Back in September of 2021, I was alerted to a “virus” that I had never heard of before known as the Nipah “virus.” After having a good laugh over the name (there were a few nipple jokes thrown about), I had decided to investigate this mysterious “virus” to see what all of the fuss was about. At the time, stories were circulating regarding the threat of this “virus” due to the death of a 12-year-old boy in Kerala, India. The only symptom reported for the boy was a low-grade fever for which his parents’ sought treatment at the local health clinic on August 29th, 2021. What treatments were provided for this low-grade fever were not disclosed, but over the course of 2 days, his condition deteriorated, and he was transferred to several hospitals. On the 4th of September, the “presence” of the Nipah “virus” in the plasma, cerebrospinal fluid and serum samples was “confirmed” via the fraudulent real-time polymerase chain reaction (RT-PCR), along with the unreliable findings of IgM antibodies in the plasma sample by ELISA serology test. Sadly, the boy passed away the next day:
Nipah virus disease – India
“On 4 September 2021, the Kerala State Health department reported an isolated case of Nipah virus disease in Kozhikode district, Kerala state, India. Nipah has a relatively high case fatality ratio, and is an emerging zoonotic disease of public health importance in the South East Asia and Western Pacific WHO Regions. This is the fifth outbreak of the disease in India.
On 29 August, a 12 year-old boy developed low grade fever, and the family sought care at a local health care facility. On 31 August, he was transferred to several hospitals as his condition deteriorated. On 1 September, the patient’s condition continued to deteriorate, and the family requested his transfer to another hospital in Kozhikode.
On 3 September, plasma, serum and cerebrospinal fluid samples were sent to the National Institute of Virology in Pune, India. On 4 September, the presence of Nipah virus in the plasma, cerebrospinal fluid and serum samples was confirmed by real-time polymerase chain reaction (RT-PCR) and IgM antibodies was confirmed in the plasma sample by ELISA serology test. On 5 September, the patient died and a safe burial and cremation were performed the same day in Kozhikode.”
https://www.who.int/emergencies/disease-outbreak-news/item/nipah-virus-disease—india
There were no other victims of the Nipah “virus” at the time, and as I was very busy transferring my old Facebook posts to the newly created ViroLIEgy.com site, I lost track of this “virus.” Now two years later, it appears that the Nipah “virus” is back once again in order to strike terror into the unsuspecting citizens of Kerala. At the time of this writing, there have been a grand total of two deaths attributed to this invisible foe, which has led to a state of panic and mass testing. Public gatherings were “curbed” while schools have been shut down indefinitely.
Sound familiar?
The Nipah “virus” is claimed to have a fatality rate between 40-75% and, as there are no vaccines or treatments said to be effective at combating it, the old school methods of rest, hydration, and treating symptoms are all that can be offered. However, there is hope for the perpetually frightened as there are several new vaccines undergoing clinical trials as we speak, including an mRNA-based injection. Thus, it won’t be long before people are able to roll up their sleeves for even more toxic jabs failing to protect them against the same symptoms of disease.
As it slipped past me the first time around, it seems like now is the perfect opportunity to pull the curtain back and look into the mysterious origins of the Nipah “virus.” How did this “virus” come about and when did it first appear? What symptoms are associated with the disease? Are there other possible explanations for any signs of illness? Let’s take a look at all of this as well as the foundational study that alerted the world to the threat of this nasty little Nipah in order to see if there is any actual scientific evidence supporting the need for mass testing, vaccines, and public curbings. While I failed to tackle Nipah two years ago, let’s see if we can nip this one in the bud this time around.
In order to properly drum up the desired level of fear necessary to get people to go along with the new round of mass testing, the mainstream media loves to spotlight the exotic animal origins of these lesser known “viruses.” Case in point, in a September 18th, 2023 The Guardian article, we are told that this rare but serious bat-borne “virus” can cause fever, vomiting, and respiratory infections, including seizures, brain inflammation, and coma. Of course, the fact that the Nipah is a bat-borne “virus” is highlighted below the title of the article. Nothing drums up fear quite like bat-nipples.
What is Nipah virus? Kerala starts mass testing after outbreak in India
Rare but serious bat-borne virus that can cause fever, vomiting and respiratory infections in humans has killed two in Kerala
“Indian authorities have instituted mass testing to halt the spread of the deadly Nipah virus, which has killed two people in the southern state of Kerala.
Public gatherings were curbed and some schools were shut last week, officials said on Thursday. It is the fourth outbreak in the region since 2018.
Nipah is a rare but serious bat-borne virus that can cause fever, vomiting and respiratory infections in humans. Severe cases can involve seizures and encephalitis – inflammation of the brain – and result in a coma.
The virus has a fatality rate between 40-75%, according to the World Health Organization (WHO). It has no known vaccine, and the usual treatment is to provide supportive care.
So how did the world first learn about this deadly bat-nipple “virus?” The first cases were recorded in 1998 after Nipah was said to spread among pig farmers in Malaysia and Singapore. It is claimed that the bat-borne “virus” was first transmitted to humans from the fluids of the “infected” pigs. Thus, it would seem that this bat-borne “virus” is truly a pig-borne “virus,” but perhaps pig nipples are not as scary as Mr. Clooney’s.
