“What is now proved was once only imagin’d”
It’s kind of ironic that the above William Blake quote headlined the Rockefeller University’s Research Profile on Simon Flexner seeing how everything virology claims to have “proven” amounts to nothing but pure imagination. Simon Flexner, brother of Abraham Flexner of the infamous Flexner Report, was the first director of the Rockefeller Institute for Medical Research. He is also one of the original trustees of the Rockefeller Foundation. If you are unaware of why this matters, I implore you to research the Rockefeller’s substantial influence on shaping the modern medical system and how the 1910 Flexner Report by Abraham Flexner was used to hijack the medical educational system in America. Unfortunately, it is far too much to delve into here and I plan to do a post sometime in the future breaking this all down. In the meantime, for a nice brief overview, this is a good resource:
In 1910, Simon Flexner (the Flexner bros were busy that year) provided a shining example of the incredibly horrific lengths virology went to in order to “prove” an invisible “virus” was the cause of Polio. The 31-page paper presents an in-depth look at how virologists tried to experimentally recreate the symptoms of Polio seen in humans by grinding up spinal cords and other tissues from deceased children and monkeys which were then injected into the brains and bodies of monkeys and other unfortunate animals. This is a long read and I had to edit some sections out. I provided the most relevant highlights but I do recommend reading the entire paper if the chance arises:
EXPERIMENTAL EPIDEMIC POLIOMYELITIS IN MONKEYS
Up to the present time there has existed no convincing knowledge of the nature of the agent causing epidemic poliomyelitis. Various bacteria and especially certain cocci 6 have from time to time been isolated in cultures from fluids obtained by lumbar puncture from patients suffering from epidemic poliomyelitis, or from specimens of the central nervous system removed at autopsy. These bacteria did not conform to one species or group of microorganisms and did not suffice to set up poliomyelitis in animals. They can be accounted for more satisfactorily as contaminations or secondarily invading bacteria than as the cause of the disease.“
Our studies are limited to the two epidemics which affected New York and vicinity in I907 and I909. In I907, one of us (Flexner) studied in various ways a number of fluids, obtained by lumbar puncture, from cases in different stages of the disease. The cellular nature, proteid strength, bacteriological content, and infectivity were investigated. The lymphocytes were increased in number, the proteid was not markedly increased, and aerobic and anaerobic cultivations were, as a rule, unsuccessful. Rarely, bacteria were present in the fluid; but the bacteria were not of uniform species. The fluids, obtained by lumbar puncture, were injected into laboratory animals, including monkeys, but without setting up any recognizable pathological condition. During the epidemic of I907, we did not secure organs from a case of pure infantile paralysis and we failed, therefore, in our intention to inoculate monkeys from the spinal cord.
In September I909, we secured the spinal cord from two cases of infantile paralysis in human beings. For these valuable specimens we are indebted to Dr. Ridner, of Lake Hopatcong, N. J., and Dr. Le Grand Kerr, of Brooklyn, N.Y. Dr. Ridner’s patient died on the fifth or sixth day following the appearance of the paralysis, which affected the legs. The lumbar cord was obtained in
a sterile condition, twenty-six hours after death, and employed for inoculation of animals. Dr. Kerr’s patient had been widely paralyzed and died on the fourth day of the disease. The lesions in the cord were wide-spread and severe and affected gray matter and white. The entire spinal cord was obtained twelve hours after death and inoculated into animals four hours later.
In order to favor the transmission of the disease to monkeys, we chose the brain as the site of inoculation, which was made under ether anesthesia, through a small trephine opening. After the operations, the animals were at once lively and normal. The injected material consisted, first, of emulsions in salt solution of the spinal
cord from the children and, later, of emulsions and filtrates from the spinal cord and other organs from the monkeys developing paralysis.
Before proceeding to a detailed account of our experiments and results, it is desirable to review two publications, which immediately preceded ours, dealing with the experimental production of poliomyelitis. The first and more important is the report of Landsteiner and Popper, which appeared in the summer of I909, and which marks the beginning of the new era in the study of epidemic poliomyelitis.
