Monkey Business

If you have been paying attention to the (fake) news recently, you may have heard a little something about a crop of monkeypox cases popping up around the world. Normally, most people wouldn’t bat an eye at any headlines concerning the monkeypox yet the mainstream media is making a strong push to ensure that these headlines catch your attention. As can be seen, the usual suspects such as President Biden, the CDC, and the WHO are all involved in sounding the alarm over what is considered to be a mild and relatively hard to transmit “viral” disease.

Cue the FEAR propaganda.

It makes one wonder what (or who) could possibly be behind such a push to strike fear into the minds of a populace already on high alert over the emerging “6th wave of Covid-19.” It’s not like they have these things planned out well in advance now, do they?

Monkeypox outbreak exercise. Reminds me of something…

In March of 2021, the Nuclear Threat Initiative (NTI), a nonprofit group created in 2001 by Senator Sam Nunn and philanthropist Ted Turner, hosted a monkeypox pandemic exercise that just so happened to be forecasted to take place in May 2022. What an interesting coincidence, right? If you are unfamiliar with NTI, according to the organization’s homepage, it is a “nonprofit, nonpartisan global security organization focused on reducing nuclear and biological threats imperiling humanity.” From the Wikipedia page, it states that NTI “serves as the Secretariat for the ‘Nuclear Security Project’, in cooperation with the Hoover Institution at Stanford. It is guided by former Secretary of State George P. Shultz, former Secretary of Defense William J. Perry, former Secretary of State Henry A. Kissinger and Nunn,” who are collectively known as the “four horsemen of the nuclear apocalypse.” Nothing suspicious about that.

If we look at the summary of the monkeypox pandemic exercise, we can gather some additional insight:

Strengthening Global Systems to Prevent and Respond to High-Consequence Biological Threats

“In March 2021, NTI partnered with the Munich Security Conference to conduct a tabletop exercise on reducing high-consequence biological threats. The exercise examined gaps in national and international biosecurity and pandemic preparedness architectures—exploring opportunities to improve prevention and response capabilities for high-consequence biological events. Participants included 19 senior leaders and experts from across Africa, the Americas, Asia, and Europe with decades of combined experience in public health, biotechnology industry, international security, and philanthropy.”

Exercise Summary

“Developed in consultation with technical and policy experts, the fictional exercise scenario portrayed a deadly, global pandemic involving an unusual strain of monkeypox virus that first emerged in the fictional nation of Brinia and spread globally over 18 months. Ultimately, the exercise scenario revealed that the initial outbreak was caused by a terrorist attack using a pathogen engineered in a laboratory with inadequate biosafety and biosecurity provisions and weak oversight. By the end of the exercise, the fictional pandemic resulted in more than three billion cases and 270 million fatalities worldwide.

Discussions throughout the tabletop exercise generated a range of valuable insights and key findings. Most significantly, exercise participants agreed that, notwithstanding improvements following the global response to COVID-19, the international system of pandemic prevention, detection, analysis, warning, and response is woefully inadequate to address current and anticipated future challenges. Gaps in the international biosecurity and pandemic preparedness architecture are extensive and fundamental, undermining the ability of the international community to prevent and mount effective responses to future biological events—including those that could match the impacts of COVID-19 or cause damage that is significantly more severe.”

Strengthening Global Systems to Prevent and Respond to High-Consequence Biological Threats

https://www.nti.org/wp-content/uploads/2021/11/NTI_Paper_BIO-TTX_Final.pdf

Upon opening the report of the event, we find some interesting representatives listed among the 19 senior leaders and experts who attended the drill including:

  1. Dr. Ruxandra Draghia-Akli
    • Global Head Johnson & Johnson Global Public Health R&D 
    • Janssen Research & Development
  2. Dr. Chris Elias President, Global
    • Development Division Bill & Melinda Gates Foundation
  3. Sir Jeremy Farrar
    • Director Wellcome Trust
  4. Dr. George Gao
    • Director-General, Chinese Center for Disease Control and Prevention (China CDC)
    • Vice President, the National Natural Science Foundation of China (NSFC)
    • Director and Professor, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences
      Dean, Medical School, University of Chinese Academy of Sciences
  5. Dr. John Nkengasong
    • Director Africa Centres for Disease Control and Prevention
  6. Dr. Michael Ryan
    • Executive Director WHO Health Emergencies Programme
  7. Dr. Petra Wicklandt
    • Head of Corporate Affairs Merck KGaA

We have representatives from pharmaceutical companies (J&J, Merck, GlaxoSmithKline), the Bill and Melinda Gates Foundation, the African and Chinese CDC, and the WHO. As is always seemingly the case, the very people who control the response and who profit off of these “pandemics” are the very ones executing the drills that “predict” the pandemics. Don’t believe me? Let’s take a trip down memory lane back to October 2019 with Event 201:

Event 201

“The Johns Hopkins Center for Health Security in partnership with the World Economic Forum and the Bill and Melinda Gates Foundation hosted Event 201, a high-level pandemic exercise on October 18, 2019, in New York, NY. The exercise illustrated areas where public/private partnerships will be necessary during the response to a severe pandemic in order to diminish large-scale economic and societal consequences.”

The Event 201 scenario

“Event 201 simulates an outbreak of a novel zoonotic coronavirus transmitted from bats to pigs to people that eventually becomes efficiently transmissible from person to person, leading to a severe pandemic. The pathogen and the disease it causes are modeled largely on SARS, but it is more transmissible in the community setting by people with mild symptoms.”

https://www.centerforhealthsecurity.org/event201/about

As can be seen, the Bill and Melinda Gates Foundation was once again heavily involved with this “pandemic” exercise which accurately predicted a “coronavirus” outbreak resulting in a pandemic 6 weeks before the “real pandemic” emerged. Among the participants in Event 201 that also participated in the NTI monkeypox drill were:

  1. Dr. Chris Elias President,
    • Global Development Division Bill & Melinda Gates Foundation
  2. Dr. George Gao
    • Director-General, Chinese Center for Disease Control and Prevention (China CDC)

We can also find representatives from Johnson & Johnson (again), the UN, and the CDC.

Why do we regularly see such drills and exercises taking place before the exact same events play out? Are these pandemic drills, which are sponsored by the same players who eerily predict the very “virus” within months, merely coincidences or something else entirely?

While the timing of these pandemic drills should raise red flags in regards to showing that this media push is a carefully controlled narrative, the threat of the “virus” behind the media stories is just as fictional as that presented in the drills. If you are here reading this article, you are either questioning the official narrative or you understand that whatever “virus” is chosen, they have never been scientifically proven to exist. This holds true for the monkeypox just as it does for any other “virus.”

Previously, I wrote about how the monkeypox was just the rebranding and relabelling of smallpox. In 1958, the WHO decided to make a push to eradicate smallpox through the use of what is considered the deadliest vaccine known to man, even though smallpox had steadily declined throughout the proceeding decades. Coincidently (or not), the monkeypox “virus” was “discovered” in two colonies of test monkeys in a Danish lab that same year. In my previous article, I did not highlight the papers related to the isolation of this “virus” in monkeys and humans so it seems to be the perfect time to do so now. As the initial 1958 paper itself is rather long, I am only focusing on the methods used to “isolate” the monkeypox “virus” originally in monkeys. You will be able to see that, as always, it is just another unpurified tissue/cell cultured creation that was compared to other unpurified cultured concoctions with indirect immunological testing. At no point were the particles assumed to be monkeypox ever purified and isolated directly from the fluids of the monkeys. Upon separation from the monkeys, the samples were immediately subjected to numerous chemical additives such as McIlvain’s buffer saline and Bacto-tryptose “Difco” containing Penicillin and Streptomycin. The samples were then inoculated onto the chorio-allantoic membrane of 11-12 day old Leghorn embryos and into tissue cultures of monkey kidney, human amnion and HeLa cells. Also interesting to note is that the “virus” was said to be cultured and “isolated” from healthy monkeys as well, thus showing that whatever they were “isolating” was not pathogenic at all as it fails Koch’s first Postulate for proving a microbe causes disease:

  1. The microorganism must be found in abundance in all cases of those suffering from the disease, but should not be found in healthy subjects.

A POX-LIKE DISEASE IN CYNOMOLGUS MONKEYS

“During the summer and fall of 1958 two outbreaks of a non-fatal pox-like disease in cynomolgus monkeys have been observed in the
monkey colony in this institute. Both outbreaks occurred rather late after the monkeys had been received, i.e. 51 and 62 days after arrival and only a small percentage of the exposed animals showed signs of illness.

This paper presents observations on the epidemiological and clinical 
manifestations of the disease. The isolation of a virus from the diseased animals will also he described as well as some studies on the properties of the agent which in this paper will be referred to as monkey pox virus. 

MATERIAL AND METHODS 

Virus isolation: Material for egg inoculation was collected from the pustular lesions and diluted approximately 1:10 in 0.004 hl. McIlvain’s buffer saline pH 7.2. Material for tissue culture experiments was collected from the pustules by means of a cotton swab, which was immediately immersed into 2 ml of Bacto-tryptose “Difco”. Both diluents contained Penicillin (100 mg per ml) and Streptomycin (0.1 mg per ml). After clarification by low speed centrifugation the supernatants were used for inoculation onto the chorio-allantoic membrane of 11-12 day old Leghorn embryos and into tissue cultures of monkey kidney, human amnion and HeLa cells. A total of three virus strains was isolated, one during the first and two during the second outbreak. Most of the studies to be reported were carried out using the strain which was isolated first. 

