By Julie Beal
On the 19th of January, 2020, a 35-year-old man walked into an urgent care clinic in Washington, America. He was worried he might be infected with the 2019-nCoV virus because he’d just got back from Wuhan and had seen a health alert from the CDC about the coronavirus outbreak. He’d had a cough for four days and was worried he might have a fever because he felt a bit hot. The medical team checked him out and said the fever was ‘subjective’ (imagined?) and his lungs were fine as well, so they took a swab from his nose so they could check it for various pathogens, along with some other samples to test for 2019-nCoV, then sent him home.
The next day, the CDC said he was positive according to a PCR test so they put him back in hospital – in isolation. This PCR test may have used the protocol published by Drosten et al, as this was released on the 17th of January (the same day the NIH finished annotating the Wuhan-Hu-1 genome).
For the next few days, the man experienced some hot spells and some fast heartbeats. He still had a cough and he seemed to be tired. He also did two runny poos and a had a bit of a tummy ache. By the 24th of January, there was some evidence of pneumonia and he had some trouble breathing so they started giving him oxygen and administered antibiotics intravenously. On the 25th, the hospital did another X-ray and saw there were some streaky opacities in his lungs so they started giving him Remdesivir. On the 26th of January, they stopped the antibiotics, and the next day, the man was feeling a bit better. He had a tiny cough and a bit of a runny nose, but his lungs were okay again so they stopped the oxygen treatment. He was still in hospital on the 30th but by this point, all he had was a bit of a cough.
Samples taken from this man were cultured in monkey kidney cells and some viruses grew out of the culture. They were said to match the genomes sequenced in China, and so this man became the first official case of ‘covid’ in America and the genome of the virus is the US reference strain. It’s known as WA1/2020 and it was tested on some macaque monkeys a couple of months later, as described in a paper published by the NIH on 12 May, 2020. This paper was called, ‘Respiratory disease in rhesus macaques inoculated with SARS-CoV-2’, and was summed up in the introduction like this:
“Here, we show that SARS-CoV-2 causes respiratory disease in infected rhesus macaques, with disease lasting 8–16 days. Pulmonary infiltrates, a hallmark of human disease, were visible in lung radiographs. High viral loads were detected in swabs from the nose and throat of all animals as well as in bronchoalveolar lavages; in one animal we observed prolonged rectal shedding. Taken together, the rhesus macaque recapitulates moderate disease observed in the majority of human cases. The establishment of the rhesus macaque as a model of COVID-19 will increase our understanding of the pathogenesis of this disease and will aid development and testing of medical countermeasures.”
Eight rhesus macaques were infected with WA1/2020, which was “isolated from an oropharyngeal swab” from the patient described above. Four of the macaques were ‘sacrificed’ (i.e. killed) on Day 3. The four remaining macaques all recovered (by Days 9, 10, 13 and 17). During the first week of infection, their clinical symptoms included hunched posture, goosebumps, slow/fast/heavy breathing, reduced appetite and a snotty nose. One of them was even said to have anorexia for a day! (As if it didn’t have much of an appetite that day!)
“Coughing was occasionally heard in the room where animals were housed but could not be pinpointed to individual animals.”
By the second week, two of the macaques were a bit perkier, but the other two were much the same. (Here are the symptoms.)
Deducing deadliness
SARS-CoV-2 is supposed to be a deadly virus and yet there is little evidence for this – there are plenty of doctors who say they’ve got patients for covid, but the total number of deaths remained mostly normal until the injections began. For a virus to be classed as ‘deadly’, most people would expect there to be a higher than average death toll, but this hasn’t happened with SARS-CoV-2. Why, then, do most of the experts continue to believe that SARS-CoV-2 is a dangerous and deadly virus? It could be partly because they’ve been convinced for a long time that coronaviruses are dangerous (both SARS-CoV and MERS-CoV were thought to be lethal, based on the case:fatality ratio). They might also be caught up in the mass hysteria being sustained by the media, but on the whole, it seems to be a function of the way viruses are studied:
Epidemiology – virologists and molecular biologists often study viruses that are flagged as being significant based on certain statistics. It seems to be standard practice to trust these statistics without questioning their reliability, or other issues such as running too many cycles for the PCR, the lack of diagnosis for ‘cases’, and the significance of co-morbidities.