The material employed for inoculation of two monkeys consisted of the emulsified spinal cord in salt solution obtained from a child nine years old, who died on the fourth day of attack from infantile paralysis. The emulsion was injected into the peritoneal cavity of the monkeys. One of the latter became severely sick on the sixth day and died on the eighth day after inoculation. The other monkey became paralyzed on the seventeenth day and was killed on the nineteenth day after inoculation. The spinal cord of the first monkey was not used for further inoculation, while that from the second monkey was used to inoculate, probably by intraperitoneal injection, two other monkeys that did not, however, develop the symptoms of the disease. Apparently they were unaffected by the injection.Landsteiner and Popper, Zeit. f. Immunitiitsforsch., Orig., 1909, ii, 377.
“Owing to their inability to transmit the disease from one monkey to another, Landsteiner and Popper discuss the three following possible explanations of the failure, namely: (1) whether the disease in the first monkey was caused by a transferred poison or by the infectious agent; (2) whether a successful transfer from monkey to monkey might not have been secured had the cord of the monkey, dying on the sixth day of the disease, been used; and (3) whether the infectious agent may not have become attenuated in virulence in its passage through the monkey and thus have lost its power of further transmission. They inclined to the last explanation.
At the time our studies of 1909 were begun, we were familiar with the foregoing publication; but before our first report n appeared in print, a second account of a successful transfer of poliomyelitis to a monkey was published from Vienna, whence the first appeared, by Knoepfelmacher. 1-0
On December 22, 1908, 14 hours post-mortem, the spinal cord was removed from a child of one year, who had died on the sixth day of the disease, and 10 centimeters of the cervical portion, after emulsification in salt solution, were injected into the peritoneal cavity of a Macacus rhesus. The first evidence of sickness was noted on the eighth day, and the first evidence of paralysis on the twelth day, after the inoculation. On the fourteenth day the animal was killed with chloroform and 10 centimeters of the spinal cord were rubbed up in salt solution and the emulsion was injected into a second monkey (presumably by way of the peritoneum) which was unaffected. The anatomical and histological findings agreed with those described by Landsteiner and Popper.l=Knoepfelmacher, Med. Klin., 19o9, v, I67I. Strauss and Huntoon (New York Med. Jour., 191o, xci, 64) have since reported a successful intraperitoneal inoculation of a monkey and failure to transmit the disease further.
We have observed with care the monkeys inoculated successfully with the virus of epidemic poliomyelitis and have classified them into groups according to the symptoms recognized. The description to be given is based upon a study of 81 monkeys w.hich became infected with the virus.
Iucubation Period.–The incubation period has been taken to be the interval elapsing between the time of inoculation and the appearance of the first definite paralysis. During this interval certain other clinical manifestations of illness may be noted and these will be considered separately as prodromal symptoms. The latter besides being inconstant call frequently for the exercise of personal judgment for their detection and hence they can be defined less accurately than the paralysis. In several instances the monkeys fell ill and died without paralysis having occurred or been noted. These animals were included among the series of successful inoculation only when the typical lesions were present in the nervous system. The incubation period in them was calculated from the inoculation to the onset of definite symptoms of illness.
The shortest period thus far noted as elapsing between the inoculation and the onset of paralysis has been 4 days and the longest period, 33 days. The average period has been 9.82 days. The number of animals developing paralysis after the twelfth day was 16, and the number developing paralysis before the eighth day was 18. Hence the extremes of the incubation period are probably simple variations from a mean which represents the activity of the virus for monkeys. We possess some evidence that the virus may suffer, in certain strains, an enduring alteration through which its activity is diminished. When the site chosen for inoculation is some other than the brain, or the material used some other than an emulsion of the spinal cord, the incubation period has not usually been at either extreme period.
Prodromal Signs.—The inoculation of the virus into the brain or other parts produces no immediate effects. As soon as the effects of the anesthetic disappear, the monkeys appear normal. This condition persists until a period of from six to forty-eight hours before the onset of paralysis when certain abnormal signs may be noted. The animals become nervous and excitable; on being disturbed and made to move about the cages, they tire quickly; a tremor of the head, face or limbs develops; when the attention can be attracted the gaze is shifting, rather than fixed as in the normal monkey, and the face is wrinkled and mobile rather than smooth and placid; the hairs are erected somewhat, and the animals prefer to remain quiet. All these symptoms are almost never noted in a given animal and they occur in varying combinations. The temperature does not rise constantly during the incubation period and gastro-intestinal symptoms rarely occur. A few animals have shown diarrhoea but this condition may well have been a coincidence.”
