Monkeypox and the Covid-19 Vaccine

UK Column has covered various aspects of the Covid-19 virus and has looked in depth at the significant negative effects of the Covid-19 vaccine, including clotting, and also the change in immunological mechanisms after vaccination. Those mechanisms were used to explain the poor performance of the Covid-19 vaccine campaign, highlighted by an increased relative risk of infection for those vaccinated compared to the unvaccinated.

This article will address the current atypical spread of monkeypox virus around the world. To be clear, up until now, monkeypox hasn’t caused large clusters of infection in separate countries at the same time—that is highly unusual.

Monkeypox is one of the four genera of pox viruses that can infect humans. There are two distinct clades of monkeypox virus; the current infections are the West African version and are typically mild, with a death rate of less than one per cent. Chicken pox is an unrelated herpes virus, specifically Varicella.

It needs to be explained why we are seeing such a highly unusual pattern of infections. The medical concern is that we are witnessing an increase in human-to-human transmission.

Basic data

Current data indicate that there are 107 confirmed cases—of which 19 have been hospitalised—and 85 suspected cases, with four hospitalisations among them. Taking only the confirmed cases, we thus obtain an 18% hospitalisation rate; combining the cases of all statuses, we get a 12% hospitalisation rate. However, those percentages will change as the cases increase.

Early data suggest that there is an increased risk amongst men who have sex with men.


In Stabilising the Code, we learned that:

In 2005, Drs. Weissman and Kariko discovered a way to protect foreign mRNA from the body’s immune system. That scientific milestone would be key to the advancement of the mRNA vaccines in 2020.

Specifically, they altered the genetic code of RNA.

Their key discovery, that modifying the RNA code (modifying the nucleoside uridine) resulted in ablating the innate immune response, involved toll-like receptors (TLR).

This discovery was adopted in the mRNA technology used in Covid vaccines, in order that the foreign vaccine mRNA could enter cells without being destroyed.

The RNA alteration results in the body’s immune defences—specifically, toll-like receptors (TLR)—not recognising foreign invaders like viruses. As I continued to set out in Stabilising the Code:

The key TLRs affected are TLR 3, TLR 7 and TLR 8. They act as sentries, whose job is to recognise foreign invaders by way of their form or patterns […]

That technology—altering RNA—was adopted for the Covid-19 mRNA vaccines.

Dominguez-Andres et al. discovered that not only had that technology worked well, but it appeared to have induced long term immune tolerance in the vaccinated: 

The response of innate immune cells to TLR4 and TLR7/8 ligands was lower after BNT162b2 vaccination[.]

Toll-like receptors were found not to work as well after vaccination as before. That was not supposed to happen. Obviously, you need your TLRs to be working in order to fend off viruses like monkeypox.


Toll-like receptors

Stack and Bowie investigated monkeypox virus and the role of TLR 4:

Toll-like receptors (TLRs) have an anti-viral role in that they detect viruses, leading to cytokine and IFN induction, and as such are targeted by viruses for immune evasion. TLR4, although best known for its role in recognizing bacterial LPS, is also strongly implicated in the immune response to viruses […] This work reveals the molecular basis for poxviral antagonism of TLR4.

Harte et al. demonstrated that pox virus suppresses the host defence by blocking TLR 3:

Toll-like receptors (TLRs) are crucial in the innate immune response to pathogens, in that they recognize and respond to pathogen associated molecular patterns, which leads to activation of intracellular signaling pathways and altered gene expression […]
This study reveals a novel mechanism used by VV [pox virus] to suppress the host immunity. We demonstrate viral disabling of TLRs, providing further evidence for an important role for this family of receptors in the antiviral response.


We also know that TLRs, upon detecting a virus, will activate other parts of the immune system. Khanmohammedi and Rezaei write:

Toll‐like receptors (TLR) play an important role in recognition of viral particles and activation of the innate immune system. Activation of TLR pathways leads to secretion of pro‐inflammatory cytokines, such as interleukin‐1 (IL‐1), IL‐6, and tumor necrosis factor‐α, as well as type 1 interferon […]
Robust induction of type I IFN through the activation of TLRs constitutes a critical aspect of antiviral immunity.

It being the case that TLRs activate other parts of the immune system—and given that, due to alterations in the vaccine mRNA, TLRs are no longer as responsive—we should expect to see a difference in downstream immunological profiles as well after vaccination.