Vaccinia strain: Lot NO. 1/50 111 received from the smallpox vaccine department in this institute was used in some experiments in order to compare it with the monkey virus. This strain had heen maintained for several years by serial cutaneous passages in rabbits and calves. Either the glycerinated third calf passage or a subsequent first passage of this material on the chorio-allantois was used. 

Egg passages: The technique descrihed by Westwood et al. was employed. After inoculation the eggs were incubated for 48 hours at 37° C when vaccinia virus was used for infection and for 72 hours when the monkey virus was used. 

Neutralization tests on the chorio-allantoic membrane: Undiluted serum was mixed with equal volumes of increasing dilutions of virus. After incubation for 2-3 hours at room temperature 0.1 ml amounts of the serum-virus mixtures were inoculated onto the chorio-allantoic membranes of groups of five 11-12 day old embryos. The membranes were harvested after 48-72 hours continued incubation and the reduction effected in the number of typical pocks was determined.

Tissue cultures: The techniques employed for the preparation of tissue cultures for infectivity titrations and for neutralization tests have been described in earlier publications. An inoculum of 0.2 ml was used for tissue culture passages and the tubes were kept stationary at 35° C. During the first experiments they were examined daily for cytopathic changes but in later ones microscopic examination was carried out only every fourth or fifth day. Serial passages were usually made with 0.2 ml amounts of undiluted nutrient fluid harvested 5 days after inoculation.

Hemagglutination: The pattern method of Salk was employed. The technique has been described in detail in previous papers.

Complement-fixation tests were carried out according to the method of Fulton & Dumbell as modified by Svedmyr et al. Antigens were prepared from nutrient fluid of tissue cultures as well as from chorio-allantoic membranes infected with monkey-pox or vaccinia virus.

Rabbit immune sera: Hyperimmune sera against monkey pox and vaccinia viruses were prepared in rabbits by repeated intravenous injections of 0.5 to 2.0 ml amounts of 10 percent suspensions of infected chorio-allantoic membranes. The animals received a total of 7 intravenous injections (on day 1, 9, 11, 16, 18, 23 and 25). They were bled 10 days after the last injection.

Another hyperimmune serum prepared by immunizing rabbits with calf-lymph vaccinia antigen which had been inactivated by heating at 70° C for 60 minutes was also used. In addition, an hyperimmune vaccinia rabbit serum kindly supplied by
dr. F. 0. MacCallum, England was used in some experiments.

A human hyperimmune serum was finally used in some egg-neutralization tests.

Diffusion-precipitation test was performed according to the method described by Gispen.

Electron microscopy: A prototype of the Phillips electron microscope type EM 100 B was used. Exposures were made at a magnification of 3000 X and photographically enlarged as desired.

The pus-like material from the pustular lesions of a monkey was removed by means of a capillary pipette, placed on formvar coated grids and allowed to dry. Following the method of Van Royen & Scoff the grids were treated with 0.25 percent crystalline trypsin solution for 4 hours at 37° C after which they had 2 brief washings in distilled water. Fixation was carried out in the vapours of a 1 percent osmiumtetroxide solution for 15 minutes, and in order to minimize the risk of infection the grids were heated to 70″ C for one hour (1) prior to shadowcasting with platinum. The egg adapted virus grown on chorio-allantoic membranes was purified for electron microscopy by means of differential centrifugation and precipitation with citric acid according to the method of Henderson & McClean. The final suspension was placed directly on formvar coated grids, dried and further treated as stated above with the exception that no digestion with trypsin was carried out.”

Virus Isolation

“Virus isolation was attempted only from one monkey during outbreak No. 1 and from two monkeys during outbreak No. 2. Virus was recovered from all three animals. The strain isolated first has been most extensively studied but there is no indication of any difference between this strain and those isolated during outbreak No. 2. 

Virus isolation in eggs: Scrapings from several papules which were diluted lO^-3, 10^-5, and 10^-7 produced greyish oedematous changes in the membranes. In addition small discrete lesions showing a tendency to spread along the blood vessels could be seen in the eggs inoculated with the highest dilution of virus (Fig. 4). 

On continued passage, using dilute membrane suspensions as seed, the oedematous reaction disappeared and the small opaque dome-shaped pocks became predominant ( Fig. 5). In membranes harvested after incubation for 3 days these pocks resembled closely those described for variola virus. The lesions developed later and were much smaller than those seen with vaccinia virus (Fig. 6). The titer of the original pustule material was 7 x 10^8 and no significant increase in titer was observed on continued passage in eggs. 

Virus isolation in tissue cultures: Pustular scrapings were emulsified in tryptose-broth, clarified by low speed centrifugation, and the supernatant was inoculated into tissue cultures of monkey kidney, human amnion, and HeLa cells. Cytopathic lesions developed in all cell types after continued incubation for 2-3 days and destruction was almost complete after 5 days.

The cytopathogenic effect was characterized by a rounding of the affected cells which subsequently became granulated and condensed.
The cells retained their rounded shape for several days, eventually slipping off the side of the tube leaving macroscopically visible holes in the cell sheet. In the monkey kidney and human amnion cell cultures the affected cells were interconnected by threadlike syncytial elongations (Fig. 7). In the HeLa cell cultures these formations were not observed but otherwise the cytopathogenic effect was similar to that observed in the other cell types used.

On continued tissue culture passage the cytopathogenic changes developed somewhat more slowly, suggesting that the passage fluid contained less virus than the pustular material. This assumption was supported by egg titrations. Tissue culture passage fluid contained only 10^6 to 10^7 pock forming units while the pustular material had a titer of about 10^8. On titration in tissue cultures the titer of passage fluid varied between 10^-4 and 10^-6.”

PHESENCE OF MONKEY-POX VIRUS IN TISSUE CULTURES PREPARED FROM KIDNEYS OF APPARENTLY HEALTHY MONKEYS

“During the first outbreak of the pox disease some apprently healthy cynomolgus monkeys which belonged to the affected shipment had been sacrificed for other purposes. The kidneys from these animals were trypsinized and culture tubes were prepared from the cell suspensions. In some of the tubes (approximately 5 percent) cytopathic changes developed 7 to 12 days later and monkey-pox virus was isolated from these cultures.

During the 2nd outbreak monkey-pox virus was again present in a small percentage of the tubes prepared from kidneys of apparently healthy-but exposed-animals. On this occasion virus was recovered from cultures of a monkey which had been sacrificed 4 days before the outbreak. This was the only occasion when monkey-pox virus was encountered in cultures which had been prepared at a time when clinical illness was not present in the colony. In all instances the cytopathic manifestations in the cultures were not recognisable until 7 to 10 days after the tubes had been prepared indicating that only small amounts of virus had been present in the cell stock suspension.”

“The results obtained by electronmicroscopy are presented in Figs. 11 and 12. Fig. 11 shows particles obtained directly from the pustular lesions of a monkey, whereas the elementary bodies of the virus obtained from the third passage on chorio-allantoic membranes of material isolated from another monkey are given in Fig. 12. Although the fields presented are not particularly well free of accompanying impurities they do bring out the outlines of quite a few particles ciearly enough to allow the well known rectangular appearance characterizing the viruses of the pox-group to be distinguished. In a few cases the dimensions of well isolated particles have been measured. They all fell within the range of the pox viruses, i.e. 200 hy 250 mu. Especially one of the clusters of particles shown in Fig. 11 appears somewhat smaller, but this is probably the result of shrinkage during the preparation. Isolated particles of both types of material generally measure approximately 200-250 mu as stated above.”

https://doi.org/10.1111/j.1699-0463.1959.tb00328.x

“Partially purified.”

It is rather interesting that this new “virus,” which just so happens to share the exact same symptoms of smallpox, was conveniently discovered at the same time that the WHO declared that they would eradicate smallpox through a mass vaccination campaign.  It is also interesting to note that many of the symptoms associated with both smallpox and monkeypox can be side-effects from the very vaccine given to protect against the diseases. This could lead one to believe that the “discovery” of the monkeypox in monkeys and subsequently in humans a decade later was the perfect scapegoat to blame for any cases of the same symptoms of disease that occurred after the WHO officially declared smallpox eradicated.

In any case, the monkeypox itself was said not to be able to infect humans, only monkeys. That all changed in 1970 when a case of smallpox was identified in a 9-month-old unvaccinated child from the village of Bokenda in Basankusu Province, Democratic Republic of the Congo. The whole village (and presumably the mother and father of the child) had been mass vaccinated for smallpox the year before. No one was said to have become infected with the “virus” from the child. Upon clinical examination and “isolation” of the “virus,” it was originally said to be smallpox (i.e. variola) that the child was suffering from. However, after further incubating the sample in an egg, which was subjected to toxic culturing conditions for a longer period of time, the membrane broke down some more and it was decided by the researchers that the pock formations noticed were now different than those observed in smallpox.

As in the previous paper from 1958, you will see that the “virus” is once again an unpurified mixture of host material (skin lesions) along with other materials such as chicken eggs, chick embryo fibroblast, monkey kidney cells, and four continuous cell lines (VERO, A-1, PEK, HEP-2). Sadly, the actual ingredients added beyond the cell type were left to methods utilized in previous unreferenced research but it was stated by the researchers that they used the “usual” isolation techniques which means that antibiotics/antifungals, fetal bovine serum, and other additives were most likely applied in the creation of this “virus.”

