Did Thomas Francis Jr. Isolate Influenza B in 1940?

After “isolating” the influenza A “virus” in 1934 and supposedly “isolating” it again on tissue culture and egg membrane in 1937, Thomas Francis Jr. was back in 1940 to perform more grotesque serial passages of ground up chemically altered diseased animal tissue goo from one animal into another. He must have decided that the  perfect way to cover-up any past and future “isolation” failures of his current strain was to claim the discovery a new one:

“Dr. Francis had a leading part in the discovery and isolation of both virus A and B. Type A was isolated for the first time in the Western Hemisphere in 1934 at Rockefeller Institute, where he was a member, and Type B was discovered under his direction in the New York University bacteriological laboratory which he headed from 1938 to 1941.”

“Thomas Francis was an American physician, virologist, and epidemiologist. Francis was the first person to isolate influenza virus in America, and in 1940 showed that there are other strains of influenza, and took part in the development of influenza vaccines.”

http://um2017.org/Thomas_Francis.html

Keep in mind while reading his paper, no “virus” was ever properly purified/isolated directly from a sick patient. He took throat washings from patients and injected ferrets and mice up the nose with the washings in attempts to make the animals sick. The animals were killed after observation and then the lungs and nasal turbinates (bone/cartilage) were ground up and mixed with chemicals which were then injected into the nose of healthy animals. This process of killing/grinding up tissue/nasal injection was repeated (known as serial passaging) until he got the results (i.e. symptoms) he wanted to see. Francis Jr. then assumed a “virus” was present in the toxic animal goo and ran useless indirect antibody tests to back up his claims.

Below is the full paper with a summary:

A NEW TYPE OF VIRUS FROM EPIDEMIC INFLUENZA

In February and March of 1940, an epidemic of acute respiratory disease, simulating epidemic influenza, occurred at Irvington House, a convalescent home for children with rheumatic cardiac disease, located at Irvington on Hadson. Through the courtesy of Dr. Ann G. Kuttner, throat washings were received from 4 cases in the first 3 days of illness and, in addition, samples of serum were taken in the acute and convalescent stages. Neutralization tests done with these sera revealed no rise in antibody titer during convalescence against 1000 M.L.D. of the PR8 strain of the virus of epidemic influenza. Mice and ferrets were inoculated intranasally with 3 of the throat washings. Two of the ferrets failed to exhibit recognizable signs of infection and their sera, taken 8 and 51 days later, respectively, failed to neutralize the standard PR8 strain of virus. Attempts to isolate a virus directly in mice from any of the throat washings were unsuccessful through 5 serial passages at 4-day intervals or 10, 21 and 23 passages, respectively, at 7-day intervals.

The temperature of the ferret inoculated with throat washings from the third patient (Lee) fell to subnormal on the 5th and 6th days. The animal stopped eating, was abnormally quiet and had some respiratory distress. At autopsy on the 6th day the only gross finding was a mild, bluish discoloration of the left lower lobe of the lung. Passage to a normal ferret was made with a suspension of lung and turbinates and 13 serial transfers were made at 4- to 6-day intervals in this species of animal. After the 5th passage a double series was maintained. In 2 of the 20 ferrets, the highest temperature was above 105′ F.; in 7, it was 104-5′; in 6, between 103.5′ and 104′; in 3, no evidence of fever was obtained and in 2 the temperature was subnormal. In 13 of 18 autopsied ferrets mild pulmonary lesion, usually spotty, were noted and the majority presented abnormalities of the respiratory turbinate tissue. Serum taken from the sole convalescent ferret (B77-9th passage) on the 21st day failed to neutralize 1000 or 100 M.L.D. of the mouse passage PR8 strain of virus. Hence, by the criteria established in 1937 this outbreak of respiratory disease was not associated with the virus of epidemic influenza.