Ivanova et al. have observed:

Myeloid cells with high expression of Toll-like receptors (TLR) and other pattern-recognition receptors are likely the first to respond to viral infection. Robust induction of type I IFN through the activation of TLRs constitutes a critical aspect of antiviral immunity[…]
IFN production is dependent on transcription factors IRF7 and IRF8, which interact with MyD88 (Lester and Li, 2014; Tailor et al., 2007; Xagorari and Chlichlia, 2008). Prior studies of immune responses during COVID-19 found increased activity of these innate immune pathways (Scagnolari et al., 2021; Xu et al., 2020; Zhou et al., 2020) […]
Differential gene expression analysis of pDCs from COVID-19 patients and immunized individuals revealed a dramatic upregulation of gene signature associated with type I and type II IFN production in the former and not the latter.

Clearly, the attenuation (weakening) of TLRs after Covid-19 vaccination is having a significant negative effect: in this case, the possible reduction of interferon in response to infection—an important defence against viruses.

Pox viruses

Pox viruses, like so many other viruses, have developed to try to outwit the human immune defences.

That has been observed in the science literature, such as Arndt et al., Evasion of the Innate Immune Type I Interferon System by Monkeypox Virus; and Johnstone et al., who demonstrate just why the virus needs to do so, in: In vitro inhibition of monkeypox virus production and spread by Interferon-β.

Indeed, pivotal to the success or failure of the monkeypox virus is its ability to overcome TLRs and switch off interferon.

Of course, once the immune system is primed to have a weaker response by TLRs and IFN, then it is more susceptible to pox infection. All that is then required to challenge it is exposure to the target virus. 

The immune system is a symphony of complex responses, so an altered TLR response does not guarantee successful infection upon exposure to monkeypox virus—but it does increase the chances of it, since a major, initial defence mechanism has been weakened; especially if other factors increase that susceptibility.

Who is being infected?

The list of those known to be infected with monkeypox in the recent outbreaks is almost exclusively male, with reports of male-to-male sex being a common factor. It is still very early in the investigation, so that picture may change. However, it is well understood that men who have sex with other men have a demonstrably increased risk of infection with such viruses.

The current published list of those infected with monkeypox has one woman on it. That, plus the relatively high percentage of gay and bisexual men suggests it may be being spread through sexual networks.

Kelleher writes in Pink News:

The UKHSA [UK Health Security Agency, formerly known as Public Health England—editorial note] has said cases are primarily being detected among gay and bisexual men, which has led to some level of concern in the LGBTQ+ community.

It’s thought that monkeypox is not sexually transmitted, but it’s possible that the virus is spreading through close contact in sexual networks, according to Mateo Prochazka, an epidemiologist with the UKHSA.

On 17 May, Prochazka said on Twitter that 57 per cent of the cases they had detected at that stage were among gay or bisexual men. That figure is “highly suggestive of spread in sexual networks”, he said.

The question has to be asked, though: why now? Men haven’t just started having sex with other men. And are all the cases connected?

The global incidences of monkeypox—and the apparent, highly unusual, velocity of spread—argues that something new has entered the equation; something has changed.

What is the new factor?

Lockdown my have played a part in immune reduction in adults, due to the deprival of human contact, as described in Medical News Today:

According to a paper by Stanford researcher Firdaus S. Dhabhar, Ph.D., in the journal Immunologic Research, “chronic stress can suppress protective immune responses and/or exacerbate pathological immune responses.”

For adults, it is the stress of isolation and the pandemic, rather than the lack of interaction with microbes, that is a concern for the immune system.

Yet most countries are relatively back to normal now, with people socialising again; and, unless there are chronic effects, the very fact that close contact is hypothesised as a mechanism of monkeypox spread argues against a policy of social isolation of those infected.

I suggest that we would be foolish to ignore chronic immune alteration due to Covid-19 mRNA vaccination, and the specific attenuation of TLRs that has been leading to altered interferon production and increasing susceptibility to viruses such as monkeypox.

Thankfully, most cases are mild, but tragically, we will see fatalities, as we do with other diseases, and the affect that the Covid-19 vaccine-induced altered immune response will have on monkeypox mortality is unknown. We will, no doubt, also be seeing more fear-mongering by the media and governments.

Of course, they have already started; in fact, long before the first reported cases this month even happened.

The Strengthening Global Systems to Prevent and Respond to High-Consequence Biological Threats tabletop exercise conducted in partnership with the Munich Security Conference (the largest annual meeting of the intelligence agencies of the Western world) in November 2021 seems accurately to have predicted this current monkeypox scenario—even down to the month it started.


Image source: Strengthening Global Systems to Prevent and Respond to High-Consequence Biological Threats, p. 10

How are these tabletop exercises so accurate in their predictions? 

According to that scenario, monkeypox is released as a biological weapon, billions across the globe will be affected, and hundreds of millions will die: 

The exercise scenario concludes with more than three billion cases and 270 million fatalities globally […]

Absent any other evidence, and on the balance of probabilities, what we are witnessing now suggests vaccine-induced immunological attenuation and foul play.