The remainder of the paper involves the indirect comparison of the size and shape of pock formations in egg embryos and antibody testing between the cultured concoctions. Differences in pock formation/morphology could easily be explained due to differences in the culture ingredients/conditions and not because of any imaginary “virus.” In fact, a change in the length of incubation periods in the eggs between smallpox (vaccinia as a stand-in) at 48 hours and monkeypox “virus” at 72 hours was noted in both the 1958 and 1972 papers. It can be seen that with 48 hours of incubation, the pocks resembled smallpox. At 72 hours, the pock formations did not match smallpox and resembled monkeypox. It was not explained why it was decided that it was necessary to incubate the monkeypox samples an extra 24 hours in either study. Thus, it can be seen that the researchers are creating the effect that they want to see by manipulating the time of incubation.

1958:

“After inoculation the eggs were incubated for 48 hours at 37° C when vaccinia virus was used for infection and for 72 hours when the monkey virus was used.”

1972:

“After incubation for 48 hours, as already stated the lesions on chick-embryo CAM differed little from those caused by ordinary smallpox virus. However, after 72 hours they had already become flatter and haemorrhages appeared in the centre of most of the pocks.”

This discrepancy was even pointed out in Chapter 29 of Smallpox and its Eradication by Frank Fenner where it is revealed that the WHO experts agreed in 1969 that the appearance of the pocks after 3 days of incubation was the first indication of monkeypox over smallpox:

“At the first meeting of the WHO Informal Group on Monkeypox and Related Viruses, in Moscow in March 1969, the experts agreed that the first indication that virus recovered from a skin lesion might be monkeypox virus would be the haemorrhagic appearance of the pocks produced on the chorioallantoic membrane after 3 days’ incubation at 35 ° C.

On 23 September 1970 Dr S. S. Marennikova, Dr E. M. Shelukhina and Dr N. N. Maltseva, of the WHO collaborating centre in Moscow, recovered a virus on the chorioallantoic membrane from material sent from a patient in Zaire. When examined after incubation for 2 days, the pocks were “perfectly typical” of variola virus. However, after another day’s incubation at 35 ° C, there was some haemorrhage around the pocks, a feature never seen with variola virus and characteristic of monkeypox virus.”

https://www.google.com/url?sa=t&source=web&rct=j&url=https://biotech.law.lsu.edu/blaw/bt/smallpox/who/red-book/Chp%252029.pdf&ved=2ahUKEwiJi_G355X1AhWKZM0KHd9IAA8QFnoECDEQAQ&usg=AOvVaw0o1ZKfIZFos-R50YesS-Wp

As for the antibody results, since antibodies have never been purified  and isolated nor scientifically proven to exist, it should be obvious that using one fictional entity (antibodies) to identify another fictional entity (“virus”) is not proof that a “virus” exists nor that it is either the same or different from other fictional “viruses” also assumed to exist. Sadly, this simple bit of logic never seems to enter into the minds of these researchers for some reason.

The entirety of the 1972 paper identifying the first case of human monkeypox infection and the “isolation” of the “virus” is presented below:

Isolation and properties of the causal agent of a new variola-like disease (monkeypox) in man

The causal agent of a case of disease in man occurring in the Democratic Republic of the Congo with a similar clinical picture to smallpox was isolated and studied. The agent was identified as monkeypox virus. A comparative study of the isolated strain (Congo-8) and of viruses isolated from similar cases of illness in Liberia (Liberia-i and Liberia-2 strains) and Sierra Leone (V-70 1 266 strain) showed that they were identical. A number of local species of monkeys and apes were examined serologically in the Congo region to determine the probability of human infection with monkeypox virus. It was confirmed that the animals had had contact with an agent of the poxvirus group. In 2 of the 7 sera examined, antibodies of the variola-vaccinia group of poxviruses were discovered (virus-neutralizing
antibodies, precipitins, and antihaemagglutinins). In a chimpanzee, antihaemagglutinins
were found in a titre of 1:1,280, and in the same animal a variola-like virus was isolated from the kidneys. In the course of the investigation, it was shown conclusively that monkeypox virus and the strains under investigation could be distinguished from ordinary variola and vaccinia viruses on the basis of their behaviour in pig embryo kidney continuous cell line culture.

Until fairly recently it was believed that only two poxviruses other than variola and alastrim viruses could cause generalized infection in man accompanied by skin lesions. These were the true cowpox agent and the vaccinia virus. As a rule, both these
viruses cause lesions at the point of infection, and the infection becomes generalized only in occasional cases. In 1958 a new representative of the poxvirus group, the monkeypox virus, was discovered (Magnus et al., 1959). Since then a number of outbreaks of monkeypox among trapped animals kept in nature reserves and zoological gardens have been recorded and studied (Prier et al., 1960; McConnell et al., 1962; Peters, 1966; Gispen, Verlinde & Zwart, 1967).

It has been established that the infection caused by the virus can be transmitted to some other animals (anteaters) and to various species of monkey and ape, including the anthropoid apes. The severity of the disease in monkeys varies and depends to a considerable extent on the species. The disease follows its most severe course in anthropoid apes. Nevertheless, no illness in man caused by monkey-pox virus has been noted in any of these outbreaks. The data quoted in this paper, however, indicate that monkeypox virus can cause a disease similar to ordinary smallpox in man. The virus was isolated from material obtained from a 9-month-old unvaccinated child (A. I.) from the village of Bokenda in Basankusu Province, Democratic Republic of the Congo, who was suffering from a disease suspected to be smallpox. The village concerned is situated in a remote locality in the depths of a tropical rain forest. No cases of smallpox had occurred during the 2 previous years either in the village or in the surrounding area. No cases of infection with the variola-like disease spreading from the child A. I. were recorded (Ladnyj, Ziegler & Kima, 1971). Practically the whole population of Bokenda village had been vaccinated against smallpox a year before this case occurred during a mass smallpox vaccination campaign throughout the country.

In addition to reporting the results of the isolation and identification of the Congo-8 strain of virus from the child A. I. this paper gives the results of a serological examination of a group of monkeys and apes from the focus, and also the results of a study of Liberia-i, Liberia-2, and V-70 1 266 viruses isolated in the Center for Disease Control, Atlanta, Ga., USA, from patients suffering from similar variola-like illnesses in Liberia and Sierra Leone.

MATERIAL AND METHODS

Material from the patients in the Democratic Republic of the Congo was obtained through the World Health Organization by air in a special packing, and consisted of the contents of skin lesions (scabs and smears on slides). The Liberia-I, Liberia-2, and V-70 1 266 strains were obtained through WHO on 11 December 1970, 18 December 1970, and 30 April 1971, respectively, in the form of suspensions of chorioallantoic membrane (CAM), infected CAM, and scabs from a patient (Liberia-1). These strains had been passaged once or twice in the laboratory and were used in the experiments in the form of first-or second-passage suspensions of CAM (disregarding passages undergone before they were received in the laboratory).

Strains Congo-8, Liberia-1, Liberia-2, and V-70 1 266 were compared with viruses of variola (strains MT-60 and MK-60-Harvey), cowpox (Brighton strain), monkeypox (Copenhagen strain), and vaccinia (strains Tanzania-3 and France). The viruses were used in the form of a suspension of infected CAM after one or two further passages in chick embryos.

The sera and organs of monkeys caught in the area of Bokenda village were received in the laboratory in a frozen state in a container of liquid nitrogen.

The usual methods were used to isolate the virus from materials taken from patients and from the organs of monkeys and to investigate them by means of the agar gel microprecipitation test (World Health Organization, 1969).

In studying the genetic features of the viruses (the type of pock on CAM and the plaques in cell cultures, haemagglutinating activity, pathogenicity for rabbits following infection by intradermal inoculation or scarification and other properties), standard methods were used (Marennikova & gafikova, 1969; Marennikova, Gurvic & geluhina, 1970). The animals used in the experiments were white chinchilla rabbits weighing 2.5 kg, and randomly bred white mice weighing 10-11 g.

The type of cytopathic effect was determined in the following cell cultures: two primary (chick embryo fibroblast and monkey kidney cells) and four continuous (VERO, A-1, PEK, HEP-2). The morphology of the plaques was studied both with and without agar overlay (Porterfield & Allison, 1960; Gendon & ternos, 1964).

In the comparative studies equal doses of the viruses were used. The doses given to rabbits intradermally and by scarification were 10^6 pock-forming units per 0.1 ml. The doses used to study pathogenicity in chick embryos ranged from 10 to 10^7 pock-forming units per 0.1 ml, the results being read after 72 hours. In studying the ceiling temperature for the development of specific lesions, 100 and 1,000 pock-forming units were used. Except in special tests, the morphology of pocks was determined on CAM after
72 hours, when there were 10-100 pocks on the membrane. The type of cytopathic effect was studied by infection with doses of virus ranging from 10 to 10^7 TCD50, the results being read from 24 hours to 7 days after infection.

Before examination the monkey sera were thawed and heated at 56°C for 30 minutes. The haemagglutination-inhibition test was carried out with 2 agglutinating units (AU) of the test virus and a 1% suspension of chick red cells. The neutralization test was carried out by the usual method (Boulter, 1957),
while the Ouchterlony method (1949) was used in the agar gel precipitation test.