Fruit bats, a.k.a. flying foxes, are claimed to be the natural carriers of the “virus.” Nipah is also said to be related to the Hendra “virus” that originated in horses. Thus, we have quite the inerspecies “viral” jamboree going on with the Nipah. One of the hypothesized ways that fruit bats are said to spread the “virus” is by sitting in trees and urinating all over the precious fruit. This “virus”-laden urine-covered fruit is then ingested by unsuspecting humans. Possibly due to the fear that people will forget to wash their urine-soaked fruit before consuming, scientists are frightened that a mutated, highly transmissible strain will emerge from these nasty Nipah bats.
What is the Nipah virus?
The first Nipah outbreak was recorded in 1998 after the virus spread among pig farmers in Malaysia and Singapore. The virus is named after the village where it was discovered.
It is able to infect humans directly through contact with the bodily fluids of infected bats and pigs, with some documented cases of transmission among humans.
Flying foxes are the natural carriers of the virus. “It’s carried by fruit bats who sit in the tops of trees,” said Joanne Macdonald, an associate professor of molecular engineering at the University of the Sunshine Coast. “They can urinate and contaminate fruit, and when people eat that they get the virus and then they get sick.”
“Once you get it, [the only treatments are] rest, hydration, treatment of symptoms.”
Scientists fear a mutated, highly transmissible strain will emerge from bats. Outbreaks are rare but Nipah has been listed by the WHO as one of several diseases deserving of priority research for their potential to cause a global epidemic, alongside Ebola, Zika and Covid-19.
Nipah is a type of Henipavirus, and is related to Hendra virus, which was first discovered in Australia and has caused deaths in humans and horses.
According to the article, the first pig-borne outbreak of the Nipah that occurred in 1998 “infected” nearly 300 people in Malaysia, with more than 100 deaths attributed to it. Just as we saw with the Avian flu and the mass killing of birds, the fear of the zoonotic spread of the “virus” prompted the culling of one million pigs in an effort to contain the “virus.” However, this did not stop the Nipah from spreading to Singapore where 11 more cases and one death amongst slaughterhouse workers who came into contact with pigs were reported. Since then, the Nipah has made its home in Bangladesh and India, with cases recorded beginning in 2001. Between 1998 to 2015, there have been around 600 cases of the Nipah “virus.” This current outbreak of the Nipah in Kerala is the fourth in five years, after other instances in 2018, 2019 and 2021. Thus, the alarm bells are being rung due to this increased frequency. However, despite the lack of vaccines and treatments, as luck would have it, the outbreaks of the past have been contained through widespread mass testing and the strict isolation of those who came into contact with patients. See a pattern?
What has happened during previous outbreaks?
The first Nipah outbreak in 1998 infected nearly 300 people in Malaysia, killing more than 100, and prompted the culling of one million pigs in an effort to contain the virus.
It also spread to Singapore, with 11 cases and one death among slaughterhouse workers who came into contact with pigs imported from Malaysia.
Since then, the disease has mainly been recorded in Bangladesh and India, with both countries reporting their first outbreaks in 2001. Bangladesh has borne the brunt in recent years, with more than 100 people dying of Nipah since 2001.
More than 600 cases of Nipah virus human infections were reported between 1998 to 2015, according to WHO data.
Two early outbreaks in India killed more than 50 people before they were brought under control.
The southern state of Kerala has recorded two deaths from Nipah and four other confirmed cases since last month. This marks Kerala’s fourth recorded outbreak of Nipah in five years, after other instances in 2018, 2019 and 2021.
The state has managed to stamp out previous outbreaks within a matter of weeks through widespread testing and strict isolation of those in contact with patients.
Regardless, the threat of the zoonotic origins of new “viruses” is prominently pointed out in the closing remarks of the article. We are reminded that “viruses” jumping from animals to humans has multiplied in the last 20-30 years. Industrial farming and deforestation are given the credit for this increase as humans must now be in closer contact with the scary animals. And wouldn’t you know it, the climate crisis also gets a shout out as another reason for this “increased” spread. Sientists are warning that climate change is increasing the risk of “zoonotic spillover” events, with 15,000 instances “predicted” to occur over the next 50 years:
Are animal-to-human viruses becoming more frequent?
Zoonotic diseases – those that can be transmitted from animals to humans – have multiplied over the past 20 to 30 years.
Industrial farming increases the risk of pathogens spreading between animals while deforestation heightens contact between wildlife, domestic animals and humans.
Scientists have warned that the climate crisis is increasing the risk of “zoonotic spillover” events, with 15,000 instances of viruses jumping between species predicted over the next 50 years.”
As the bat-Nipah “virus” is said to be a rare but deadly “virus” presenting with non-specific symptoms of disease, how is it supposed to be differentiated and diagnosed clinically from the many other identical illnesses? Let’s see what the leading “experts” have to say on the matter. According to the CDC, the way to diagnose Nipah is via the usual suspects with PCR and antibody tests. They admit that early diagnosis via clinical symptoms is challenging due to the non-specific nature of the symptoms:
“Nipah virus (NiV) infection can be diagnosed during illness or after recovery. Different tests are available to diagnose NiV infection. During early stages of the illness, laboratory testing can be conducted using real time polymerase chain reaction (RT-PCR) from throat and nasal swabs, cerebrospinal fluid, urine, and blood. Later in the course of illness and after recovery, testing for antibodies is conducted using an enzyme-linked immunosorbent assay (ELISA).
