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27.12.2021 Feature Article

Who was "Patient Zero"?

Author: Radu GolbanAuthor: Radu Golban
27.12.2021 LISTEN

Professor Karl Lauterbach, Germany's newly appointed health minister, is an expert on COVID-19. Last year Lauterbach twittered that we may expect brain lesions induced by another wave of the Encephalitis lethargica [1] after the current pandemic expires. He's telling us, that these injuries will follow the plague in the same way that they did in the world after the Spanish Flu (1918-1920) [2]. Apparently, he knows something, which we don't know. He knows what caused the deadliest illness in history, which produced in addition to flue like symptoms, severe neurological, psychiatric, cardiovascular disturbances and death [3]. There are still many rumours and myths surrounding the so-called “Spanish influenza”. The mysterious Encephalitis lethargica [4] in the 1920s and 1930s, well known for its beta-amyloid deposition, similar to the “Spanish Flue” was the second devastating disease of the century [5]. Viruses, in comparison to synthetic amyloids, were unknown back then, since the first virus was discovered in 1933. Luckily, German medicine had with Salvarsan and Suramin medicaments available against the two pandemics. Salvarsan (Arsphenamin) was discovered by Paul Ehrlich about a hundred years ago, after he tried it out at the turn of the 19th century on Africans suffering from the sleeping disease [6] (Encephalitis lethargica). And fortunately, Germanin [7] (Suramin), also proves successful today against COVID-19 [8]. What a coincidence in the history of medicine, relevant in the present times. Could his statement help us to find the “patient zero”? Let me explain:

Scientists are on the hunt for clues to identify coronavirus “patient zero”, yet many experts around the world are still at odds on the origin of the ongoing outbreak, in particular to identify when, how, and why it started. I believe that “patient zero” may have been identified either as Dr Hans Gerhard Creutzfeldt's patient, the 22-year-old woman, Bertha Elschker from Breslau (8.12.1890-11.8.1913) or a native from the Papua New-Guinea Fore tribe, whom Nobel Laureate Dr Daniel Carlton Gajdusek (1923-2008) investigated in 1957, some fifty years later. At that time, the US-American scientist reported that typical signs of an infectious disease were not observed, though the patient's general feeling resembled that of acute respiratory infection [9]. The prodromal ill-defined period lasting for up to 23 months [10], which the natives used to call (kuru laik i-kamp nau—i.e., “kuru is about to begin”) was characterized by a headache and pains in the limbs, often in the joints; frequently, knees and ankles were affected first, followed by elbows and wrists; sometimes, interphalangeal joints were initially affected, along with abdominal pains and loss of weight [11]. Dr Gajdusek was convinced that “A virus from the Inorganic World...” is causing this new disease [12]. Neuropathologically, kuru is characterized by the presence of amyloid “kuru” plaques, often called, “corona”, because of their circular shape on the brain tissue [13].

In 1986 Dr Gajdusek communicated, that the molecular weight of this controversial “virus”, causing physiological and neurological effects is somewhere between 33- to 35-kDa [14] (“kDa” is a unit of molecular mass equal to 1000 Daltons). Coincidently, analysis of physicochemical parameters revealed that the SARS-CoV-2 is 306 amino acids long with a molecular weight of 33,796.64 Da [15] (33.8 kDa). In his last published article, 2008, Dr Gajdusek explains what might have caused this “fantasy virus” [16]. The amyloid [17] (abnormal protein) formation is associated with a few other devastating diseases as well. According to Dr Gajdusek et.al. [18], in the case of TSE (transmissible spongiform encephalopathy) amyloid deposits in man or animals are always found to be contaminated with other proteins similarly polymerized into fibrils—even co-polymerized. The process is as simple as it is fascinating, since it works according to the same principles that make a diamond hold together or the twinning of minerals [19]. “A diamond is the hardest of minerals; it can scratch steel, yet it is still only made of carbon, similar to carbon black, coal or graphite[20]. Dr Gajdusek was convinced, that an amyloid enhancing factor, either a synthetic or a scrapie like agent (animal TSE) was accelerating the amyloid toxicity. Before having a closer look to this “fantasy virus”, let's stay with history and geography for a while, since it could provide us valuable information.