RESULTS

Research on the laboratory diagnosis of smallpox carried out in this institute in 1970, with material taken from patients during the period 18 December 1969 to 22 October 1970, enabled us to confirm the presence of smallpox in a number of provinces of the Democratic Republic of the Congo (Dendale Kinshasa, Kalomy, Longo Ngaba Kinshasa, and Kabulo Kalukivu). The strains of variola virus isolated did not differ from the typical virus of natural smallpox.

During the same period a virus was isolated from material taken on 1 September 1970 in the village of Bokenda in the province of Basankusu from the child A. I. as already stated. On the basis of an examination of infected CAM after 48 hours and serological identification by means of the agar gel microprecipitation test, this virus was initially identified as variola virus (23 September 1970). However, the character of the pocks on CAM had changed sharply after 72 hours and this observation, together with results of haemagglutinating activity tests, suggested that the agent isolated was of a different nature. A detailed study was then undertaken and the virus was also re-isolated from material taken from the patient.

Table I shows the results of isolating the virus from material taken from the patient and testing the basic properties of the strain. Investigations showed that the isolated virus (strain Congo-8) produced a peculiar type of pock on CAM, distinguishing the strain from both vaccinia virus and ordinary variola virus. This virus also showed a high degree of haemagglutinating activity and a marked tendency to cause lesions on scarified rabbit skin. On the third to fourth day after infection of the rabbit, the scarified area stood out above the healthy skin surrounding it as a result of the development of confluent papular eruptions without any marked induration of the underlying tissues. The confluent elements took the form of moist ridges along the lines of scarification (see Fig. 1).

When the rabbits were infected intradermally, necrosis developed in the centre of the dense infiltrated area that formed at the site of inoculation. The area of infiltration itself was slightly haemorrhagic. In rabbits infected by scarification and intradermally, the infection assumed a generalized character.

After incubation for 48 hours, as already stated the lesions on chick-embryo CAM differed little from those caused by ordinary smallpox virus. However, after 72 hours they had already become flatter and haemorrhages appeared in the centre of most of the pocks (Fig. 2). By that time the non-uniformity of the pocks in respect of morphology and size had become obvious; side by side with small pocks containing haemorrhages, a small number of large white pocks without haemorrhages could be observed. This feature was seen at an incubation temperature of 35°C. An increase in the incubation temperature by as little as 1 deg C led to changes in the nature of the pocks. Pocks that developed on CAM showed no haemorrhage.

The unusual combination of properties and the close similarity of a number of the features of the Congo-8 strain to those of other viruses in the pox group made it necessary to carry out a detailed comparison of the virus in experiments with cowpox, monkeypox, variola, and vaccinia viruses. The strains of Liberia-1, Liberia-2, and V-70 1 266 from Liberia and Sierra Leone, which had been isolated from cases of variola-like illness in man, similar to that from which A. I. was suffering, were included in the same tests. The results of the comparative study showed that Congo-8, Liberia-I, Liberia-2, and V-70 1 266 did not differ substantially one from another according to the tests used, nor did they differ from the classical type of monkeypox virus of the Copenhagen strain (Tables 2 and 3).

Not only was these a close affinity between these four strains according to the tests already described (type of pock on CAM, skin lesions in rabbits, and haemagglutinating activity) but they all produced plaques of identical morphology and size, whether agar overlay was used (in chick embryo fibroblast cells) or not (Vero continuous cell line). Unlike ordinary variola virus, which under agar overlay produces small plaques less than 1 mm in diameter, monkeypox virus and the Congo-8, Liberia-1, and Liberia-2 isolates formed larger plaques with a visible internal structure and an uneven margin. In experiments without agar overlay, variola virus gave scarcely visible plaques with an intensely stained rim, whereas the isolates formed large plaques with a transparent centre and two peripheral zones: an inner reticular zone with an uneven edge and an outer intensely stained zone (Fig. 3). The differences in the type of cytopathic effect between these viruses and the variola virus were less marked than the differences in plaque formation. The isolates produced a cytopathic effect of focal type in the initial stages with breaks in the cell layer and a zone of cell proliferation on the periphery. The cells bounding the focus were rounded and highly refractive. In the centre of the focus were cells or groups of cells that had lost the capacity for process formation. At higher doses of the virus (over 10^5 TCD5O) there was a “diffuse” cytopathic effect throughout the cell layer (Fig. 4).

The study of a number of cell cultures infected with Congo-8, Liberia-2, and Copenhagen viruses showed that the most sensitive were VERO cells (titres of 107-5 and 106.2 TCD5O) compared with chick embryo fibroblast cells (titres of 105-5-106 5 TCD,O) and the A-1 cells (titres of 105.5-106 5 TCDS,O). These viruses showed marked haemadsorption phenomena in chick embryo fibroblasts, monkey kidney cells, Vero cells, A-1 cells, and HEP-2 cells.

It has been shown previously (Marennikova, Gurvic & Seluhina, 1970) that a feature of monkeypox virus that distinguishes it from variola and vaccinia viruses is its incapacity for active replication and the absence of the haemadsorption phenomenon in a culture of the continuous pig embryo kidney (PEK) cell line. Study of the behaviour of Congo-8, Liberia-1, and Liberia-2 strains showed that they behave similarly: their titre in PEK cells did not exceed 10^2-6 TCD50/ml and the haemadsorption phenomenon did not occur even when cytopathic changes had taken place (Table 2).

Determination of the ceiling temperature for the development of pocks on chick embryo CAM showed, that, unlike vaccinia and cowpox viruses, strains Congo-8, Liberia-1, and Liberia-2, as well as monkeypox virus, did not cause lesions at a temperature of 39.6°C following the administration of 100 and 1,000 pock-forming units. However, this group of strains and the monkeypox virus caused the development of pocks on CAM at a temperature at which no lesions developed following infection with the MT-60 strain of variola virus (38.6.39°C). The test strains differed from variola virus and cowpox virus in their higher haemagglutinating activity (see Table 3). The Congo-8 strain and the three other isolates tested proved highly pathogenic for chick embryos. Following intracerebral infection of white mice, these strains, like monkeypox virus, were considerably more pathogenic than variola virus for adult mice (Table 3).

In the serological studies use was made of hyper-immune rabbit sera against vaccinia and variola viruses. In the haemagglutination-inhibition test with both antisera, the test viruses produced titres identical with those produced by monkeypox virus (Table 4). In the agar gel precipitation test, all the viruses except cowpox virus were found to have an identical antigenic structure (Fig. 5).

In view of the fact that the experimental material obtained enabled the Congo-8 virus to be identified as monkeypox virus, it seemed useful to investigate monkeys and apes living in the area of the infective focus. In January 1971 Dr I. D. Ladnyj and Dr P. Ziegler trapped a group of monkeys of different species whose blood, serum, and organs (liver, spleen, and kidneys) were studied. The results of serological examinations of the animals are given in Table 5. Of 7 sera tested, 2 showed antihaemagglutinins in titres of 1:16 and 1:1,280. In these same sera (Nos 4 and 9), virus-neutralizing antibodies, in a titre of more than 1:40, and precipitins were discovered. The detection of antibodies to vaccinia virus shows that an agent of the poxvirus group is circulating among certain local species of monkey. Furthermore, the presence of precipitins and the high level of antihaemagglutinins found in a chimpanzee suggested that it had been infected. This view is supported by the isolation from the kidneys of the same chimpanzee of a variola-like virus. The results of this study are given by Marennikova et al. (1971).

DISCUSSION

Experience gained in recent years in studying variola virus has shown that it is distinguished, like a number of other viruses, although to a lesser degree, by intraspecific variability or natural variation (Bedson, Dunbell & Thomas, 1963; Sarkar & Mitra, 1967; Marennikova & gafikova, 1969). The differences found were related to the degree of pathogenicity of the strains for chick embryos and white mice, the ceiling temperature for pock development, and some other indices. However, not one of  the strains of variola and alastrim viruses investigated proved capable of causing the development of lesions on scarified skin in rabbits. The Congo-8 strain isolated from the patient A. I. with an illness resembling smallpox caused a marked specific reaction when it was placed on scarified rabbit skin. This feature of the Congo-8 virus, combined with other characteristics (the haemorrhagic type of pocks on CAM, types of plaque in tissue culture, high degree of haemagglutinating activity, ceiling temperature for the development of lesions, etc.) makes it impossible for it to be considered as a variant of variola virus. On the other hand, the properties of Congo-8 proved to be indistinguishable from those of the classic representative of monkeypox virus (the Copenhagen strain), and provided good grounds for identifying it as a monkeypox virus itself. The evidence thus indicates that the monkeypox virus can cause disease in man.