Early diagnosis of NiV infection can be challenging due to the non-specific early symptoms of the illness.”
https://www.cdc.gov/vhf/nipah/diagnosis/index.html
The CDC even states that symptoms may not be present for years after exposure, thus confirming that Nipah is detected via PCR in healthy people without disease:
“Infections that lead to symptoms and sometimes death much later after exposure (known as dormant or latent infections) have also been reported months and even years after exposure.”
https://www.cdc.gov/vhf/nipah/symptoms/index.html
These asymptomatic “infections” in healthy people is also confirmed by the WHO, who state that symptoms range from none to fatal encephalitis. Non-specific symptoms such as fever, headaches, myalgia (muscle pain), vomiting and sore throat are mentioned, which can be followed up by dizziness, drowsiness, altered consciousness, and neurological signs that indicate acute encephalitis. Respiratory distress, encephalitis, and seizures are left to severe cases. While the CDC stated that symptoms could take years to develop, the WHO stated 45 days, so it depends on which of these organizations you distrust the least when it comes to whom to believe on the matter:
Signs and symptoms
“Human infections range from asymptomatic infection to acute respiratory infection (mild, severe), and fatal encephalitis.
Infected people initially develop symptoms including fever, headaches, myalgia (muscle pain), vomiting and sore throat. This can be followed by dizziness, drowsiness, altered consciousness, and neurological signs that indicate acute encephalitis. Some people can also experience atypical pneumonia and severe respiratory problems, including acute respiratory distress. Encephalitis and seizures occur in severe cases, progressing to coma within 24 to 48 hours.
The incubation period (interval from infection to the onset of symptoms) is believed to range from 4 to 14 days. However, an incubation period as long as 45 days has been reported.”
As for diagnosing this disease, the WHO agreed that the symptoms for Nipah are non-specific and that the diagnosis is often not suspected at the time of presentation. This inability to diagnose based upon symptoms alone hinders getting an accurate diagnosis, as does the quality, quantity, type, timing of clinical sample collection, and the time needed to transfer samples to the laboratory. Thus, there are many reasons why the laboratory results that are required for an accurate diagnosis are not so accurate:
Diagnosis
“Initial signs and symptoms of Nipah virus infection are nonspecific, and the diagnosis is often not suspected at the time of presentation. This can hinder accurate diagnosis and creates challenges in outbreak detection, effective and timely infection control measures, and outbreak response activities.
In addition, the quality, quantity, type, timing of clinical sample collection and the time needed to transfer samples to the laboratory can affect the accuracy of laboratory results.”
Interestingly, the WHO states that, while the fruit bats are the natural hosts of the “virus,” they suffer no symptoms of disease whatsoever:
Natural host: fruit bats
“Fruit bats of the family Pteropodidae – particularly species belonging to the Pteropus genus – are the natural hosts for Nipah virus. There is no apparent disease in fruit bats.”
Meanwhile, the “virus” is said to be highly “infectious” in pigs, even though they may not show any symptoms at all. Unlike the 40-75% fatality rate seen in humans, the disease does not result in high mortality in pigs. If symptoms do occur, they are not dramatically different from other respiratory and neurological illnesses suffered by pigs. In other words, the symptoms of disease are non-specific:
Nipah virus in domestic animals
“Outbreaks of the Nipah virus in pigs and other domestic animals such as horses, goats, sheep, cats and dogs were first reported during the initial Malaysian outbreak in 1999.
The virus is highly contagious in pigs. Pigs are infectious during the incubation period, which lasts from 4 to 14 days.
An infected pig can exhibit no symptoms, but some develop acute feverish illness, labored breathing, and neurological symptoms such as trembling, twitching and muscle spasms. Generally, mortality is low except in young piglets. These symptoms are not dramatically different from other respiratory and neurological illnesses of pigs. Nipah virus should be suspected if pigs also have an unusual barking cough or if human cases of encephalitis are present.”
https://www.who.int/news-room/fact-sheets/detail/nipah-virus
Thus, we know that the Nipah is a bat-borne “virus” that does not cause disease in the bats it “infects.” Somehow, this harmless “virus” in bats is highly “infectious” to pigs, but it is regularly asymptomatic or presents with non-specific symptoms of disease. It does not result in high fatality in pigs, unlike in humans where this “virus” is highly “infectious” with a high fatality rate of 40-75%. As with pigs, the disease in humans can be asymptomatic, even for years, and when symptoms do occur, they are non-specific. This means that clinical diagnosis is impossible based upon symptoms alone, and it requires fraudulent PCR and antibody tests as a means of obtaining an “accurate” diagnosis.