Infectivity – scientists usually assess infectivity by creating a synthetic virus, adding it to a bit of blood, then examining it with a microscope, e.g. to see how the virus gets into certain cells, how well it replicates, and if the virus is shed (which might mean it can be transmitted to others). Infected animals can also be dissected and analysed to quantify the amount of virus in their tissues and assess them for damage. SARS-CoV-2 is said to be very good at getting into cells.
Pathogenicity –a virus is said to be pathogenic if it causes damage or leads to a disease (e.g. based on chest X-rays of patients, see HRCT Chest and CO-RADS Classification System, A Pictorial Review). The pathogenicity of a virus is also assessed by deliberately infecting animals with it, usually by blasting a ‘full dose’ deep inside their chests and noses, monitoring them for clinical signs of illness, then killing them a week or two later to examine their body tissues, etc. (This 2007 study has photos of damaged lungs.) One of the main reasons SARS-CoV-2 is said to be highly pathogenic is because of the way it affects animals who are artificially infected with the virus, but it’s also due to reports from doctors.
Alleged Illness and Deaths with Covid
According to Pfizer, people with covid usually have a cough and a fever, with “ground-glass opacities or patchy shadowing” visible in chest X-rays, although some people develop ARDS (acute respiratory distress syndrome), and even “multi-organ failure and death”. Nonetheless, the ‘case fatality rate’ is highest in people who are already in poor condition and/or near the end of life.
“According to the WHO, the population most at risk of severe disease and death from the SARSCoV- 2 virus are individuals over the age of 60 and individuals with underlying conditions of cardiovascular disease, diabetes, hypertension, cancer and chronic respiratory disease. The highest mortality rate reported is for people 80 years of age and older at 21.9-percent. …… The SARS-CoV-2 virus appears to not attack children, unlike other infectious diseases like influenza.”
Testing different versions of SARS-CoV-2 on monkeys
An article co-authored by Zeng Li Shi said that tests done on animals were useful because they display the same clinical features as humans, such as viral shedding and having high viral loads. In terms of pathogenicity, various animals had been used to test the effects of SARS-CoV-2. These include several types of monkey, plus mice, ferrets and hamsters, and the studies are listed in the article’s footnotes. One of the monkey experiments is described above, and here are two more:
Comparative pathogenesis of SARS-CoV-2, MERS-CoV, and SARS-CoV infections in cynomolgus macaques; Rockx et al (authors include Drosten and Fouchier); 17 April, 2020. This experiment involved infecting cynomolgus monkeys; the first group consisted of four young and four old monkeys, each infected with SARS-CoV (the virus that was identified in 2002), whilst MERS-CoV was used in the second group containing four young monkeys. The third group consisted of 2 x young and 2 x old monkeys who were deliberately infected with something thought to be SARS-CoV-2; it was a strain that was obtained from a German traveller returning from China, and described as “a low-passage clinical isolate of SARS-CoV-2, which resulted in productive infection in the absence of overt clinical signs”. It seems quite remarkable that the only clinical sign seen in any of the groups was when “one aged animal” had a snotty nose on Day 14. No significant weight loss was seen in any of the animals, and they all had antibodies by Day 14. The older animals had higher levels of SARS-2 RNA in their noses than the younger ones did. “Increased age did not affect disease outcome.” (Link to symptoms). Four of the monkeys used in these experiments were killed on Day 4. The researchers concluded:
“These data show that cynomolgus macaques are permissive to SARS-CoV-2 infection, shed virus for a prolonged period of time, and display COVID-19–like disease.”