“Concomitantly with the appearance of paralysis of any large muscle group, other muscle groups are found either weak or partially paralyzed. The exceptions to this rule are present among the cases of slight affection. The onset of symptoms in the bulbar or cerebral group has not been the same in any two cases, and death has occurred before the developments of flaccid paralysis. The striking features of the cases have been spasticity of the limbs, marked incoordination resulting in violent pseudo-convulsions; epileptiform convulsions with tonic and clonic muscle-spasms; and, finally, sudden death of apoplectiform type. Death has occurred within thirty minutes of the first appearance of cerebral symptoms.”
“Termination.–This division of our subject cannot be discussed with the completeness of the other sections. Since the main object of our study required that we maintain an active virus, we have been obliged to sacrifice a considerable number of the affected animals within twenty-four to forty-eight hours of the onset of the paralysis.
The affected monkeys may recover. When this happens, the paralysis reaches a maximum, becomes stationary, and then recedes more or less. When the affection has been severe, the animals appear sick for several days, but when recovery commences the general symptoms of sickness quickly disappear. The muscles which were weak, but not definitely paralyzed, regain strength. Hence, the actual paralyses are more sharply demarcated. Although the
variations are considerable, it happens that within a week of a severe or critical state the animal has regained health and general strength, except for the actually paralyzed muscles. In other instances, two or three weeks have not sufficed for the restoration of strength to muscles apparently intact. In some instances in which the paralysis affecting a single limb appeared to be complete, it has entirely disappeared within a few weeks.
When paralysis has been marked it usually persists. There has not yet been sufficient time to show what the end result of these cases will be; but present indications, based on several animals paralyzed from three to ten weeks, are that further recovery will be very slow and incomplete. Within a month or so, the paralyzed limb tends to stiffen and to contract, the kind of contracture depending somewhat upon the position assumed by the paralyzed limb in the meantime.
The animals may die. When the first force of the affection is exerted upon the medulla, death may occur within a short time of the first appearance of symptoms. When the limbs are first affected, the progress and extension of the paralysis may be very rapid and death be caused quickly through involvement of the medulla. Again, the progress may be slow and the prostrated animal may gradually grow weak and die after one or several days. When the period of disease is prolonged, then other factors, such as secondary infections and general nutritive and trophic disturbances, must be considered.
The accompanying table exhibits the mortality in the cases considered in this paper. It requires a few words of explanation, since, while a part of the recoveries and deaths noted are facts, another part are surmises. Each set is clearly indicated. The necessity for this division has been explained already and was caused by the need of maintaining an active virus for inoculating other animals. We are of the opinion that we have put the number of probable recoveries rather too high, but this was done to avoid over-statement of the probable fatality of experimental poliomyelitis in monkeys. When the probable outcome of certain sacrificed animals could not be predicted, the animals were excluded from the tabulation.
From the figures given it follows that in 54.3 percent of the monkeys, in this series, which developed poliomyelitis, the issue would in all probability have been fatal. Hence, the experimental disease is more highly fatal than is the spontaneous disease in human beings.”
“Gross lesions of the brain have been observed rarely. In a few instances, hemorrhages along the needle-track have been present, but they were of traumatic origin and are not to be regarded as part of the pathological anatomy of the experimental disease. In one or two instances, small Cysts with clear contents were found at the inoculation-site long after the operation. They gave rise to no symptoms. The substance of the brain has been excessively moist in some instances; and in a few cases yellowish dots, not clearly distinguishable, have been noted which, on microscopic study, proved to be areas of necrosis. There occurred, a few times, small subdural hemorrhages, present on one or both sides.”
“To resume, therefore, the lesions in the spinal cord and medulla of the monkeys, visible to the naked eye, consist of congestion and hemorrhage into the gray matter chiefly, but not exclusively confined to the anterior horns. The general appearances of the spinal cord, medulla and brain are not greatly altered, and the visible effects are no proper measure of the damage inflicted by the virus.“
AVENUES AND SOURCES OF INFECTION.