As this very familiar story of “viruses” jumping from animals to humans resulting in “different” diseases with non-specific symptoms is repeated over and over again, let’s turn our attention to the original study that brought this latest retelling to the world’s attention to see if there is any scientific validity to it. I will interject commentary throughout the study in order to highlight certain points, beginning with the summary. You will see from the very start that this study is based upon a relatively small sample size as it is limited to the first three people who died during the 1999 outbreak. Blood and cerebrospinal-fluid (CSF) samples that were taken before death were cultured for “viruses” as well as tested for antibodies to “viruses.” Thus, we are not dealing with any attempts to actually purify and isolate the assumed “viral” particles directly from the fluids of these three men. The researchers assumed a “virus” was present in the blood and CSF and attempted to create the “virus” through cell culture. They then used antibody testing to claim that their new cultured “virus” was related to the Hendra “virus” as there was a cross-reaction. The symptoms experienced by all three men were non-specific, and consisted of fever, headache, and altered level of consciousness. Inclusion bodies “likely to be of viral origin” were noted in neurons near vasculitic blood vessels. From these results, the researchers concluded that they had discovered a Hendra-like “virus” stemming from direct contact with pigs that was the cause of the outbreak.
Fatal encephalitis due to Nipah virus among pig-farmers in Malaysia
Summary
Background Between February and April, 1999, an outbreak of viral encephalitis occurred among pig-farmers in Malaysia. We report findings for the first three patients who died.
Methods Samples of tissue were taken at necropsy. Blood and cerebrospinal-fluid (CSF) samples taken before death were cultured for viruses, and tested for antibodies to viruses.
Findings The three pig-farmers presented with fever, headache, and altered level of consciousness. Myoclonus was present in two patients. There were signs of brainstem dysfunction with hypertension and tachycardia. Rapid deterioration led to irreversible hypotension and death. A virus causing syncytial formation of vero cells was cultured from the CSF of two patients after 5 days; the virus stained positively with antibodies against Hendra virus by indirect immunofluorescence. IgM capture ELISA showed that all three patients had IgM antibodies in CSF against Hendra viral antigens. Necropsy showed widespread microinfarction in the central nervous system and other organs resulting from vasculitis-induced thrombosis. There was no clinical evidence of pulmonary involvement. Inclusion bodies likely to be of viral origin were noted in neurons near vasculitic blood vessels.
Interpretation The causative agent was a previously undescribed paramyxovirus related to the Hendra virus. Close contact with infected pigs may be the source of the viral transmission. Clinically and epidemiologically the infection is distinct from infection by the Hendra virus. We propose that this Hendra-like virus was the cause of the outbreak of encephalitis in Malaysia.
The researchers stated that, as this outbreak occurred amongst people in close contact with pigs, the differential diagnoses included Japanese encephalitis. The Japanese encephalitis “virus” is said to come from mosquitoes that feed on “infected” pigs, and the disease shares the same non-specific symptoms observed in the farmers. However, they decided that this was not Japanese encephalitis for a few reasons.
- Infection was predominantly in adults rather than children
- There were clustering of cases in members of the same household
- There was a high proportion of patients in direct contact with pigs as opposed to other individuals living in the same neighbourhood, which is claimed as evidence against a mosquito-borne disease
- A history of illness in the pigs belonging to affected farmers
- The fact that many patients have had previous immunization against Japanese encephalitis
This previous immunization to Japanese encephalitis “virus” is presented as a main reason for the conclusion that the non-specific symptoms experienced in these cases belong to a new “virus” rather than the one that these farmers were immunized against. Creating new “viruses” that bring about the same disease is how they are able to keep the myth that the vaccines are effective against the previous “virus” alive.
Introduction
Between February and April, 1999, there was a severe outbreak of viral encephalitis among pig-farmers in the Bukit Pelandok area in Negri Sembilan state, Malaysia, that affected more than 200 individuals. 91 patients from the outbreak area were admitted to the University of Malaya Medical Centre, Kuala Lumpur, and there were 28 deaths. Because this outbreak occurred among people in close contact with pigs, the differential diagnoses included Japanese encephalitis. Features that distinguished this outbreak from Japanese encephalitis included: infection predominantly in adults rather than children; clustering of cases in members of the same household, which suggests an infection with high disease attack rate (as opposed to the Japanese-encephalitis virus which causes symptomatic encephalitis in one in 300 of those infected); a high proportion of patients in direct contact with pigs as opposed to other individuals living in the same neighbourhood (evidence against a mosquito-borne disease); a history of illness in the pigs belonging to affected farmers; and the fact that many patients have had previous immunisation against Japanese encephalitis.
The researchers planted the seed that there is a connection to pigs as all three farmers had a history of direct contact with the animals. Interestingly, the fact that all three patients had received multiple vaccines against the Japanese encephalitis “virus” was once again highlighted. For patient 1, he had received two doses of Japanese-encephalitis vaccine, with the second dose said to be more than a month before the onset of illness. Patient 2 had received three doses of Japanese-encephalitis vaccine with the last dose being 3 weeks before the onset of illness. Patient 3 had received two doses of Japanese-encephalitis vaccine, with the second dose 1 month before admission to the hospital. Thus, we can see that all three men had multiple and recent vaccinations against Japanese encephalitis. Unsuprisingly, the Japanese encephalitis vaccine is linked to every symptom these patients experienced, including encephalitis.