Another study was published by Chinese researchers on 30 March, 2020, with the title, ‘Age-related rhesus macaque models of COVID-19’. They had three young rhesus macaques in one group, and two aged ones in the other. (One monkey from each group was killed on Day 7.) They were all infected with a strain from the Chinese CDC called HB-01 (“obtained from a virus isolated from a patient”, from either bronchoalveolar-lavage fluid or epithelial cells). There were few clinical signs of illness in any of the monkeys.
Young ones: Week one – two of the three monkeys had some weight loss and seemed somewhat weak, but none had fever. Week two – one of the two remaining monkeys still had weight loss, and weakness until Day 9.
Aged ones: Week one – both of the monkeys had weight loss and weakness but neither of them had a fever. Week two – the last remaining monkey still had weight loss, and weakness until Day 11, but no fever.
What happened to their lungs?
None of the monkeys in any of these experiments died until they were euthanized in order to harvest their organs and examine them under a microscope. As expected, the monkeys displayed signs of pathology, such as lung lesions, and this is viewed as evidence of disease. For example, the young monkeys in the Chinese study had ground glass opacities, whilst the aged monkeys had lesions from interstitial pneumonia which were said to be “remarkable”. These pathology tests are then used to support various claims, such as: “SARS-CoV-2 caused more severe interstitial pneumonia in old monkeys than that in young monkeys. Rhesus macaque models infected with SARS-CoV-2 provided insight into the pathogenic mechanism and facilitated the development of vaccines and therapeutics against SARS-CoV-2 infection.”
First there was SARS-CoV
“Severe acute respiratory syndrome (SARS) was recognized in late 2002, and by the end of the outbreak in July 2003 more than 8000 cases and 774 deaths were attributed to SARS worldwide (Kuiken et al., 2003). A new coronavirus, termed the SARS coronavirus (SARS-CoV), was isolated from patients with SARS (Drosten et al., 2003; Ksiazek et al., 2003; Poutanen et al., 2003). Soon after the disease was recognized, the ability to experimentally infect and induce interstitial pneumonitis in cynomolgus macaques with SARS-CoV was demonstrated, thus fulfilling Koch’s postulates and confirming that SARS-CoV was the causative agent of SARS (Fouchier et al., 2003; Kuiken et al., 2003).”
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Back in July, 2003, a landmark study was published in The Lancet which claimed to have proven Koch’s postulates for SARS. The authors of the paper (‘Newly discovered coronavirus as the primary cause of severe acute respiratory syndrome’) included experts such as Fouchier, Drosten and Peiris. The paper describes how they “tested clinical and postmortem samples from 436 SARS patients in six countries for infection with SARS-CoV” and found that 75% of them tested positive, whereas most of them were found to be negative for other types of respiratory viruses. They also attempted to replicate the suspected disease by infecting four cynomolgus macaques with an isolate from a patient thought to have SARS, which was passaged four times. Three of the monkeys became lethargic after a few days, and two had a temporary skin rash on Day 4. One macaque “had respiratory distress” (breathing quickly, with some difficulty) from Day 4, and only one of the animals had normal looking lungs afterwards. They were all euthanized on Day 6.
Proof of SARS in people was said to come from an experiment performed in April by Peiris et al (‘Coronavirus as a possible cause of severe acute respiratory syndrome’); tissue from two people diagnosed as having the new disease were grown in monkey cells and the stuff that grew seemed to be similar to the ones in the original samples. They produced 30 clones from this process, and one of them had an unknown section of DNA that seemed to be a coronavirus because a fair bit of it matched a cow coronavirus and a mouse virus called MHV. This matching piece was a fragment of DNA that was only 646 base pairs long (the total virus is about 30,000 base pairs), and it was used to devise a PCR test. Then they tested 44 patients thought to have SARS and half of them tested positive, whereas 40 people with unrelated diseases tested negative.