Groups of mice were inoculated intranasally with suspensions of lung, turbinate or both from ferrets of the 5th, 7th, 8th, 9th, 10th and 13th passages and multiple transfers were made with lung snspensions by the intranasal route at 4- to 6-day intervals. Using 10 percent suspensions, only small lesions were as a rule observed in mice of the first 5 passages. Thereafter, an increase in severity of the disease occurred so that by the 10th transfer infections were frequently fatal within the 5-day period. With continued passage the virulence increased so that at present virus of the two series which have been continued through 40 passages produces fatal infection within 10 days when used in a 1:1000 dilution, occasionally 1:10,000, of infected mouse lung.

Throughout its development the lesions produced by the virus in the lungs of mice have been of the uniform reddish blue type seen in infections with the virus of epidemic influenza. Nevertheless, when tested against rabbit or ferret serum prepared against numerous different strains of epidemic influenza virus, no neutralization of 200 M.L.D. or less of the Lee virus was effected. It was not neutralized by rabbit sera prepared against several strains of poorly defined agents, probably of origin, or by serum against normal mouse virus obtained from Dr. P. L. Horsfall, Jr. (Table I). 0n the other hand, rabbit serum prepared against one passage strain of the Lee virus completely neutralized 3 substrains established in mice with material from 3 different ferret passages (8, 8A, 13A). It was then found that the convalescent serum of ferret B77, which had failed to neutralize the PR8 strain, completely neutralizecl the Lee strain. The virus transferred in mice and ferrets appeared therefore to be identical.

The sera of the Irvington House patients which had exhibited no rise in convalescent titer against the standard PR8 strain were tested against a 10 percent mouse lung suspension (100 M.L.D.) of the Lee virus. The titers of both acute and convalescent sera of patient, Lee, were approximately the same when measured against PR8. Against the Lee strain the acute titer was 0; the convalescent titer, 120. A similar result was obtained with sera of 2 others, while in one instance no difference was detected. Sera from 3 other patients who had been sick during the epidemic were fortunately available. All these also showed in convalescence a pronounced rise in antibodies to the Lee virus but not to PR8 (Table II). These results seem clearly to establish the causal assassociation of Lee virus with the Irvington house epidemic and to demonstrate the lack of serological relationship of that virus to strains of virus isolated from other epidemics of influenza.

In January and February of 1940 an extensive epidemic of what appeared to be epidemic influenza extended throughout the southeastern portion of the United States. Through the kindness of Dr. D. T. Smith and members of the medical staff of Duke University Hospital, patients were made available for study. Since these investigations were undertaken toward the end of the epidemic, throat washings or sputum and serum taken during the acute and convalescent stages of illness were obtained from but 7 patients. Four of the throat washings were given intranasally to ferrets. In two instances serial passages through 4 ferrets were made. While some of the ferrets exhibited signs suggestive of infection with influenza virus, attempts to maintain the infection or to isolate a virus in mice were unsuccessful. The fourth passage ferrets (B35, B46) were bled on the 12th day; another (B32) on the 28th day. Their sera failed to neutralize the PR8 strain. Furthermore, when neutralization tests with the acute and convalescent sera of the patients were performed, using 100 and 1000 M.L.D. of the standard PR8 strain of epidemic influenza virus, no diagnostic rise in antibodies was detected. In this instance, again, the customary procedures had indicated that the virus of epidemic influenza was not involved.

In view of the studies of the Irvington outbreak, the various sera were retested against 100 M.L.D. of the Lee virus. In 6 of the 7 patients a definite rise in titer of the convalescent serum was seen (Table II). Furthermore, serum of 3 ferrets receiving throat washings from these patients neutralized the Lee virus, although
they had failed to neutralize the PR8 strain. In addition, serum from 6 ferrets inoculated by Dr. Horsfall with throat washings of patients from the North Carolina epidemic were tested. Four of them neutralized the Lee virus, all failed to neutralize 100 M.L.D. of the PR8 strain. The serum of 3 patients which had been found by Dr. Horsfall to show no increased convalescent titer against the PR8 strain, when tested against the Lee virus, exhibited marked rises in neutralizing antibodies. It is evident, ttherefore, that the Lee virus was the cause of the earlier general outbreak in North Carolina and adjoining areas.