Geographically speaking, the area where Dr Gajdusek investigated this rare human neurodegenerative disease, classified as a TSE, or prion disease, is in the north-western part of Papua-New Guinea [21]. Between 1884 and 1914 this part of the country was called “German New-Guinea” and was a German protectorate within the German colonial empire [22].

Dr Creutzfeldt was a distinguished German neuropathologist during the first half of the 20th century [23]. In August 1909, he embarked on a three-month training course at the Bernhard-Nocht-Institute in Hamburg in tropical medicine [24] which he then followed by nine-month medical training course at the Imperial Marine. He then embarked on a long journey to the Pacific Ocean as a naval surgeon. After his return, he decided to become a neurologist. Just like that. I wandered where he had been in the Pacific for almost one and a half years, if not in the German protectorates, and what inspired him to change his career after his return. Most historians focus on his activity during the Third Reich, as a medical reviewer at the euthanasia court. I consider the period prior to 1913 at least as interesting, since there are no entries in the German official military record [25] . Nor does the Bernhard-Nocht-Institute have any entries in their catalogue about him.

If one reads German biographies about Dr Creutzfeldt, one would wonder why a young physician interested in botany while travelling as a ship's doctor then made up his mind to this sharp change in his career path. A few months later he started working in a famous clinic in Breslau. One of his patients there was Bertha Elkscher, who was admitted with severe neurological symptoms to the hospital. Dr Creutzfeldt, a young German, who was not yet a neurologist, performed the autopsy after her death [26]. The case would become famous in 1920, when Dr Creutzfeldt found the time, after specializing in neurology, to publish a report on his special patient. She was theoretically the first reported case of the later-called Creutzfeldt-Jakob disease. At the autopsy there was bronchopneumonia, diffuse bronchitis, and neuropathological lesions, similar to the later findings of another German neurologist, Professor Alfons Maria Jakob. Interestingly, Dr Creutzfeldt's “star- or rosette-shaped” formations have also been documented in post-mortem examinations today of COVID victims by Dr Maura Boldrini, [27] who observed a brain tissue resembling “a galactic crush of stars stretched across a darkened sky”. Few questions arise from this unusual biography. How could a would be neurologist have realized that he was dealing with a new disease, if he had not the knowledge of other neurological symptoms and diseases? Why did he wait for almost seven years to publish the autopsy report in 1921?

Worse still, for decades experts considered that his findings did not match the later-named classical CJD until the 1990s when a new version, the variant CJD (vCJD) appeared in Europe and the United States. [28]. Ironically, Bertha Elschker was the only case to resemble vCJD. Robert Williams [29], a neuroscientist from University of Tennessee Health Science Center (UTHSC), Memphis, United States, pointed out that in her last two years, Bertha Elschker's life was entirely consistent with those observed in cases of vCJD [30]. Interestingly, Dr Gajdusek himself thought of having discovered something new, much like Dr Creutzfeldt, but due to nomenclature aspects of the classical CJD disease, the kuru similar vCJD variant had indeed been known to him since 1913 [31]. Prior to the vCJD, scientists agreed upon using the name CJD, despite the fact the Elschker's case didn't properly match the symptoms and neuropathology of the classical form of the disease. Gajdusek's cases were not new either, since according to a study from 1971 by Professor Shirly Lindenbaum, a famous Australian anthropologist notable for her medical anthropological work on kuru, the first cases had already occurred during the 1920s [32]. The tenacious German colonial bureaucracy has no entries about these cases either, though this new disease erupted during the German administration of these territories. Further research as to the extent where the Germans might have experimented with amyloids is thus useless, but not discouraging, since this is exactly Dr Gajdusek's point: A synthetic virus consisting of artificial polypeptides inducing TSE disease. Could he have had artificial amyloids [33] in his mind? They were not that new in the 1950s, once the German scientist Rudolph Virchow introduced this term 1854 [34]. At least Dr Gajdusek had some serious doubts about the origin of kuru, which he had pointed out during his speech in Stockholm 1976, when he received his Nobel Prize award. He clearly stated that the origin of kuru is more than suspect, as is the incidence of one per million cases of CJD in the world [35]. Dr Jonathan Wadsworth, an MRC Investigator and Programme Leader within the MRC Prion Unit at UCL and Reader in Prion Diseases in the UCL Institute of Prion Diseases et.al. concluded that kuru and vCJD are caused by a peripheral route of exposure to infectious proteinaceous agents [36].