A year later, another study was conducted by NIAID researchers (‘Replication of SARS coronavirus administered into the respiratory tract of African Green, rhesus and cynomolgus monkeys’, 2004). This study involved infecting three species of monkey with SARS, and showed that the virus, “replicated in the respiratory tract but did not induce illness”. Another NIAID report from 2004 described how monkeys infected with the Urbani strain of SARS-CoV (the one Baric patented) showed no signs of clinical illness. The authors suggested this was due to having used a different strain of SARS to previous researchers.
An FDA/NIAID experiment with ferrets in 2007 (‘Severe Acute Respiratory Syndrome Coronavirus Infection in Vaccinated Ferrets’) assessed the effects of a SARS vaccine. Without having been previously infected, the ferrets were either given no vaccine, or they were given vaccine containing an inactivated SARS-CoV virus. They were then subjected to a challenge test, where they were deliberately infected with SARS; they were killed on Day 23 and their lungs were checked for lesions that indicated lung disease. The lesions were graded and these were the results:
No vax + No challenge = no lesions
No vax + Challenge = 3 x mild, 1 x moderate
Vax + Challenge = 1 x minimal, 1 x mild, 2 x moderate
Vax + No challenge = no lesions
The vaccinated ferrets cleared the virus in the pharynges by Day 7, and the unvaccinated cleared it by Day 14.
What happened to the monkeys?
None of the studies described above include details about the health of the monkeys afterwards (most of them are killed, anyway), and they don’t say whether or not the damage might be permanent, or what health problems could manifest. However, there are known consequences to having pneumonia, which is alleged to be the main type of disease caused by SARS-CoV-2.
Covid Pneumonia
Covid pneumonia is said to be characterized by the lungs filling with fluid, which causes shortness of breath; if it gets worse, it can lead to acute respiratory distress syndrome (ARDS), which is basically lung failure and can be fatal. Historically, the main symptoms of pneumonia have been “cough, sputum production, fever, and feeling generally ill, sometimes with shortness of breath and chest pain on breathing in.” The disease is usually mild and might only last for a few days; most people are better after two weeks. Pneumonia used to be diagnosed by checking for bacterial infection and signs of consolidation (thickening) in the lungs using X-rays or CT scans. Before 2020, most types of pneumonia were thought to be caused by bacteria; about 50% of all cases were linked to Streptococcus and about 25% to other types of bacteria, such as mycoplasma and chlamydia. Pneumonia caused by bacteria can be treated with antibiotics and most people recover even if their lungs are damaged:
“Pneumonia is an acute infection from which most patients will make a rapid recovery. Many patients do suffer from easily getting tired for a couple of months after having had pneumonia, but this gradually improves. Amazingly, even with severe pneumonia, the lung usually recovers and has no lasting damage, although occasionally there might be some scarring of the lung (rarely leading to bronchiectasis) or lung surface (the pleura).”
Lung damage
When a lung nodule (or mass) is found during a CT scan of the chest, they’re usually “the result of old infections, scar tissue, or other causes”; and, apparently, it’s quite common to have lung lesions by the time you die, for a variety of reasons.(i) A 2017 pathologist report (‘Prevalence of Lung Lesions at Autopsy: A Histopathological Study’) said that 68% of the lungs they autopsied had “significant microscopic finding”, and the rest were normal (another similar study found abnormalities in 90% of samples). Apparently, congestion and oedema are the most commonly found changes, along with “changes in interstitium” which, they say, “could be due to pollution, smoking or any restrictive lung disease leading to fibrosis”. An article called ‘Pulmonary Lung Conditions Found at Autopsy’ notes, “There are innumerable conditions that may affect the lungs, producing findings that can be found at autopsy.” Lungs affected by viral and early bacterial pneumonia go through a series of stages related to inflammation. They might start off like heavy, wet sponges but this can change to a more congested state, known as consolidation, where the lungs “begin to have a more firm and solid appearance in the affected areas.” The initial “red hepatization” phase is followed by a pattern called “gray hepatization”, after which “the affected area either completely heals or is replaced by residual scar tissue.” Lungs that are scarred following an episode of severe pneumonia would end up with “some degree of chronic, permanent impairment of gas exchange (chronic respiratory failure)”. People with acute respiratory distress syndrome (ARDS) may have lungs with diffuse alveolar damage.
