus is mutating up to 12 times faster than expected."
And where have we seen this before?
Somebody ask Dr. Baric.
You could say, this puts the crown* on monkey business.
* (lat. corona)