The fact that examinations of numerous samples over a number of years of material from patients from different countries with suspected smallpox have not previously revealed an agent identical with, or close to, the Congo-8 virus in its properties, and that no such cases have been reported by other authors, may indicate that this infection has a low degree of contagiousness and a comparatively limited area of distribution. This view is supported particularly by the results of examinations of other material taken from patients in the Democratic Republic of the Congo. Except for Congo-8, the virus isolated in each case did not differ from the variola virus. However, the results of examining Liberia-1 and Liberia-2 strains, which according to the results we obtained did not differ substantially in their properties from the Congo-8 strain, suggest that monkeypox in man is not strictly limited in distribution since the Democratic Republic of the Congo and Liberia have no common frontier and are fairly far apart. It may be assumed that cases of monkeypox in man are caused by the presence of a reservoir of the virus in certain species of monkeys and apes in the areas concerned. This view is supported by the results of serological examinations of animals trapped in the focus of infection. The low degree of contagiousness of monkeypox to man or the complete absence of infectivity for other persons in the patient’s household may be the reason why the disease was not discovered earlier. There is no doubt that the discovery of this infection was aided by the establishment of an epidemiological surveillance system sufficiently sensitive to discover single cases of illness.

https://apps.who.int/iris/bitstream/handle/10665/263482/PMC2480798.pdf?sequence=1&isAllowed=y

In Summary:

  • In March 2021, NTI partnered with the Munich Security Conference to conduct a tabletop exercise on reducing high-consequence biological threats
  • Participants included 19 senior leaders and experts from across Africa, the Americas, Asia, and Europe with decades of combined experience in public health, biotechnology industry, international security, and philanthropy
  • Developed in consultation with technical and policy experts, the fictional exercise scenario portrayed a deadly, global pandemic involving an unusual strain of monkeypox “virus” that first emerged in the fictional nation of Brinia and spread globally over 18 months
  • Ultimately, the exercise scenario revealed that the initial outbreak was caused by a terrorist attack using a pathogen engineered in a laboratory with inadequate biosafety and biosecurity provisions and weak oversight
  • By the end of the exercise, the fictional pandemic resulted in more than three billion cases and 270 million fatalities worldwide
  • Most significantly, exercise participants agreed that, notwithstanding improvements following the global response to “COVID-19,” the international system of pandemic prevention, detection, analysis, warning, and response is woefully inadequate to address current and anticipated future challenges
  • The Johns Hopkins Center for Health Security in partnership with the World Economic Forum and the Bill and Melinda Gates Foundation hosted Event 201, a high-level pandemic exercise on October 18, 2019, in New York, NY
  • Event 201 simulates an outbreak of a novel zoonotic “coronavirus” transmitted from bats to pigs to people that eventually becomes efficiently transmissible from person to person, leading to a severe pandemic
  • The pathogen and the disease it causes are modeled largely on “SARS,” but it is more transmissible in the community setting by people with mild symptoms
  • Two outbreaks of smallpox-like disease occurred in lab monkeys in 1958 rather late after the monkeys had been received, i.e. 51 and 62 days after arrival and only a small percentage of the exposed animals showed signs of illness
  • Material for egg inoculation was collected from the pustular lesions and diluted approximately 1:10 in 0.004 hl. McIlvain’s buffer saline pH 7.2
  • Material for tissue culture experiments was collected from the pustules by means of a cotton swab, which was immediately immersed into 2 ml of Bacto-tryptose “Difco”
  • Bacto™ Tryptone is a pancreatic digest of casein. It was developed by Difco Laboratories while investigating a peptone particularly suitable for the elaboration of indole by bacteria. It is also notable for the absence of detectable levels of carbohydrates. https://www.americanpharmaceuticalreview.com/25246-Cell-Culture-Media-Supplements/5821993-Bacto-Tryptone/
  • Both diluents contained Penicillin (100 mg per ml) and Streptomycin (0.1 mg per ml)
  • After clarification by low speed centrifugation the supernatants were used for inoculation onto the chorio-allantoic membrane of 11-12 day old Leghorn embryos and into tissue cultures of monkey kidney, human amnion and HeLa cells
  • Vaccinia strain (i.e. not variola) lot NO. 1/50 111 received from the smallpox vaccine department in this institute was used in some experiments in order to compare it with the monkey “virus”
  • This strain had heen maintained for several years by serial cutaneous passages in rabbits and calves
  • Either the glycerinated third calf passage or a subsequent first passage of this material on the chorio-allantois was used
  • After inoculation the eggs were incubated for 48 hours at 37° C when vaccinia “virus” was used for infection and for 72 hours when the monkey “virus” was used (i.e. the samples being compared were not treated the same)
  • For neutralization tests, undiluted serum was mixed with equal volumes of increasing dilutions of “virus”
  • After incubation for 2-3 hours at room temperature 0.1 ml amounts of the serum-“virus” mixtures were inoculated onto the chorio-allantoic membranes of groups of five 11-12 day old embryos
  • Tissue culture methods were not described in this paper yet it was stated that during the first experiments they were examined daily for cytopathic changes but in later ones microscopic examination was carried out only every fourth or fifth day
  • Serial passages were usually made with 0.2 ml amounts of undiluted nutrient fluid harvested 5 days after inoculation
  • For complement fixation tests, antigens were prepared from nutrient fluid of tissue cultures as well as from chorio-allantoic membranes infected with monkey-pox or vaccinia “virus”
  • Hyperimmune sera against monkey pox and vaccinia “viruses” were prepared in rabbits by repeated intravenous injections of 0.5 to 2.0 ml amounts of 10 percent suspensions of infected chorio-allantoic membranes
  • The animals received a total of 7 intravenous injections (on day 1, 9, 11, 16, 18, 23 and 25)
  • They were bled 10 days after the last injection
  • Another hyperimmune serum prepared by immunizing rabbits with calf-lymph vaccinia antigen which had been inactivated by heating at 70° C for 60 minutes was also used
  • In addition, an hyperimmune vaccinia rabbit serum kindly supplied by dr. F. 0. MacCallum, England was used in some experiments
  • In other words, the sera used for antibody experiments came from many sources with different preparation methods
  • Electron microscopy followed the method of Van Royen & Scoff:
    1. The grids were treated with 0.25 percent crystalline trypsin solution for 4 hours at 37° C after which they had 2 brief washings in distilled water
    2. Fixation was carried out in the vapours of a 1 percent osmiumtetroxide solution for 15 minutes
    3. In order to minimize the risk of infection the grids were heated to 70° C for one hour (1) prior to shadowcasting with platinum
    4. The egg adapted “virus” grown on chorio-allantoic membranes was “purified” for electron microscopy by means of differential centrifugation and precipitation with citric acid according to the method of Henderson & McClean
    5. The final suspension was placed directly on formvar coated grids, dried and further treated as stated above with the exception that no digestion with trypsin was carried out
  • In other words, the “purified virus” from egg membranes was heavily treated and coated with platinum before imaging
  • “Virus” isolation was attempted only from one monkey during outbreak  No. 1 and from two monkeys during outbreak No. 2
  • Most of the studies were done from the “isolate” of the first monkey
  • For “virus isolation” in eggs, scrapings from several papules which were diluted lO^-3, 10^-5, and 10^-7 produced greyish oedematous changes in the  membranes
  • In addition small discrete lesions showing a tendency to spread along the blood vessels could be seen in the eggs inoculated with the highest dilution of “virus”
  • On continued passage, using dilute membrane suspensions as seed, the oedernatous reaction disappeared and the small opaque dome-shaped pocks became predominant
  • In membranes harvested after incubation for 3 days these pocks resembled closely those described for variola “virus”
  • For “virus isolation” in tissue cultures, pustular scrapings were emulsified in tryptose-broth, clarified by low speed centrifugation, and the supernatant was inoculated into tissue cultures of monkey kidney, human amnion, and HeLa cells.
  • Cytopathic lesions developed in all cell types after continued incubation for 2-3 days and destruction was almost complete after 5 days
  • In other words, the longer they incubated their toxic cell soup, the more the cells died
  • In the HeLa cell cultures, formations were not observed as in the other cell lines but otherwise the cytopathogenic effect was similar to that observed in the other cell types used
  • On continued tissue culture passage the cytopathogenic changes developed somewhat more slowly, suggesting that the passage fluid contained less “virus” than the pustular material
  • This assumption was supported by egg titrations
  • During the first outbreak of the pox disease some apprently healthy cynomolgus monkeys which belonged to the affected shipment had been sacrificed for other purposes
  • The kidneys from these animals were trypsinized and culture tubes were prepared from the cell suspensions
  • In some of the tubes (approximately 5 percent) cytopathic changes
    developed 7 to 12 days later and monkey-pox “virus” was isolated from these cultures
  • During the 2nd outhreak monkey-pox “virus” was again present in a small percentage of the tubes prepared from kidneys of apparently healthy-but exposed-animals
  • On this occasion “virus” was recovered from cultures of a monkey which had been sacrificed 4 days before the outbreak
  • This was the only occasion when monkey-pox “virus” was encountered in cultures which had been prepared at a time when clinical illness was not present in the colony
  • The fields presented in EM images were admitted to not be free of accompanying impurities, yet the researchers were able to make out the outlines of quite a few particles ciearly enough to allow the well known rectangular appearance characterizing the “viruses” of the pox-group to be distinguished
  • One of the clusters of particles appeared somewhat smaller than normal pox “virus” particles, but they chalked it up as probably the result of shrinkage during the preparation
  • In other words, the samples imaged by EM were not purified as there were impurities within the samples imaged and the rectangular particles were picked as the “virus” as they looked like a typical “pox virus”…i.e. point and declare
  • The causal agent of a case of disease in man occurring in the Democratic Republic of the Congo with a similar clinical picture to smallpox was said to be isolated and studied
  • The agent was identified as monkeypox “virus”
  • A number of local species of monkeys and apes were examined serologically in the Congo region to determine the probability of human infection with monkeypox “virus”
  • In the course of the investigation, it was shown “conclusively” that monkeypox “virus” and the strains under investigation could be distinguished from ordinary variola and vaccinia “viruses” on the basis of their behaviour in pig embryo kidney continuous cell line culture
  • In other words, they looked at the INDIRECT chemical reactions and determined different “viruses” based on this rather than DIRECT evidence of purified/isolated particles directly from the fluids
  • It was believed that only two “poxviruses” other than variola and alastrim “viruses” could cause generalized infection in man accompanied by skin lesions: the cowpox and vaccinia “virus”
  • In 1958 a new representative of the “poxvirus” group, the monkeypox “virus,” was discovered
  • Since then a number of outbreaks of monkeypox among trapped animals kept in nature reserves and zoological gardens have been recorded and studied (no outbreaks in animals in the wild?)
  • The severity of the disease in monkeys varies and depends to a considerable extent on the species
  • The disease follows its most severe course in anthropoid apes
  • No illness in man caused by monkeypox “virus” had been noted in any of these outbreaks
  • The data quoted in this paper, however, was said to indicate that monkeypox “virus” can cause a disease similar to ordinary smallpox in man
  • The “virus” was “isolated” from material obtained from a 9-month-old unvaccinated child (A. I.) from the village of Bokenda in
    Basankusu Province, Democratic Republic of the Congo, who was suffering from a disease suspected to be smallpox
  • No cases of infection with the variola-like disease spreading from the child A. I. were recorded
  • Practically the whole population of Bokenda village had been vaccinated against smallpox a year before this case occurred during a mass smallpox vaccination campaign throughout the country
  • Material from the patients in the Democratic Republic of the Congo was obtained through the World Health Organization by air in a special packing (no mention of what this consisted of), and consisted of the contents of skin lesions (scabs and smears on slides)
  • The Liberia-I, Liberia-2, and V-70 1 266 strains were obtained through WHO on 11 December 1970, 18 December 1970, and 30 April 1971, respectively, in the form of suspensions of chorioallantoic membrane (CAM) (highly vascularized membrane found in the eggs of certain amniotes like birds and reptiles), infected CAM, and scabs from a patient (Liberia-1)
  • These strains had been passaged once or twice in the laboratory and were used in the experiments in the form of first-or second-passage suspensions of CAM (disregarding passages undergone before they were received in the laboratory)
  • Strains Congo-8, Liberia-1, Liberia-2, and V-70 1 266 were compared with “viruses” of variola (strains MT-60 and MK-60-Harvey), cowpox (Brighton strain), monkeypox (Copenhagen strain), and vaccinia (strains Tanzania-3 and France)
  • The “viruses” were used in the form of a suspension of infected CAM after one or two further passages in chick embryos
  • The sera and organs of monkeys caught in the area of Bokenda village were received in the laboratory in a frozen state in a container of liquid nitrogen
  • The usual methods (i.e. tissue and cell culture) were used to “isolate” the “virus” from materials taken from patients and from the organs of monkeys and to investigate them by means of the agar gel microprecipitation test
  • Standard methods used for studying the genetic features of the “viruses” included:
    1. The type of pock on CAM and the plaques in cell cultures
    2. Haemagglutinating activity
    3. Pathogenicity for rabbits following infection by intradermal inoculation or scarification and other properties
  • The type of cytopathic effect was determined in the following cell cultures:
    1. Two primary (chick embryo fibroblast and monkey kidney cells)
    2. Four continuous (VERO, A-1, PEK, HEP-2)
  • The doses given to rabbits intradermally and by scarification were 10^6 pock-forming units per 0.1 ml.
  • The doses used to study pathogenicity in chick embryos ranged from 10 to 10^7 pock-forming units per 0.1 ml, the results being read after 72 hours
  • The type of cytopathic effect was studied by infection with doses of “virus” ranging from 10 to 10^7 TCD50, the results being read from 24 hours to 7 days after infection
  • In other words, the doses used and the timing to determine results varied
  • Before examination the monkey sera were thawed and heated at 56°C for 30 minutes
  • On the basis of an examination of infected CAM after 48 hours and serological identification by means of the agar gel microprecipitation test, this “virus” was initially identified as variola “virus” (23 September 1970)
  • However, the character of the pocks on CAM had changed sharply after 72 hours and this observation, together with results of haemagglutinating activity tests, suggested that the agent isolated was of a different nature
  • In other words, the initial examination and serological investigation told them that the boy had smallpox but after 72 hours of further culturing, the pocks in the chorioallantoic membrane changed and they decided it was no longer smallpox
  • Investigations showed that the isolated “virus” (strain Congo-8) produced a peculiar type of pock on CAM, distinguishing the strain from both vaccinia “virus” and ordinary variola “virus” (i.e. they could not see the “virus” particles but assumed a difference in the type of pock in CAM meant it was different)
  • This “virus” also showed a high degree of haemagglutinating activity and a marked tendency to cause lesions on scarified rabbit skin (how shocking that lesions occurred where rabbits were scraped and cut)
  • When the rabbits were infected intradermally, necrosis (the death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply) developed in the centre of the dense infiltrated area that formed at the site of inoculation
  • In rabbits infected by scarification and intradermally, the infection assumed a generalized character
  • After incubation for 48 hours, as already stated the lesions on chick-embryo CAM differed little from those caused by ordinary smallpox “virus”
  • However, after 72 hours they had already become flatter and haemorrhages appeared in the centre of most of the pocks
  • The unusual combination of properties and the close similarity of a number of the features of the Congo-8 strain to those of other “viruses” in the pox group made it necessary to carry out a detailed comparison of the “virus” in experiments with cowpox, monkeypox, variola, and vaccinia “viruses”
  • The results of the comparative study showed that Congo-8, Liberia-I, Liberia-2, and V-70 1 266 did not differ substantially one from another according to the tests used, nor did they differ from the classical type of monkeypox “virus” of the Copenhagen strain
  • The 4 strains all produced plaques of identical morphology and size, whether agar overlay was used (in chick embryo fibroblast cells) or not (Vero continuous cell line)
  • Unlike ordinary variola “virus,” which under agar overlay produces small plaques less than 1 mm in diameter, monkeypox “virus” and the Congo-8, Liberia-1, and Liberia-2 isolates formed larger plaques with a visible internal structure and an uneven margin
  • In other words, they determined similarity of the invisible “viruses” by plaques produced and not by showing purified/isolated particles in EM
  • The differences in the type of cytopathic effect between these “viruses” and the variola “virus” were less marked than the differences in plaque formation (i.e. the CPE was not distinct)
  • The study of a number of cell cultures infected with Congo-8, Liberia-2, and Copenhagen viruses showed that the most sensitive were VERO cells (titres of 10^7-5 and 10^6.2 TCD5O) compared with chick embryo fibroblast cells (titres of 10^5-5-10^6 5 TCD5O) and the A-1 cells (titres of 10^5.5-10^6 5 TCD5O)
  • These “viruses” showed marked haemadsorption phenomena in chick embryo fibroblasts, monkey kidney cells,Vero cells, A-1 cells, and HEP-2 cells
  • It had been shown previously (Marennikova, Gurvic & Seluhina, 1970) that a feature of monkeypox “virus” that distinguishes it from variola and vaccinia “viruses” is its incapacity for active replication and the absence of the haemadsorption phenomenon in a culture of the continuous pig embryo kidney (PEK) cell line (more indirect non-specific chemical reactions)
  • As the behaviour of Congo-8, Liberia-1, and Liberia-2 strains showed that they behave similarly, they were determined to be monkeypox rather than smallpox
  • Following intracerebral infection of white mice, these strains, like monkeypox “virus,” were considerably more pathogenic than variola “virus” for adult mice
  • Upon investigating monkeys and apes, the detection of antibodies to vaccinia “virus” showed that an agent of the “poxvirus” group was circulating among certain local species of monkey
  • The presence of precipitins and the high level of antihaemagglutinins found in a chimpanzee suggested that it had been infected
  • This view was supported by the “isolation” from the kidneys of the same chimpanzee of a variola-like “virus”
  • The lesions upon scarification of rabbits from the Congo-8 “virus,” combined with other (indirect) characteristics (the haemorrhagic type of pocks on CAM, types of plaque in tissue culture, high degree of haemagglutinating activity, ceiling temperature for the development of lesions, etc.) made it impossible for it to be considered as a variant of variola “virus” (even though they originally claimed that it was)
  • The evidence indicated that the monkeypox “virus” can cause disease in man (even though this was never shown)
  • It may be assumed that cases of monkeypox in man are caused by the presence of a reservoir of the “virus” in certain species of monkeys and apes in the areas concerned
  • This view is supported by the results of serological examinations of animals trapped in the focus of infection
  • The low degree of contagiousness of monkeypox to man or the complete absence of infectivity for other persons in the patient’s household may be the reason why the disease was not discovered earlier