Interestingly, the Nipah outbreak was originally assumed to be Japanese encephalitis, and there were “confirmed” cases of the JE disease right before Nipah, which ultimately led to a local program of vector control against mosquitoes as well as an immunization campaign against the JE “virus.” However, it is apparent that neither the potential environmental toxicity from the vector control programs nor the JE vaccine were ever looked at as potential causes for the symptoms experienced by the three farmers or anyone else during the outbreak. Instead, the vector control was ignored and the vaccine was used as an excuse not to blame the Japanese encephalitis “virus” as the potential cause, as well as to justify the existence of a brand new “virus.”
We report on the first three fatal cases seen at our hospital. All three patients were farmers with a history of direct contact with pigs.
Case reports
Patient 1
This 51-year-old man was admitted to hospital with fever (2 days since onset), acute confusion (1 day), and pain associated with myoclonus in the left arm. He had received two doses of Japanese-encephalitis vaccine, the second dose more than a month before onset of illness. On admission, his temperature was 38°C and he was disoriented. The patient’s pupils were reactive, and doll’s eye reflex was present. There was no focal limb weakness and no meningism. Examination of the heart and lungs showed no abnormalities, and chest radiographs were normal. Brain computed tomography (CT) scan was normal. Cerebrospinal fluid (CSF) examination showed a pressure of 13 cm water, no white blood cells, glucose concentration of 46 mmol/L, and protein concentration of 0·6 g/L. The next day his condition deteriorated; there were signs of deepening coma and flaccid tetraparesis and he needed mechanical ventilation. Electroencephalography (EEG) showed continuous diffuse slow waves with bitemporal independent sharp waves. Intravenous aciclovir was started empirically. Persistent tachycardia and high blood pressure (maximum 230/122 mm Hg) were noted despite sedation with intravenous midazolam and propofol infusion. He deteriorated further and on day 6 had pinpoint unreactive pupils and no doll’s eye reflex. The patient developed hypotension and bradycardia and died.
Patient 2
This 34-year-old man was admitted with fever (3 days since onset) drowsiness, and lethargy, but without headache. He had received three doses of Japanese-encephalitis vaccine, the last being 3 weeks before onset of illness. A month before his illness, some of the patient’s pigs became ill and died suddenly. On admission he was oriented but drowsy, and his temperature was 38°C. Examination of the lungs showed no abnormalities, and chest radiography was normal. Blood pressure ranged from 130/70 mm Hg to 170/95 mm Hg with a heart rate of 100–160 beats per min. There were no focal neurological deficits and no neck stiffness. The patient refused lumbar puncture. He remained febrile and became comatose 2 days after admission, only responding to painful stimuli with facial grimacing. He developed jerking of the abdominal wall and right leg; this feature suggested segmental myoclonus. The patient was intubated and ventilated. EEG showed continuous diffuse slow waves with intermittent bitemporal sharp waves. The next day the doll’s eye reflex was absent but his pupils remained reactive. He did not improve, and on day 7 developed hypotension (unresponsive to fluid and inopressor therapy) and died. A CSF sample was obtained at necropsy.
Patient 3
This 52-year-old man was admitted after having headache and nausea for 14 days, and fever and chills for 7 days. He had received two doses of Japanese-encephalitis vaccine, the second 1 month before admission to hospital. At presentation he was alert and conscious but had horizontal nystagmus to the left. No other focal neurological abnormalities were noted. Examination of the lungs showed no abnormalities, and the chest radiographs were normal. Blood pressure ranged from 122/76 mm Hg to 200/70 mm Hg with a heart rate range of 100–127 beats per min. CSF examination showed a pressure of 16 cm water, white blood cell count of 720 per L (88% lymphocytes), glucose concentration of 4·0 mmol/L, and protein 1·75 g/L. 2 days later his consciousness deteriorated and mechanical ventilation was started. On the next day he had no doll’s eye reflex, although his pupils remained reactive. EEG showed continuous diffuse slow waves. He did not improve and died 5 days after admission.
In the histopathological examination, it was stated that many neurons adjacent to vasculitic vessels had eosinophilic cytoplasmic and nuclear “viral” inclusions as seen in the brain with other “paramyxovirus infections.” These aggregates of proteins were taken as an indicator by the researchers that they were dealing with a “virus.” However, it is well-known that inclusion bodies are not specific to “viruses” and can be found in those without a “viral” disease. They are also not found in all cases of a particular disease, found in those without the disease, and are even found in uninoculated cell cultures, as seen with RSV. In fact, a 1941 paper by Alfred M. Lucas stated that the “existence of an object which appears to be an inclusion body is not proof of the presence of a virus but merely an indication that a virus should be considered if no bacterial agent can be found.” In other words, inclusion bodies are nothing but non-specific indirect evidence used to infer an assumed “virus.” Thus, the finding of inclusion bodies is essentially meaningless as a specific sign of the presence of a “virus.” Perhaps this is why the authors stated in the opening summary that the inclusion bodies observed were only “likely to be of viral origin.”