“The intracerebral mode of infection is not the only successful one. It has been determined that the virus of epidemic poliomyelitis when introduced into the body by means of the blood, subcutis, peritoneum, spinal canal and large nerves, tends to localize in the spinal cord and brain and set up the specific lesions, in the same manner as when injected into the brain. It remains to be determined whether these several routes give uniformly as good results as the intracerebral route. Our impression is that infection is readily accomplished by way of the subcutis and less readily by way of the peritoneal cavity. We have made several unsuccessful attempts to produce infection through intratracheal inoculation and by feeding. But the number of experiments will have to be considerably greater before a final conclusion can be ventured on these points. On the other hand, it has been shown that the cerebrospinal fluid, at the beginning of the paralysis, is capable when injected into the brain, of setting up paralysis in other animals. Hence at this period, at least, this fluid contains the virus.
The blood contains the virus at the beginning of the infection, but how richly has not been accurately determined. As little as two cubic centimeters may fall to cause infection while as much as twenty has caused typical paralysis.“
“The naso-pharyngeal muscosa also contains the virus. The excised membrane, including the tonsils and turbinate mucosa, on being rubbed up with quartz sand, macerated and filtered, yielded a fluid which, on being injected into the brain, caused paralysis. Thus far infection has not been secured with the spleen, bone-marrow, liver or retro-vertebral glands.
NATURE AND RESISTANCE OF THE VIRUS.
Film preparations and sections prepared from the spinal cord of human beings and monkeys examined, prepared and stained in the most various ways, showed no parasites, either bacterial or protozoal, that could account for the infection. The readiness with which epidemic poliomyelitis could be transmitted to monkeys and the absence of visible and stainable parasites, early suggested the possibility that the infectious agent belonged to the minute filterable viruses. To determine this point, the spinal cords, removed from monkeys just paralyzed, were triturated with sterile quartz sand, thoroughly shaken, and pressed through a Berkefeld filter which had previously been tested and found bacteria-tight. These clear and bacteriologically clear filtrates have been used repeatedly to inoculate monkeys, both by the intracerebral and subcutaneous routes, and have regularly caused paralysis. From these paralyzed animals, the virus has been transferred to other monkeys, so that it can be asserted that the effects it produces are caused not by a filterable toxic substance but by a true virus or living micro6rganism.
It was because of the fact of the filterability of the virus that we succeeded in detecting the presence of the organism in the muscosa of the mouth and nose.
The clear fluids obtained by filtration when examined under the dark field microscope show innumerable bright, dancing points devoid of definite size and form and not truly motile. This fluid prepared and stained by means of Loeffler’s flagella stain shows minute particles of roundish or oval form which were absent from a similar filtrate prepared with the nervous system of a rabbit. That the particles represent the microorganism of poliomyelitis cannot be affirmed at present.“
“The parasite of epidemic poliomyelitis is, therefore, very minute and cannot, for the moment, be further classified, since the precise position among living things held by the filterable viruses has not been determined. At least one of these viruses, that of pleuro-pneumonia of cattle, has been cultivated artificially. An attempt has been made to cultivate the virus of poliomyelitis in test tubes.
The result has seemed to be successful, but it is still in doubt. What has thus far been determined is that the filtrates when added to bouillon prepared with human blood serum or ascitic fluid become clouded and retain their virulence for four days in the thermostat. The transfer of a fraction of a cubic centimeter of such turbid fluids to a second set of tubes may cause a turbidity to develop in them. The staining of these turbid fluids with Loeffler’s flagella stain brings out the oval or roundish particles in numbers. But thus far we have not induced paralysis by inoculating the culture fluid of the second or third transfer of the original virus.”
“Experimental poliomyelitis develops, as a rule, quickly and after an incubation period of only a few days. It is not probable, therefore, that protective inoculation can be accomplished, by way of the subcutis, that shall prevent the onset of paralysis after an intracerebral inoculation. We have made an unsuccessful effort to achieve such protection. Emulsions of active spinal cord, warmed to 55 ° to 57 ° C. for one hour or to 60 ° C. for one half hour were injected beneath the skin at the same time that a usual intracerebral injection of virus was given. The two monkeys employed in the experiment developed paralysis in the usual manner.”
VARIATION IN VIRULENCE OF THE VIRUS.
There is at present no reliable way of estimating the degree of activity of the virus since the number of organisms inoculated is not subject to control. The inoculated materials consisted of heavy suspensions in salt solution of the spinal cord, for preparing which portions from several levels were employed, or filtrates obtained from the suspensions, of which from two to four cubic centimeters were injected.”