Should everybody be concerned about monkeypox as Joe Biden has warned? If you understand that the original evidence for the monkeypox “virus” in both animal and man lacks the physical evidence of purified and isolated particles directly from the host fluids which were then proven pathogenic in a natural way, you will be able to easily brush aside the latest attempt at fear propaganda. Taking samples from monkeys and subjecting them to tissue, egg, and cell culturing with the addition of various other chemicals and looking for patterns formed after incubation does not prove a “virus” is present. Taking this toxic soup and injecting it in numerous ways and/or scarifying it onto the skin of animals and seeing lesions form is not a recreation of the same disease. It is an unnatural experimental reaction to various forms of torture and abuse the animals are subjected to and does not prove a “virus” as the cause. Performing various tests mixing the blood of animals and humans and claiming the results mean that there is a specific antibody reacting to a specific “virus” when neither have been properly purified and isolated does not prove a “virus” either. All of these examples are of the indirect evidence used to state the existence of an invisible “virus” which are the result of unnatural lab-created chemical reactions and concoctions. They are performed and evaluated without physically having direct evidence of the assumed “virus” particles in question in order to infer its presence due to the resulting reactions. These researchers are trying to sell you on the idea of Santa Claus by way of half-eaten cookies, presents under the tree, and a colorful note that looks suspiciously like your mother’s handwriting.