Findings
Histopathology
Samples from all three patients showed similar histological findings of endothelial damage and vasculitis (mainly in arterioles, capillaries, and venules, although these features were also seen in some large muscular arteries). The brain was the most severely affected organ, but other organs including the lung, heart, and kidney were also affected. Vasculitic vessels were characterised by vessel-wall necrosis, thrombosis, and inflammatory-cell infiltration of neutrophils and mononuclear cells (figure 1). Syncytial-cell formation was seen in the endothelium of affected blood vessels in the brain and lung, and in the Bowman’s capsule of the glomerulus (figure 2). Zones of microinfarction and ischaemia were commonly found around or adjacent to vasculitic blood vessels.
In the brain, many neurons adjacent to vasculitic vessels had eosinophilic cytoplasmic and nuclear viral inclusions as seen with other paramyxovirus infections. Neuronophagia and microglial-nodule formation were noted in focal areas. Perivascular cuffing and meningitis were generally mild. There was no evidence of perivenous demyelination. The distribution of vasculitis and zones of microinfarction and ischaemia suggested a random process, equally affecting the grey and white matter of the cerebrum, basal ganglion, cerebellum, brainstem, and spinal cord. Overall, the main cause of death was widespread focal infarction of the brain and possibly direct viral infection of the neurons.
As stated previously, no attempts were made to purify and isolate the assumed “virus” directly from the blood and CSF of any of the patients. Unpurified cell cultures using Vero cells from the kidneys of African green monkeys was performed instead. No details were provided outlining the exact steps used to culture the “virus.” The researchers only performed culturing of the “virus” from 2 of the 3 patients due to fear of “infection” from patient 2, and only the culture from patient 1 gave a “strong positive reaction” with antibodies to Hendra “virus” by indirect immunofluorescence assay with hyperimmune mouse ascitic fluid. Based upon the use of fictional antibodies, it was decided that the results from this single patient was proof that the non-specific reaction meant that their new fictional “virus” was related to the old fictional Hendra “virus.” The researchers stated that preliminary nucleotide-sequence studies showed that the Nipah “virus” was a new “paramyxovirus.” The “viruses” associated with measles, mumps, respiratory syncytial “virus,” and other respiratory diseases are said to also belong to this family.
Virology
A virus causing rapid syncytial formation on vero-cell cultures (ATCC, CCL81) was isolated from the CSF of patients 1 and 3 on day 5 of inoculation (figure 3). The infected vero cells in patient 1 gave a strong positive reaction with antibodies to Hendra virus by indirect immunofluorescence assay with hyperimmune mouse ascitic fluid. The infected cells did not stain by indirect immunofluorescence assay with specific monoclonal antibodies against respiratory viruses (adenovirus, influenza A, influenza B, parainfluenza 1–3, respiratory syncytial virus, and measles virus), enteroviruses (coxsackievirus A and B, echovirus, and enterovirus 70 and 71), human herpesviruses 1, 2, and 5, and Japanese-encephalitis virus, and other flaviviruses. The result indicates that the virus is related to Hendra virus.
Preliminary nucleotide-sequence studies show that this virus, now called Nipah virus, is a new paramyxovirus related to but distinct from Hendra virus.
We did not attempt to isolate the virus from the CSF of patient 2 because of concerns about laboratory-acquired infection. At some stage of the illness, all three patients had IgM antibodies against Hendra viral antigens by IgM capture ELISA in CSF (table). In patient 3, the appearance of specific IgM against the virus in the serum preceded the IgM response in the CSF. IgM antibodies against the Japanese-encephalitis virus were not detected in the serum or CSF of any of the three patients.
The researchers attempted to make the case that, based upon their 3 patients, the disease caused by their Nipah “virus” was distinct from the Hendra “virus” because Nipah came from pigs, while Hendra came from horses. They might as well have just claimed that the “viruses” were different because Nipah was Malaysian while Hendra was Australian. The researchers also tried to differentiate the “viruses” based upon symptoms that were seen in 3 cases of Hendra against those that were seen in the 3 cases of Nipah. They concluded that Hendra had respiratory involvement and only one case of encephalitis while Nipah was primarily a central-nervous system disease with no pulmonary involvement. However, according to the CDC, both Hendra and Nipah are respiratory diseases with the same non-specific symptoms that can lead to encephalitis.
While the researchers stated that the histological features of Nipah in the brain are distinct from those as seen in cases of measles, it was admitted that there are some similarities to Hendra “virus” encephalitis. The researchers believed that the neurological dysfunction seen in their 3 patients was the result of widespread focal ischemia or infarction in the brain and direct neuronal “infection,” which they felt was suggested by the presence of the non-specific finding of the inclusion bodies that were claimed to be “paramyxoviral.”
Discussion
The virus implicated in this outbreak is related to but distinct from the Hendra virus. Clinically and epidemiologically the disease in our three patients differed from the previously described Hendra-virus infection. Hendra virus was transmitted from horses, and two of the three reported patients with Hendra infection had respiratory involvement, with only one patient showing a severe meningoencephalitis. In our patients, however, the infection involved direct contact with pigs and predominant central-nervous-system disease with no clinical or radiological evidence of pulmonary involvement.
The features of the brain in this illness are distinct from other disorders in that there is clear histological evidence of necrotising vasculitis and syncytial formation in all cases, which is not found in postinfectious encephalomyelitis, including measles, or in many primary viral encephalitides, including measles. However, there are some similarities to Hendra virus encephalitis.