How is it that Dr Creutzfeldt, once he made such a huge discovery, became a servant of the Third Reich and hasn't continued with further impressive research? Could Dr Creutzfeld have been aware of a mechanism of transmissible, synthetic amyloids inducing a fatal illness? Could he have known that poor Bertha Elschker, was inoculated with synthetic amyloids inducing transmissible dementia? Did he conduct similar experiments in the Pacific, in German New-Guinea? Is this what motivated him to become a neuropathologist? This remains unknown. At least we know that he married Clara Sombart, the daughter of the German economist Werner Sombart and author of “The Jews and Modern Capitalism[37]. Sombart obstinately accused the Jews, the “Saharists” of being unable to sustain an economy in comparison to the “Silvanists” (Nordic, Germanic people) [38]. His concept was decisive for the later race and ideology idea of the Third Reich [39] and even today is shamefully preserved in terms of sustainability and common good, certainly purified of the ethnic terms. One would say that Sombart, an economist, together with his son-in-law Dr Creutzfeldt, a neuropathologist would not have had much to talk about, unless they had known then that Dr Gajdusek would publish almost seventy years later his work titled: “The transmissible amyloidoses: genetical control of spontaneous generation of infectious amyloid proteins by nucleation of configurational change in host precursors: kuru-CJD-GSS-scrapie-BSE[40]. Once more Dr Gajdusek and other famous scientists were looking closer at the “slow virus” and were analysing the higher susceptibility for amyloid disease among the Sephardic Jews [41]. What a coincidence. Literally, the genetical control of infectious amyloid proteins, would have been something Professor Sombart and Dr Creutzfeldt, could have talked about, if synthetic amyloids were to be a later biological weapon that their nation might employ in order to build a pure, economically and socially sustainable race.

Amyloids, or prions are weaponizable toxic pathogen agents [42]; there is no doubt about that. To the extent that Dr Gajdusek's virus resembles COVID-19 would require scientists to look for analogies. The “slow virus” provokes no immune response nor evidencing and has no nonhost antigen, it has an enormous resistance to physical and chemical inactivation, it is a subviral pathogen devoid of nucleic acid or a non-host protein, it develops scrapie-associated fibrils, autoantibody directed against 10-nm neurofilaments, and no other component of the CNS (Central Nervous System) in over 60 per cent of the cases, is less detectable with an electron microscope etc. These are, according to the legendary kuru expert, the characteristics of this “fantasy virus” [43]. I have no doubt that you would start doing your own research if it does or not resemble the Coronavirus. You'd be better off doing it now than later.

Yet another genetical mutation determines COVID-19 susceptibility. TMPRSS2 expression dictates the entry route used by SARS‐CoV‐2 to infect a host [44] since this gene encodes a relevant protein in the case of the COVID-19 virus. According to the database for population genetic variants, there are about 378 different mutations of this gene [45]. The only mutation, the rs12329760, disrupts the function of TMPRESS2 and has thus a protective impact on the disease susceptibility. The lowest frequency of this mutation is in Latino and Jewish-Ashkenazi populations in comparison to East-Asian and Nordic people [46]. And it is related to the amyloid [47] formations, which we're also trying to understand in an historical context. Once more genetic control and amyloid formations seem to be playing a central role.