A similar conclusion about the lack of evidence regarding the existence of the monkeypox “virus” was made by Dr.’s Sam and Mark Bailey in their recent excellent article on this topic:

“In any case, a review of the scientific evidence revealed that with regards to monkeypox: (a) there is no evidence of a physical particle that meets the definition of a virus, (b) there is no evidence of anything transmitting between humans, and (c) there is no way to confirm a diagnosis of monkeypox unless you believe in clinically-unvalidated tests such as the PCR kits that have been produced. In other words, if we see a monkeypox “pandemic” that is used as an excuse to role out more globalist terrorism, it will be on the back of another PCR pandemic, not one that has any basis in nature.”

Monkeypox Mythology

They go into great detail breaking down the CDC’s deceptive practices in a supposed monkeypox outbreak in the US in 2003 and the (surprise surprise) misuse of PCR to diagnose cases. I highly recommend reading the whole article.

The bottom line is that there is no reason to fear monkeypox today any more than there was before the drill and the ensuing fear-mongering headlines. Monkeypox is nothing but the reclassification of the same symptoms of disease that belong to a select group including smallpox, chickenpox, shingles, measles, etc. They are all varying levels of the same detoxification process. Could there be an increase in the amount of people suffering these sets of symptoms? Sure, as a vast amount of people have repeatedly subjected themselves to experimental injections over and over again during the last two years. Eventually, the body must rid itself of the toxic overload which may result in a similar set of symptoms as seen in cases of so-called monkeypox. However, as always, there is no need to fear any “virus” nor any infection. There is nothing to this monkeypox business other than a well-orchestrated fear-campaign. The only thing to fear regarding this media blitz in need of a poster child is this:

36 comments

  1. I have never liked monkeys for some reason. Amazing how monkey pox can suddenly be found in a dozen countries like magic. How did it spread so quick? I would think there would be trials left behind where people in-between contacted this virus. The experts never offer any explications for how these viruses move around, so in my world they are all fake…the experts and the viruses.

    I have read something interesting from Paul Craig Roberts who says that all those who have had their immune systems compromised by taking the mRNA gene therapies will be at risk for getting smallpox if they get the monkey-pox vaccine…which will be rebranded small pox vaccines. This could be dangerous as even those with good immunity will be at risk from these horrid injections. Maybe that’s the plan.

    All the worry and fear that some “virus” will kill off mankind. Even if there was some killer disease that could kill billions, neither the CDC or WHO would have much of a bear-butt clue as to what to do that would prevent it. Certainly no “vaccine” will make any difference as we have seen throughout history.

    Like

  2. Thanks Mike, you’re relentless!

    So you’re thinking that if this pox becomes their next set-piece, the unvaxxxed will not be coming down with it because the Covid vaxxxes will be the true cause?

    Liked by 1 person

    1. It seems like that scenario would lead to full disclosure which would catalyze a worldwide anti-globalist ‘revolution’ as in, out with the old boss in with the new. I’ve been of the mind for several years now that this ‘WEF’ business is a misdirection play in service of a reactionist ‘revolutionary’ swing to populist nationalisms because that’s the obvious structural future for the first (and last?) 5-10 years of collapse.

      I’m wondering, though — given the close historical correlation of ‘pox’ with famine, if disclosure will not be necessary nor even desirable since, respectively, the catastrophic and wholly manufactured Russo-Ukie ‘war’ politics will suffice and germ theory is such a good mechanism for control.

      Africa naturally will be on the cutting edge of the famines so should contract plenty of ‘pox,’ and since Africa is ever-so mysteriously unvaxxxed yet Covid resistant lol, that will serve as perfect cover for the shots heard round the world.

      Liked by 1 person

    2. I have to be. If it’s not vaccine shedding, it’s stealth omicron. If it’s not stealth omicron, it’s snake venom. If it’s not snake venom, it’s monkeypox…Yada Yada yada.. 😉

      I’m not sure as far as if the unvaccinated will come down with these symptoms or not. It depends on their toxicity level. I imagine more vaxxed will be in an unhealthier state requiring detoxification, especially with repeated injections. This may lead to an increase in these symptoms as they are associated with vaccination. Time will tell. My guess is it is mostly fear propaganda as usual. I’m just waiting for the asymptomatic Monkeypox cases.

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      1. Yeah it’ll probably be like the Covid dynamic where wherever famine dynamics are equal the vaxxxed will be measurably worse off with pox.

        Beware the asymptomatic cases you monkeys. 🙂

        Liked by 1 person

      2. Lol, I’m sure it’s just around the corner if this January 2020 study is any indication:

        Asymptomatic Orthopoxvirus Circulation in Humans in the Wake of a Monkeypox Outbreak among Chimpanzees in Cameroon

        “The ASYMPTOTIC or undetected circulation of OPXVs in humans in Cameroon is likely, and contact with monkeypox reservoirs is common, raising the need for continued surveillance for human and animal disease.”

        “We identified the presence of anti-OPXV antibodies in participants less than the age of smallpox vaccination in Mfou district, Cameroon, SUGGESTING UNDETECTED OR POSSIBLE ASYMPTOMATIC CIRCULATION of an OPXV in human populations in this region.”

        https://pubmed.ncbi.nlm.nih.gov/31769389/

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  3. After two years of reading about the fraud of germ theory, about so-called infectious disease, I have come to the conclusion there’s nothing of the sort. In regards to all the categorized “poxes”, I see them as nothing but detox through the skin. These eruptions are the body’s chosen method to rid itself of certain types of unwanted matter. This perceived uptick, called Monkeypox, might well be connected to the millions (billions?) of injections recently given, foreign matter introduced directly into body tissue. Intramuscular is a very artificial pathway for substances to gain access to the body. There’s no protection from the GI system, the normal route being ingestion. For protection from inhaled unwanted substances, there are thick mucous layers lining the mouth, nose, trachea, bronchi, etc. A recent post reminded me of the almost nine pages of Pfizer reported adverse events stemming from their mRNA jab trial. One was, “Autoimmune blistering disease.” Sounds like, perhaps, a pox? Down the list are dozens of herpes and shingles conditions. I have no doubt this gene hterapy experiment is contributing to skin issues of many varieties.

    Liked by 3 people

    1. Agree 💯 “Autoimmune blistering disease” is most likely the new name for the same detox/vaccine injury previously designated smallpox/monkeypox. They love to relabel in order to confuse.

      Liked by 1 person

  4. I have never liked monkeys for some reason. Amazing how monkey pox can suddenly be found in a dozen countries like magic. How did it spread so quickly? I would think there would be trials left behind where people in-between contacted this virus. The experts never offer any explications for how these viruses move around, so in my world they are all fake…the experts and the viruses.

    I have read something interesting from Paul Craig Roberts who says that all those who have had their immune systems compromised by taking the mRNA gene therapies will be at risk for getting smallpox if they get the monkey-pox vaccine…which will be rebranded small pox vaccines. This could be dangerous as even those with good immunity will be at risk from these horrid injections. Maybe that’s the plan.

    All the worry and fear that some “virus” will kill off mankind. Even if there was some killer disease that could kill billions, neither the CDC or WHO would have much of a whisper of a bear-butt clue as to what to do that would prevent it. Certainly no “vaccine” will make any difference as we have seen throughout history.

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    1. I’ll assume by “good immunity” you mean good overall health, but one thing that’ll remain true no matter what they try to inject everyone with is that a lethal dose for say half the world is unlikely to kill the very healthy, and an irreversibly harmful dose for half the world is likely to leave the elite-healthy fairly unscatched, at least after they fast off any damage they do incur.

      So unless they systematically target the healthiest people for extermination or one gets unlucky in choosing one of the worst vaccine batches (but if the batches vary, one can choose the least bad batch and fair even better), maintaining an awesomely healthy lifestyle will always allow one to be fairly safe statistically I think – and that’s assuming one even ever is totally forced into getting jabbed, which is unlikely given the mostly voluntary way the establishment ultimately operates.

      Deep knowledge of health, law, and the state of the world will be important going forward, but we seem to be entering a renaissance of understanding in these areas for those with an open mind and discernment.

      Liked by 1 person

  5. Stellar job again, Mike, and also Sam and Mark Bailey, their article is well worth reading. Interesting how this is a continuation of a tradition which was at play on 9/11, an event which had been exercised for, and as it was unfolding, there were a bunch of US air defenses “exercises” going on.
    Dismaying how Unlimited Hangout and CHD are pushing monkeypox as real even if hyped (article from Unlimited Hangout, posted today in The Defender).

    Liked by 1 person

    1. Thanks Jeffrey! There is a definite similarity in the events/drills taking place before the “outbreaks” to what happened with the drills right before 9/11. It seems that there is a system they use to get their propaganda all worked out and ready for prime-time. It amazes me that people do not see nor understand this connection more often.