Our patients had widespread central-nervous-system disease due to severe vasculitis of mainly small blood vessels that resulted in endothelial damage. This damage in turn caused thrombosis and ischaemia or infarction in areas supplied by these vessels. We believe that the neurological dysfunction seen in these patients was the result of widespread focal ischaemia or infarction in the brain and direct neuronal infection, suggested by the presence of paramyxoviral inclusion bodies. Lung, kidney, and heart involvement were also noted but were not severe enough to be clinically significant.
The incubation period of the illness in our patients was short (up to a month; patient 2 reported that some of his pigs were ill and many died about 1 month before his illness). The main presentation was fever with headache followed by a rapid deterioration in consciousness. Segmental myoclonus was seen in two of three patients. No generalised or focal seizures were seen. A notable feature was hypertension associated with tachycardia, which suggested dysfunction of the medullary vasomotor centre. Brainstem signs occurred with deepening coma, impaired doll’s eye reflex, and pupillary abnormalities, and were followed rapidly by death.
The Nipah virus described here may be the agent responsible for the encephalitis outbreak in Malaysia.
https://www.jstor.org/stable/4483084
In Summary
- Nipah is said to be a rare but serious bat-borne “virus” that can cause fever, vomiting and respiratory infections in humans, with severe cases can involve seizures and encephalitis – inflammation of the brain – and result in a coma
- The “virus” is claimed to have a fatality rate between 40-75%, according to the World Health Organization (WHO)
- It has no known vaccine, and the usual treatment is to provide supportive care
- The first Nipah outbreak was recorded in 1998 after the “virus” spread among pig farmers in Malaysia and Singapore
- It is said to “infect” humans directly through contact with the bodily fluids of infected bats and pigs
- Flying foxes are the natural carriers of the “virus” and it is claimed that they contaminate fruit from urinating on them while sitting in trees
- Nipah is said to be a type of “henipavirus” that is related to Hendra “virus,” which was first “discovered” in Australia in humans and horses
- The first Nipah outbreak in 1998 “infected” nearly 300 people in Malaysia, killing more than 100, and prompted the culling of one million pigs in an effort to contain the “virus”
- Since then, the disease has mainly been recorded in Bangladesh and India
- Only 600 cases of Nipah “virus“ human infections were reported between 1998 to 2015, according to WHO data
- In other words, it appears the vast majority of Nipah “infections” (300) were recorded in 1998, with very few cases ever since
- According to the CDC, Nipah must be diagnosed via either RT-PCR or antibody testing
- Early diagnosis of NiV infection can be challenging due to the non-specific early symptoms of the illness
- “Infections” that lead to symptoms and sometimes death much later after exposure, known as dormant or latent “infections,” or otherwise referred to as ASYMPTOMATIC “infections, have also been reported months and even years after exposure
- The WHO agreed with the CDC in that human “infections” range from asymptomatic “infection” to acute respiratory infection (mild, severe), and fatal encephalitis
- The WHO provided a list of non-specific symptoms including:
- fever
- headaches
- myalgia (muscle pain),
- vomiting
- sore throat
- They state that these non-specific symptoms can be followed by:
- dizziness
- drowsiness
- altered consciousness
- neurological signs that indicate acute encephalitis
- Some people can also experience atypical pneumonia and severe respiratory problems, including acute respiratory distress
- Encephalitis and seizures only occur in severe cases
- The WHO claims that the incubation period (interval from “infection” to the onset of symptoms) is believed to range from 4 to 14 days, with incubation periods as long as 45 days have been reported
- This creates a conflict between the WHO reporting an incubation period of 45 days whereas the CDC states it can last years
- The WHO states that initial signs and symptoms of Nipah “virus” infection are nonspecific, and the diagnosis is often not suspected at the time of presentation
- This is said to hinder “accurate” diagnosis and creates challenges in outbreak detection, effective and timely “infection” control measures, and outbreak response activities
- The quality, quantity, type, timing of clinical sample collection, and the time needed to transfer samples to the laboratory can affect the accuracy of laboratory results
- While they are the “natural” host, there is no apparent disease in fruit bats
- The “virus” is claimed to be highly contagious in pigs
- However, an “infected” pig can exhibit no symptoms
- Mortality is low except in young piglets
- The symptoms are not dramatically different from other respiratory and neurological illnesses of pigs
- The researchers reported findings for the first three patients who died
- The three pig-farmers presented with non-specific symptoms such as fever, headache, and altered level of consciousness
- Blood and cerebrospinal-fluid (CSF) samples taken before death were cultured for “viruses,” and tested for antibodies to “viruses’
- A “virus” causing syncytial formation of vero cells was cultured from the CSF of two patients after 5 days
- They did not attempt culturing from patient # 2
- The “virus” stained positively with antibodies against Hendra “virus” by indirect immunofluorescence, and IgM capture ELISA showed that all three patients had IgM antibodies in CSF against Hendra “viral” antigens
- In other words, the Hendra “virus” antibodies were not specific and cross-reacted with the Nipah “virus”
- Inclusion bodies likely to be of “viral” origin were noted in neurons near vasculitic blood vessels
- Based on the indirect evidence obtained from cell culture and antibody responses, they determined that the causative agent was a previously undescribed “paramyxovirus“ related to the Hendra “virus“
- Close contact with “infected” pigs may be the source of the “viral” transmission