In the early months of 1936 a widespread epidemic of acute, respiratory disease, indistinguishable from epidemic influenza, was studied. Its etiology was not established nor was any evidence obtained relating it to known strains of the virus of epiclemic influenza. Sera from 2 typical patients which had been kept in storage since that time were now tested against 100 M.L.D. of influenza (PR8) and Lee viruses. Pronounced rises of titer against Lee virus occurred but not against PR8 (Table II). It appears, in consequence, that this epidemic 4 years earlier was also due to virus of the Lee type.

Reference was then made to acute and convalescent sera of 2 individuals from whom epidemic influenza virus was isolated during the epidemic of the winter of 1936-37 (Table II). Titered against the PR8 strain, rises from 0 to 35 and 50 to 320 were noted; against 100 M.L.D. of the Lee strain the acute and convalescent titers of both were approximately 60. Hence, infection of human subjects with virus of the PR8 type does not result in a rise of antibodies to the Lee virus and the difference in etiology of the epidemics is further demonstrated.

Again through the kindness of Dr. Horsfall, serum of ferrets inoculated with throat washings of patients observed in the epidemic of influenza current in the West Indies this summer were tested. Certain of these sera also neutralized the Lee virus but not the PR8.

The immunological evidence indicates clearly that the newly isolated virus is the cause of the epidemics of acute respiratory disease in Irvington and North Carolina in 1940 and of the extensive epidemic early in 1936. These epidemics have presented no outstanding clinical features to differentiate them from the outbreaks which have yielded the virus of epidemic influenza, typified by the original WS and PR8 strains. The serological studies reveal, however, that they are etiologically distinct. In fact, the lack of cross reactions between serum against known strains of influenza virus and the present virus suggests that the latter is entirely unrelated to the virus of epidemic influenza previously isolated. Complement fixation tests which ordinarily detect the common antigen of different strains of epidemic influenza virus have not yielded up to the present any helpful information. Hyper-immune PR8 rabbit and ferret sera have not neutralized even small amounts of Lee virus. Furthermore, mice vaccinated with 2 intraperitoneal injections of 5 percent Lee virus have died of infection with 100 N.L.D, of PR8 but staunchly resist the same amount or more of the Lee virus. The differences are clearly greater than those detected in previous studies of strains of epidemic influenza virus. The behavior of the virus in animals and the gross pathological features are, however, quite the same as those of mild strains of known influenza virus.

The usual experience has been that human subjects infected with one strain of influenza virus produce antibodies readily detected by tests with any of the ordinary strains obtained from man, or even with strains of swine influenza virus. The absence of antibodies to the Lee virus in the serum of patients.at the time of their infection and the production of specific antibodies to that virus in convalescence are independent of antibodies to the PR8 strain which remain constant during the course of this disease. It is evident, therefore, that for the purposes of differential diagnosis, the Lee virus represents a serologically distinct entity. Nevertheless, the epidemic disease associated with virus of the Lee type appears on the basis of present knowledge to be as typical of epidemic influenza as that prevalent in outbreaks from which strains of the previously recognized virus were obtained. The epidemics of 1936-37 and 1938-39 have been shown to be caused by influenza virus of the usual variety while those of early 1936 and 1940 are of the Lee txpe. The two infections apparently possess independent cycles, but until further differential studies are made they should both be considered epidemic influenza caused by viruses of different serological types. The isolation of the new type of virus and the aocompanying serological studies have established the etiology of epidemics of acute respiratory disease simulating influenza which had previously not been identified. Following the classification recently suggested in which the established form of epidemic influenza is called Influenza A, outbreaks caused by virus of the Lee type are to be designated Influenza B.”

doi: 10.1126/science.92.2392.405.