“In this connection brief reference should be made to other species of animals employed for inoculation. Besides many guinea-pigs and rabbits, one horse, two calves, three goats, three pigs, three sheep, six rats, six mice, six dogs, and four cats have had active virus introduced in the brain but without causing any appreciable effect whatever. These animals have been under observation for many weeks. It remains to be discovered whether some of these species of animals may not after all be made to develop poliomyelitis by using directly spinal cord from many human cases, on the supposition that a virus of greater virulence may be found. We inoculated rabbits and guinea-pigs directly with each of the two specimens of human virus, and additional rabbits and guinea-pigs and the other animals with virus derived from monkeys.”
“The incubation period has been worked out on the supposition that the spontaneous disease in man is contagious. We observed no instance among our monkeys of a spontaneous transfer of the infection. However, we made no purposive experiments to test this point, and yet the inoculated and uninoculated animals were not kept carefully separate.“
“Experimental poliomyelitis in the monkey is a severe and highly fatal disease and exceeds in the latter respect the spontaneous disease in man.”
- Bacteria and other organisms were found in lumbar fluid and tissue fluids but were quickly determined not to be the cause of disease and were instead considered either contaminants or secondary invaders
- Fluids from lumbar puncture were injected into monkeys and other animals without any effect
- Spinal cords from deceased children were ground up and emulsified to be injected into the brains of monkeys
- The brain was chosen in order to favor transmission of disease to monkeys
- Owing to their inability to transmit the disease from one monkey to another, Landsteiner and Popper discuss the three following possible explanations of the failure:
- Whether the disease in the first monkey was caused by a transferred poison or by the infectious agent
- Whether a successful transfer from monkey to monkey might not have been secured had the cord of the monkey, dying on the sixth day of the disease, been used
- Whether the infectious agent may not have become attenuated in virulence in its passage through the monkey and thus have lost its power of further transmission
- They inclined (i.e. assumed) to the last explanation
- Emulsions of spinal cords and other organs from diseased monkeys were mixed together and injected into other monkeys
- The emulsified monkey goo did not make two other monkeys sick after being injected in their stomachs
- Studies by Landsteiner and Popper as well as Knoepfelmacher were unable to transfer disease from one monkey to another and the assumption was made that the “virus” lost virulence upon passages
- The description of the clinical features of Polio were based upon a study of 81 monkeys which became infected with the “virus”
- The incubation period was defined as the interval elapsing between the time of inoculation and the appearance of the first definite paralysis
- However, there were monkeys who became sick without paralysis which called frequently for the exercise of personal judgment for their detection and hence they could be defined less accurately than those with paralysis
- These animals without paralysis were included among the series of successful inoculation when the typical lesions were present in the nervous system upon autopsy
- Illness began anywhere from 4 days to 33 days after injection in the brain
- Flexner claimed to possess some evidence that the “virus” may suffer and its “virulence” is diminished
- When the site chosen for inoculation is something other than the brain, or the material used some other than an emulsion of the spinal cord, the incubation period has not usually been at either extreme period
- Symptoms were highly variable and were never noted to be in all monkeys
- The onset of paralysis symptoms in the bulbar or cerebral group was never the same in any two cases and death sometimes occurred before the developments of flaccid paralysis
- Monkeys would experience neurological symptoms with pseudo(?)-convulsions and death occurred within thirty minutes of the first appearance of cerebral symptoms
- Flexner stated that since the main object of the study required that they maintain an active “virus,” a considerable amount of affected animals were sacrificed within twenty-four to forty-eight hours of the onset of the paralysis
- However, he notes that the affected monkeys may recover and when this happens, the paralysis reaches a maximum, becomes stationary, and then recedes more or less
- In some instances in which the paralysis affecting a single limb appeared to be complete, it entirely disappeared within a few weeks
- Flexnera dmitted that while a part of the recoveries and deaths noted are facts, another part are surmises (i.e guesses)
- Death may occur within a short time of the first appearance of symptoms
- It was noted that with prolonged disease, factors other than a “virus” such as secondary infections or the nutritive state and trophic disturbances should be considered
- Flexner was of the opinion that they put the number of probable recoveries rather too high, but this was done to avoid over-statement of the probable fatality of experimental poliomyelitis in monkeys
- When the probable outcome of certain sacrificed animals could not be predicted, the animals were excluded from the tabulation