- They claimed that, clinically and epidemiologically, the “infection” is distinct from “infection” by the Hendra “virus”
- The researchers proposed that this Hendra-like “virus” was the cause of the outbreak of encephalitis in Malaysia
- Because this outbreak occurred among people in close contact with pigs, the differential diagnoses included Japanese encephalitis
- However, they decided that this was not Japanese encephalitis for a few reasons:
- Infection was predominantly in adults rather than children
- There were clustering of cases in members of the same household
- There was a high proportion of patients in direct contact with pigs as opposed to other individuals living in the same neighbourhood, which is claimed as evidence against a mosquito-borne disease
- A history of illness in the pigs belonging to affected farmers
- The fact that many patients have had previous immunization against Japanese encephalitis
- Paient # 1 had received two doses of Japanese-encephalitis vaccine, the second dose more than a month before onset of illness
- Patient # 2 had received three doses of Japanese-encephalitis vaccine, the last being 3 weeks before onset of illness
- Patient # 3 had received two doses of Japanese-encephalitis vaccine, the second 1 month before admission to hospital
- All of the symptoms experienced by the three patients are listed as side effects from the Japanese-encephalitis vaccine
- In the brain, many neurons adjacent to vasculitic vessels had eosinophilic cytoplasmic and nuclear “viral” inclusions as seen with other “paramyxovirus infections”
- Inclusion bodies are non-specific and regularly found in “non-viral” cases of disease
- Overall, the main cause of death was widespread focal infarction of the brain and possibly direct “viral” infection of the neurons
- The researchers claimed that Nipah was different from Hendra as Hendra was transmitted from horses, and two of the three reported patients with Hendra “infection” had respiratory involvement, with only one patient showing a severe meningoencephalitis
- In the 3 Nipah patients the “infection” involved direct contact with pigs and predominant central-nervous-system disease with no clinical or radiological evidence of pulmonary involvement
- However, contrary to this report, both diseases share the same symptoms, with the only difference being the transmitting animal
- The researchers do admit that there are some similarities to Hendra “virus” encephalitis
- They conclude that the Nipah “virus” that they described may be the agent responsible for the encephalitis outbreak in Malaysia
As can be seen by the last sentence of the paper, the researchers concluded that their Nipah “virus” may be the agent responsible for the Malaysian outbreak. Why could the researchers not state for certain that they had discovered the causative agent? This is because the paper offered no such scientific evidence that the researchers had proven anything of the sort. They were working with a small sample size in just 3 patients. There was no attempt whatsoever to try and find the particles assumed to be the “virus” directly in the blood and CSF of any of the patients via the accepted purification methods. In fact, there were no electron microscope images of any kind showing that any new “virus” was discovered.
Instead, as is always the case, the researchers relied on indirect evidence in an attempt to infer the presence of a new “virus.” They cultured their “virus” by adding the unpurified fluids taken from only 2 of the 3 patients and added them to the kidney cells of an African green monkey. Presumably, they used “viral” transport medium of some kind as well as antibiotics, antifungals, and other chemicals/nutrients. We do not know for certain what the exact recipe was as the methods were not detailed. This concoction was mixed together and incubated for days until some sort of cytopathogenic effect (CPE) was observed. On this basis, they claimed that a ‘“virus” was present. No controls of any sort were ever mentioned as having been performed.
On top of this, the researchers used these culture fluids and mixed them with hyperimmune mouse ascitic fluid and claimed, via by indirect immunofluorescence assay, that their scientifically unproven antibodies, said to be specific to the Hendra “virus,” had cross-reacted to the fictional “virus” assumed to be present within the culture fluids. Also, as already pointed out, the researchers relied on the non-specific findings of inclusion bodies in the brain claimed to be similar to “paramyxoviruses” as evidence for the presence of a “virus.” Thus, they could claim that they had a related, but distinct, new “viral” cause without ever directly demonstrating that one ever existed.
What was strikingly missing from this paper announcing the discovery of a new “virus” was any attempt whatsoever to demonstrate pathogenicity naturally with animal experiments via the steps of the scientific method. Perhaps this is because the researchers had no “virus” to actually work with in order to vary and manipulate during experimentation. As the CDC admitted to Christine Massey FOIs on November 21st, 2021, there are no records of any purified and isolated Nipah “virus.”
Thus, the researchers had no valid independent variable, i.e. the assumed “viral” particles thought to cause disease, that could be used to demonstrate the dependent variable, i.e. the effect, or symptoms said to be associated with the disease. As they had no purified and isolated “viral” particles to experiment with as well as no demonstration of recreating the disease experimentally via the scientific method, there is no scientific evidence proving the existence of a pathogenic entity known as the Nipah “virus.” All we have is the same indirect pseudoscientific evidence seen time and time again for the same symptoms of disease classified under a new brand name that can be utilized to instill fear in the unaware whenever the need arises.
Bottom line:
Don’t be fooled by the bat-Nipah’s.
This article originally appeared on ViroLIEgy’s Antiviral Substack.
ViroLIEgy 
How did they come up with a PCR test?
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