In Summary:

• Throat washings from 4 cases of sick children were received in the first 3 days of illness and, in addition, samples of serum were taken in the acute and convalescent stages
• Mice and ferrets were inoculated intranasally with 3 of the throat washings
• Two of the ferrets failed to exhibit recognizable signs of infection and their sera, taken 8 and 51 days later, respectively, failed to neutralize the standard PR8 strain of “virus”
• Attempts to isolate a “virus” directly in mice from any of the throat washings were unsuccessful through 5 serial passages at 4-day intervals or 10, 21 and 23 passages, respectively, at 7-day intervals
• In other words, Francis Jr. was unable to get the desired symptoms he wanted after injecting toxic ground up animal tissue goo up the noses of mice, killing them after observation of either 4 or 7 days, and then grinding their tissues up with chemicals and repeating the entire process anywhere from 5, 10, 21, or 23 times – thus no “virus” was “isolated” directly using human throat washings
• The temperature of the ferret inoculated with throat washings from the third patient (Lee) fell to subnormal on the 5th and 6th days
• At autopsy on the 6th day, the only gross finding was a mild, bluish discoloration of the left lower lobe of the lung
• Passage to a normal ferret was made with a suspension of lung and turbinates and 13 serial transfers were made at 4- to 6-day intervals in this species of animal
• After the 5th passage a double series was maintained
• Serum taken from the sole convalescent ferret (B77-9th passage) on the 21st day failed to neutralize 1000 or 100 M.L.D. of the mouse passage PR8 strain of “virus”
• Francis Jr. then claims that by the criteria established by himself in 1937, this outbreak of respiratory disease was not associated with the “virus” of epidemic influenza

Francis Jr.’s Own Established 1937 Criteria:

https://viroliegy.com/2021/11/23/thomas-francis-jr-s-flu-review-1937/

• Groups of mice were inoculated intranasally with suspensions of lung, turbinate or both from ferrets of the 5th, 7th, 8th, 9th, 10th and 13th passages and multiple transfers were made with lung snspensions by the intranasal route at 4- to 6-day intervals
• Thereafter, an increase in severity of the disease occurred so that by the 10th transfer infections were frequently fatal within the 5-day period
• With continued passage the virulence increased so that the “virus” of the two series which had been continued through 40 passages produced fatal infection within 10 days
• When tested against rabbit or ferret serum prepared against numerous different strains of epidemic influenza “virus,” no neutralization of 200 M.L.D. or less of the Lee “virus” was effected
• It was not neutralized by rabbit sera prepared against several strains of poorly defined agents, probably of origin, or by serum against normal mouse “virus “obtained from Dr. P. L. Horsfall, Jr.
• Rabbit serum prepared against one passage strain of the Lee ,”virus” completely neutralized 3 substrains established in mice with material fronm 3 different ferret passages (8, 8A, 13A)
• In other words, the toxic ground up tissue from MICE injected with toxic ground up tissue from FERRETS had some sort of chemical reaction with the blood from RABBITS – and voila you have a new “virus” strain
• It was then found that the convalescent serum of ferret B77, which had failed to neutralize the PR8 strain, completely neutralizecl the Lee strain
• On the basis of this 3-way interspecies blood reaction orgy as well as the single reaction from one ferret, Francis Jr. concluded that the assumed invisible “virus” transferred in mice and ferrets appeared to be identical
• He believed these results seemed clearly to establish the causal assassociation of Lee “virus” with the Irvington house epidemic and to demonstrate the lack of serological relationship of that “virus” to strains of “virus” isolated from other epidemics of influenza
• In other words, as he could not see the “virus,” the only way Francis Jr. determined a new “virus” was present was through non-specific antibody results
• In January and February of 1940 an extensive epidemic of what appeared to be epidemic influenza extended throughout the southeastern portion of the United States
• Four of seven throat washings were given intranasally to ferrets
• In two instances serial passages through 4 ferrets were made
• While some of the ferrets exhibited signs suggestive of infection with influenza “virus,” attempts to maintain the infection or to isolate a “virus” in mice were unsuccessful
• When neutralization tests with the acute and convalescent sera of the patients were performed, using 100 and 1000 M.L.D. of the standard PR8 strain of epidemic influenza “virus,” no diagnostic rise in antibodies was detected
• In this instance, again, the customary procedures (i.e. indirect non-specific antibody tests) had indicated that the “virus” of epidemic influenza was not involved
• Based on positive antibody results from some (not all) of the patients/animals tested, Francis Jr. claimed it was evident that the Lee “virus” was the cause of the earlier general outbreak in North Carolina and adjoining areas
• In the early months of 1936 a widespread epidemic of acute, respiratory disease, indistinguishable from epidemic influenza, was studied
• Its etiology was not established nor was any evidence obtained relating it to known strains of the “virus” of epiclemic influenza
• Based on antibody results from the sera of 2 patients from 1936 where rises of titer against Lee “virus” occurred but not against PR8, it appeared to Francis Jr. that this epidemic 4 years earlier was also due to “virus” of the Lee type
• Reference was then made to acute and convalescent sera of 2 individuals from whom epidemic influenza “virus” was isolated during the epidemic of the winter of 1936-37
• Infection of human subjects with “virus” of the PR8 type did not result in a rise of antibodies to the Lee “virus” so Francis Jr. stated the difference in etiology of the epidemics was further demonstrated
• Serum of ferrets inoculated with throat washings of patients observed in the epidemic of influenza in the West Indies were tested
• Certain of these sera (i.e. not all of them) also neutralized the Lee “virus” but not the PR8
• According to Francis Jr., the immunological evidence indicated clearly that the newly isolated “virus” was the cause of the epidemics of acute respiratory disease in Irvington and North Carolina in 1940 and of the extensive epidemic early in 1936
• These epidemics presented no outstanding clinical features to differentiate them from the outbreaks which had yielded the “virus” of epidemic influenza, typified by the original WS and PR8 strains
• The serological studies revealed, however, that they were etiologically distinct
• The lack of cross reactions between serum against “known” strains of influenza “virus” and the present “virus” suggested that the latter is entirely unrelated to the “virus” of epidemic influenza previously “isolated”
• Complement fixation tests which ordinarily detect the common antigen of different strains of epidemic influenza “virus” did not yield any helpful information
• The behavior of the “virus” in animals and the gross pathological features were the same as those of mild strains of known influenza “virus”
• In other words, the only way Francis Jr. could claim there was an influenza B “virus” (which he could not see) was through serological tests that are useless without first having a purified/isolated “virus” to validate the results against (which he did not have)
• It was evident to him that for the purposes of differential diagnosis, the Lee “virus” represented a serologically distinct entity
• The epidemic disease associated with “virus” of the Lee type appeared to be as typical of epidemic influenza as that prevalent in outbreaks from which strains of the previously recognized “virus” were obtained
• Francis Jr. claims that the two infections apparently possessed independent cycles, but until further differential studies were made they should both be considered epidemic influenza caused by “viruses” of different serological types
• According to Francis Jr., the “isolation” (which never happened) of the new type of “virus” and the aocompanying serological studies established the etiology of epidemics of acute respiratory disease simulating influenza which had previously not been identified
• In other words, the Lee strain (influenza B) is exactly the same in every respect to influenza A except for a few results from nonspecific and absolutely useless for identifying new “strains” of “viruses” antibody tests