Challenge tests with the Moderna vax
Evaluation of the mRNA-1273 Vaccine against SARS-CoV-2 in Nonhuman Primates was published in July, 2020, with contributions from a whole heap of researchers, including Ralph Baric and Barney Graham. It described a challenge test where monkeys were infected with synthetic viruses modelled on the WA1/2020 virus described above, and created using the reverse genetics system developed by Baric/NIAID many years ago. The monkeys were sacrificed at various points from day 7 to day 15, and their lungs were assessed for lesions. Each monkey was given a ‘lesion score’ – those who received the mRNA jab had mostly low scores, whereas the monkeys who weren’t injected with the mRNA had lung lesion scores that were mostly moderate. The authors also claim the mRNA led to an increased Th-1 response, which is something that many researchers thinks help avoid Antibody Dependent Enhancement (ADE).(ii) Coronavirus vaccines have long been known to be associated with ADE(iii), and it’s said to be caused by a Th-2 type response, characterized by a rise in eosinophils. These are white blood cells that can fight disease, but if you make a lot of them, it can be toxic, damaging cells and tissues; it’s also associated with an increased risk of thrombosis (blood clotting). No mention is made of eosinophils in the paper, but the European Medicines Agency report notes the Moderna jab caused rats to have an increase in eosinophils up to 6.5 times higher than the control group, to a point where it was at the level of disease:
“The absolute eosinophil counts observed in LNP-mRNA studies reached values that would be classified as eosinophilia in patients”
The rats also had “increases in activated partial thromboplastin time (APTT, up to ~30%) and fibrinogen (up to ~2.5-fold)”. The EMA report also noted, “Clinical pathology changes generally reversed or were reversing by the end of the 2-week recovery period.” Is this perhaps a more optimistic assessment of disease pathology than is applied to the tests with SARS 1 and 2? What happened to the people the virus samples were taken from? Did any of them have comorbidities? And what about the animals that were experimented on? Would any of them have recovered?
The next article in this series will examine the Gain of Function (GoF) research that was done in Wuhan with coronaviruses, with funding from NIAID. This research helps explain why most molecular biologists think SARS-CoV-2 is deadly, but it also demonstrates that most of the experiments they did yielded viruses that were LESS pathogenic. The experiments also provide insights into the way the coronavirus vaccines are designed (e.g. mutations). Another article will explore the design of the virus itself, and ponder whether it could have been selected or created specifically for the Reset and the vax-ID.
Notes:
(i) Sometimes, smokers are able to achieve a degree of healing in their lungs after they stop smoking (presumably before it’s too late!). One study reported that a smoker was found to have lung nodules and cysts, but after he’d stopped smoking, the lesions started to fade and were completely gone after twelve months.
(ii) See Vaccine-associated enhanced disease: Case definition and guidelines for data collection, analysis, and presentation of immunization safety data (the Brighton Collaboration Vaccine-associated Enhanced Disease Working Group).
(iii) There is currently a widespread misconception about the history of ADE with coronavirus vaccines – some people are claiming that ‘all the animals died’ when they were challenged with SARS after being vaxxed, based partly on a study entitled Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Challenge with the SARS Virus (2012). However, as with numerous other challenge studies, the animals did not die from the virus – in this particular study, all animals were sacrificed by day 56. The concern about ADE was based mainly on lung pathology (after being challenged, the unvaccinated animals tended to have less severe lung lesions than the vaxxed ones did). The studies done with SARS and MERS vaccines led experts to conclude that vaccines should be based on the spike protein in order to avoid ADE. A DNA-based SARS vax was tested on humans in 2008 and the genetic vaccine industry continued to grow with every successive outbreak.