- The experimental disease in monkeys is more fatal than seen in man
- Upon examination of the brain, hemorrhages along the needle-track were present in a few instances, but they were of traumatic origin and were decided not to be regarded as part of the pathological anatomy of the experimental disease
- The substance of the brain was excessively moist in some instances (which shouldn’t be shocking considering spinal soup was injected directly into their brains)
- Flexner states that the general appearances of the spinal cord, medulla and brain are not greatly altered, and the visible effects are no proper measure of the damage inflicted by the “virus”
- It remained to be determined whether routes other than intracerebral injections give uniformly as good results as the intracerebral route
- Flexner’s impression was that infection is readily accomplished by way of the subcutis and less readily by way of the peritoneal cavity
- They made several unsuccessful attempts to produce infection through intratracheal inoculation and by feeding
- He states that the number of experiments will have to be considerably greater before a final conclusion can be ventured on these points
- It has been shown that the cerebrospinal fluid, at the beginning of the paralysis, is capable when injected into the brain, of setting up paralysis in other animals
- It is assumed the blood contains the “virus” at the beginning of the infection, but how richly has not been accurately determined
- As little as two cubic centimeters may fall to cause infection while as much as twenty has caused typical paralysis
- The naso-pharyngeal muscosa was also said to contain the “virus”
- They concluded this when they took excised membrane, including the tonsils and turbinate mucosa, rubbed them up with quartz sand and then macerated and filtered them which yielded an unpurified fluid that, when injected into the brain, caused paralysis
- To determine a “virus,” the spinal cords, removed from monkeys just paralyzed, were triturated with sterile quartz sand, thoroughly shaken, and pressed through a Berkefeld filter
- These filtrates were used repeatedly to inoculate monkeys, both by the intracerebral and subcutaneous routes, and were claimed to regularly (not always) cause paralysis
- From these paralyzed animals, the “virus” was transferred (i.e injected intracerebrally) to other monkeys
- Particles seen under dark field microscopy (as EM wasn’t invented for another 21 years) thought to represent the microorganism of poliomyelitis could not be affirmed
- Flexner states that the parasite of epidemic poliomyelitis is very minute and could not be further classified since the precise position among living things held by the filterable “viruses” had not been determined
- There were attempts to cultivate a “virus” in test tubes and while the results originally seemed to be successful, it was still in doubt
- They had not been able to induce paralysis by inoculating the culture fluid of the second or third transfer of the original “virus”
- They made an unsuccessful effort to achieve protection from intracerebral injection while also injecting subcutaneously
- Flexner admits that there was no reliable way of estimating the degree of activity of the “virus” since the number of organisms inoculated were not subject to control
- Two to four cubic centimeters of spinal soup mixed with a salt solution would be injected into the monkeys
- Many guinea-pigs and rabbits, one horse, two calves, three goats, three pigs, three sheep, six rats, six mice, six dogs, and four cats had active “virus” introduced in the brain but without causing any appreciable effect whatever
- Flexner states that it remained to be discovered whether some of these species of animals may not after all be made to develop poliomyelitis by using directly spinal cord from many human cases, on the supposition that a “virus” of greater virulence may be found
- The incubation period was worked out on the supposition (i.e uncertain belief) that the spontaneous disease in man is contagious
- They observed no instance among the monkeys of a spontaneous transfer of the infection
- Experimental poliomyelitis in the monkey is a severe and highly fatal disease and exceeds in the latter respect the spontaneous disease in man
If one looks at this paper objectively, it is clear that the results are nothing but experimental disease brought about by the horrific torture endured by the animals subjected to it. Based on indirect evidence acquired from these cruel practices, Flexner makes many leaps in logic, clings to his assumptions, and throws out random suppositions to try and create an explanation for an imaginary “virus” he can not find nor see. No “virus” is ever properly purified/isolated directly from a sick human. It was never observed that any monkey naturally transmitted Polio to any other monkey and, last I checked, being injected in the brain with ground up spinal and brain soup is not a natural way anyone ever “caught” Polio so proving pathogenicity is out of the question. Flexner chose the brain as the inoculation site as it gave him the best chance to recreate paralysis upon poisoning the animals with toxic tissue goo. The only thing Flexner can successfully claim is that he was able to make some monkeys sick and some monkeys paralyzed through unnatural means brought about by inhumane experimentation. He can not claim it was caused by a “virus.” To do so is nothing but pure imagination on his part for which he had no proof.