I want to reiterate the point that the Lee “strain” Francis Jr. fell in love with and labelled influenza B was nothing more than the throat washings of ONE boy injected into the nose of ONE ferret which caused only mild bluish discoloration of the lower portion of one lung which was then ground up and injected intranasally into other ferrets and repeated over 13 times until he saw the symptoms he wanted to see to claim (ASSUME) a “virus” was present. No “virus” was ever properly purified/isolated directly from the throat washings. There were no EM images of any infuenza B “virus.” There was no characterization of any particle. The throat washings of one boy is nowhere near a large enough sample size and no controls were said to be performed.

Francis Jr. then claimed through antibody testing that his new “strain,” while associated with the exact same symptoms and epidemics of that associated with the influenza A “strain,” was a SEROLOGICALLY different “virus.” However, one can not use the unproven “antibody” theory to prop up the unproven “virus” theory. That would be like stating that Santa Claus is real because elves are real yet offering no proof regarding either except for footprints in the snow. Neither “antibodies” nor “viruses” have ever been properly purified/isolated nor proven to exist so one can not use one to prove the existence of the other.

This disturbing process full of inhumane passaging of ground up animal tissue containing assumed “virus” verified indirectly by assumed “antibodies” is how Thomas Francis Jr. fooled the world into believing he isolated influenza B.