What are we to learn or find out by repeating Dr Gajdusek's tests for serial transmission or genetic control, and could they be useful in the context of COVID-19? Dr Gajdusek proved beyond doubt how the serial transmission of the “slow virus” works. Let's repeat quickly: First, the “slow virus”, these infectious amyloid proteins create themselves; second, they contain no nucleic acid and thus copies of themselves are made post-translationally from the host precursor; third, in their replication in a new individual they do not copy any mutation in the nucleating and pattern setting agent [48].

Nowadays PCR tests are using biomarkers of certain specific COVID-19-sequences (not the entire virus) in order to determine by a quantitative assay if a person is infected or not [49]. Why not use infected tissue of positive test cases, instead of the prefabricated biomarkers with only some indicated sequences in order to see how and what replicates of a certain strain? The conclusion could be a geopolitical one.

Ron Tjalkens investigates viruses that invade the neurological system and neurodegenerative diseases and sees a historical precedent for long-term neurological effects in survivors of the SARS-CoV-2 virus [50]. Given, we have been dealing for a century with an induced synthetic “slow virus”, according to Dr Gajdusek's definition, then the only escape today might be to reveal the amyloid inducing agent and thus by understanding its transmission, to act accordingly with the potential initiators of the hybrid warfare.


[1] neur_60_701.663_670.tp (silverchair.com), Encephalitis lethargica: Die rätselhafte Schlafepidemie - Spektrum der Wissenschaft, (nih.gov)

[2] Prof. Karl Lauterbach na Twitteru: "(1) In 20er/30er Jahren gab es weltweit Welle der Enzephalitis Lethargica, die auf die Spanische Grippe 1918 zurückgeführt wurde. Der Hirnschaden trat erst Jahre nach Grippe auf. Das ist leider auch bei Covid-19 nicht auszuschliessen. UC London Forscher: https://t.co/AbrTlLeoki" / Twitter, Biogenese des Prion-Proteins: Regulation und Fehlregulation bei Prion-Erkrankungen (uni-muenchen.de), 100 Jahre Salvarsan: Chemisch auf Erreger zielen | PZ – Pharmazeutische Zeitung (pharmazeutische-zeitung.de)Constructing Scientific Knowledge: The Understanding of the Slow Virus, 1898-1976, The Spanish Flu Pandemic and Mental Health: A Historical Perspective (psychiatrictimes.com)

[3] Did the 1918 influenza cause the twentieth century cardiovascular mortality epidemic in the United States? (nih.gov)

[4] Encephalitis Lethargica - an overview | ScienceDirect Topics

[5] Influenza RNA not detected in archival brain tissues from acute encephalitis lethargica cases or in postencephalitic Parkinson cases - PubMed (nih.gov), Interactions between SARS-CoV-2 N-Protein and α-Synuclein Accelerate Amyloid Formation | ACS Chemical Neuroscience, Amyloid Assemblies of Influenza A Virus PB1-F2 Protein Damage Membrane and Induce Cytotoxicity (nih.gov)

[6] RKI - Geschichte - 1911 - 1920 Die Bekämpfung der Schlafkrankheit – Kleine und Koch in Afrika

[7] Comeback von Germanin: Wirkstoff gegen Schlafkrankheit hilft auch bei Leberversagen (handelsblatt.com)

[8] Suramin inhibits SARS-CoV-2 infection in cell culture by interfering with early steps of the replication cycle — Immunology (ox.ac.uk),

[9] Kuru, the First Human Prion Disease (nih.gov),

[10] Alpers M.P. Mimeographed. Dept Med. University of Adelaide; Adelaide, Australia: 1964. Kuru: Age and duration studies; p. 12

[11] Alpers M.P. Mimeographed. US Dept Health, Education, Welfare; Washington, DC, USA: 1964. Kuru: A clinical study; pp. 1–38

[12] 481 - Fantasy of a Virus.pdf (science-connections.com)

[13] Ultrastructural study of florid plaques in variant Creutzfeldt–Jakob disease: a comparison with amyloid plaques in kuru, sporadic Creutzfeldt–Jakob disease and Gerstmann–Sträussler–Scheinker disease (ed.ac.uk)