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  6. Mike, Clarifire, just wanted to beat on a dead horse here since I noticed C that you replied under this comment of Mike’s that contained the MSU article about atrazine resistance:

    https://viroliegy.com/2022/05/18/the-natural-selection-theory-of-antibody-formation-1955/comment-page-1/#comment-3014

    This interpretation of weed resistance is bonkers. To suggest that resistance comes from outlier plants that just don’t die from these herbicides surviving what is effectively a very tight bottleneck to flourish on the other side of the bottleneck (selective pressure) is pure Darwinism.

    Atrazine destroys foundational photosynthesis mechanisms thereby starving plants to death. There is zero chance that some lambsquarter plants are structurally evolved to have a completely different photosynthetic architecture that just so happens to tolerate atrazine. Adaptation only ever happens out of necessity or, I believe brian would say, joy. Which is to say intelligence only increases due to the repeated teachings of repeated stimulations that are reasonably responded to; it happens for a reason.

    Racism doesn’t exist (it’s a political fraud) because our evolutionary heritage laid down no cause for it. There was no stimulus for the hardwiring of racism because people lived on foot and the percentage of people who ever saw anybody who looked noticeably different from themselves would have been negligible; therefore there was no *mechanism* for distrusting/hating someone based on their phenotype. Racism is just political cover (shadow play) for the imperial control of a civilization that only exists by physically forcing tribal human outgroups to cooperate in service of the State.

    In the same way the existence of ‘natural resistance’ to atrazine in lambsquarter can’t possibly precede the invention of the poison. There’s no*reason* for it to exist and, frankly, it can’t exist without a rebuild of the photosynthetic foundation, and I bet my bottom dollar that there’s no evidence for lambsquarter having done so.

    Indeed, the serious biochemical literature points to the resistant lambsquarter having an accelerated detox function. These strains would be hardcore landraces — barbarians not to be fucked with — that saddled up and got the job done. Does that mean that they can handle a full-dose of atrazine generation after generation? Hell no I don’t think so. They’re edge creatures of the barrier function. Maybe the farmer’s travelling speed with the disker was a little too fast for a second which left a few hard dirt clods that sheltered the weed seed. There could be a million reasons.

    Commodities hyperbred for yield by definition, and to the degree that they can survive it, have their metabolisms geared for one thing only. As we know, the detox function takes its toll. To be long fasting is to be bedridden. There’s no way that they could breed back these plants to have such a super heavy duty detox function.

    Clarifire, thanks for the recent leads. Do you do high meat?

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    1. Not sure whether plants can ever evolve quickly to withstand poisons, but if nature has a truly hard time doing some biological trick I’ll bet my bottom dollar scientists would never be able to do it.

      High meat is something I’m interested in but haven’t tried yet. Vonderplanitz is an very interesting figure, but his advice changed a lot. Still useful for all the leads he provided.

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      1. Plants can’t evolve quickly enough given the length of their reproductive cycle but microbes can. They live in hyperspeed relative to us cumbersome multicellular giants. And if they didn’t exist within us we’d be too slow to exist. Couldn’t adapt fast enough to the energy flux. In the existential sense we are nested within them and not the other way round.

        They farmed glyphosate resistant microbes and surgically inserted the resultant glyphosate enzyme inhibitor into the chloroplast architecture so as to block the disease pathway. Monsanto spent about ten years breeding promising microbes in “waste-fed” vats – glyphosate vats.

        The surgery came at great cost to hardiness. The plants lost about 7percent yields, and they were rendered sterile. But the lowered yield was cancelled out by the reduction in weed pressure and eliminating seed saving was an evil genius.

        One thing I don’t buy is that Monsanto says they built the sterility into the seeds intentionally so that they don’t crossbreed but I figure it’s due to the modification. People with titanium knees don’t birth titanium kneed children.

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      2. Sounds like Monsanto may gave done something sort of akin to changing out the gut flora in humans, and we know what kind of changes that can produce. Or producing bacteria-free rats. There seem to be many possibilities besides that they did anything with “genes,” which was the original matter in question IIRC.

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      3. Since plant gut flora is the soil biology, Monsanto most certainly changed out their flora by replacing it with triple-16 or whatever. 🙂

        I don’t see what exists in the fields happening without physical surgery. Surgery is what they do best. About the only thing they do well. I’d need a plausible scenario to reason otherwise.

        By surgery I mean shooting them, with a gene gun. Shooting DNA into embryonic plants until the command sticks. Devolutionary proteomics. The vaxxxes are purported to be shot into cells until the message sticks.

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      4. Surgery doesn’t mean “genes” necessarily. That’s just their explanation. The question is what they’re actually doing, and trade secrets may well prevent us from even knowing, though we might be able to figure out by guessing.

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      5. I would think that if we put our heads together we would be able to figure it out. I would also expect that others like us already would have. I thought you had previously implied that you don’t have a beef with genomics. This is still just genomics – with firearms.

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      6. I appreciate that. I don’t feel that shakiness myself. I feel a hyperenabled intelligent metaconscious framework. Industrialism is the cumulative, compressed raw intelligence (the Collective Applied Consciousness of the Past – the CACP of the Home Cosmology) of incalculable amounts of life lived (fossil fuels) being fed-through the hyper-evolved human metaconsciousness which itself is the living proof –the tip of the spear of the CACP. The pinnacle of evolution (in hyperadapted humans) may currently be in self-destruct mode for cultural reasons, but until the ponzi economy pops for good here in the next 12mos probably, the hyperintelligence made possible by a human intelligence jacked-up on the fossilized CACP running through its veins continues to grow.

        Industrialism blows mind-blowing bubbles fueled by the CACP. Industrialism literally converts/transmutes the CACP into whatever it wants. Genomics is a mind-blowing consciousness bubble no different than China real estate bubble. They’re both gargantuan feats immense raw power harnessed by intelligent engineering. Culturally they’re both obscene. Some truths hurt until we’re able to make peace with them.

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      7. I’m not trying to be manipulative and suggest that you’re unable to make peace with the true powers of industrialism. That reflection came out as an expression of my own creative process.

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      8. On the genetic front I’m wondering if they modify the plants that they plan to use as the pollinizers and pollinate non-modified plants with them, which yields viable seedstock for a sterile harvest.

        I can’t think how non-,genetic surgery could be performed at the cellular level. And how that surgery could be passed on otherwise every single seed would have to have had surgery. Oddly, I was looking at an article for layperson’s by one of the Roundup Ready inventors and he seemed to say that every seed is “injected”/modified but surely that’s impossible.

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      9. I heard it said by trusted sources that any mammal fed gmo food for three generations are rendered sterile, and Ive always taken that at face value. Granted, people don’t only eat GMO foods. Nevertheless, that is high suggestive of surgery to me.

        Do you also understand that claim of sterility to be the case?

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    2. That was a bad or maybe just incomplete analogy. What I’m saying is that because a titanium kneed parentage cant birth titanium kneed offspring, if it is forced to do so then the parentage will be effectively sterile.

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  7. Hello again.
    Are you aware of any site or location that documents specific examples of people dying from the crapcine (the “covid” one)? It seems to mostly just be numbers.
    By the way, I forgot what your counterargument to the claim that doctors are reaquired to report to the VAERS *any* side effect or death within a certain window after administering a “covid vaccine”, and that anybody can report something there without verifying the cause. What is the refutation to that?
    Thanks.
    Also, I’m sure excited for another planned and fake “pandemic” with the new fake monkeypox. What are they gonna do now, have a new “pandemic” every year?

    Liked by 1 person

    1. I’m not sure as the numbers for the vaccine deaths are hard to determine. Any statistics (either way) coming from this “pandemic” need to be taken with a grain of salt. However, this interview with Dennis Rancourt by Jerm Warfare goes in depth on death statistics. I can not remember if they touch on vaccine deaths or not but it may be worth a watch as well as finding Rancourt’s 170-page paper:

      https://odysee.com/@jermwarfare:2/denis-rancourt-no-pandemic:0

      I’m not sure there is any counterargument for VAERS. People can either believe the statistics or not. There has been claims that it is vastly underreported (less than 1%) and that doctors regularly do not know to report there. Also, many victims of vaccine injuries do not know to report there. In many cases, they don’t seem to connect their injuries to vaccination at all even if they occurred around the same time. In other words, it is very difficult to argue statistics with anyone as they can be reported, unreported, massaged, and manipulated to say whatever the interpretor wants them to say. I always fall back on the Mark Twain quote:

      “There are lies, damned lies, and statistics.”

      And yes, I imagine they will continue to milk this “virus” charade for all it’s worth until the majority say “Enough!”

      Liked by 1 person

  8. Thanks Mike. Another well researched and in depth article.

    An interesting addition from Immanuel Project.
    One really has to wonder if some of the so called ‘scientists ‘ are so indoctrinated into the dogma of viruses that they really believe their falsehoods and lies , which makes their pseudoscience even more dangerous.

    Click to access _Monkeypox_.pdf

    Liked by 2 people

    1. Thanks PC! Sadly, I believe many of them are that indoctrinated. I have spoken with many who are/were in the Microbiology field who now question all of this virology insanity. They thought wholeheartedly that what they were doing was right. The main difference is that they were open to questioning and challenging long held beliefs while those who remain blissfully ignorant are not.

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