[14] Sklaviadis T., Manuelidis L., et.al. Characterization of major peptides in Creutzfeldt-Jakob disease and scrapie 6146.full.pdf (pnas.org)

[15] Structural basis of SARS-CoV-2 3CLpro and anti-COVID-19 drug discovery from medicinal plants - ScienceDirect, Microsoft Word - Dokorarbeit komplett endgültig.doc (fu-berlin.de)

[16] Kuru and its contribution to medicine | Philosophical Transactions of the Royal Society B: Biological Sciences (royalsocietypublishing.org)

[17] Amyloid - an overview | ScienceDirect Topics

[18] The Influence of Glycosaminoglycans on the Formation of Fibers from Monomeric Tropocollagen in vitro - ÖBrink - 1973 - European Journal of Biochemistry - Wiley Online Library,

[19] The transmissible amyloidoses: Genetical control of spontaneous generation of infectious amyloid proteins by nucleation of configurational change in host precursors: Kuru-CJD-GSS-Scrapie-BSE | SpringerLink, Enhancement of amyloid induction by amyloid fibril fragments in hamster. - Abstract - Europe PMC

[20] Kuru and its contribution to medicine | Philosophical Transactions of the Royal Society B: Biological Sciences (royalsocietypublishing.org)

[21] rsos160789f01.jpg (1280×1000) (royalsocietypublishing.org) GENETIC_STUDY_OF_KURU_LIAM_QUINN.pdf (ucl.ac.uk), Kuru in the 21st century—an acquired human prion disease with very long incubation periods - The Lancet, The Possession of Kuru: Medical Science and Biocolonial Exchange | Comparative Studies in Society and History | Cambridge Core,

[22] German New Guinea - New World Encyclopedia

[23] https://www.scielo.br/j/anp/a/CBGzyP5HtB8p5RWxkLWSG6t/?lang=en&format=pdf,

[24] Universität Kiel | Große Forscher und Forscherinnen aus Kiel (uni-kiel.de)

[25] Personal mandate to an official German archive expert to investigate Creutzfeldt's activity in the German protectorate in the Pacific.

[26] Origins of the Creutzfeldt and Jakob Concept | Duckett, Serge; Stern, Jan | download (booksc.eu), Kiel University | Famous Scholars from Kiel (uni-kiel.de)

[27] Column One: How does COVID-19 change the brain? This scientist is finding out - Los Angeles Times (latimes.com)

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[29] Loop | Robert W Williams (frontiersin.org)

[30] New variant Creutzfeldt-Jakob disease: the epidemic that never was | The BMJ

[31] The neuropathology of kuru and variant Creutzfeldt–Jakob disease (nih.gov)

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[33] “Amyloid” — Historical Aspects | IntechOpen

[34] Enzymatic remodeling of heparan sulfate: a therapeutic strategy for systemic and localized amyloidoses? (nih.gov)

[35] D. Carleton Gajdusek - Nobel Lecture (nobelprize.org)

[36] Kuru prions and sporadic Creutzfeldt–Jakob disease prions have equivalent transmission properties in transgenic and wild-type mice (nih.gov), Experts comb tropics for clues to vCJD | Nature

[37] Jews (mcmaster.ca)

[38] Becke J. (2019): Saharan Zion: state evasion and state-making in modern Jewish and Sahrawi history, Journal of Israeli History. Saharan Zion: state evasion and state-making in modern Jewish and Sahrawi history | Becke, Johannes | download (booksc.eu)

[39] Race and Ideology on JSTOR

[40] The transmissible amyloidoses: genetical control of spontaneous generation of infectious amyloid proteins by nucleation of configurational change in host precursors: kuru-CJD-GSS-scrapie-BSE - PubMed (nih.gov)

[41] Mutation in codon 200 of scrapie amyloid precursor gene linked to Creutzfeldt-Jakob disease in Sephardic Jews of Libyan and non-Libyan origin - PubMed (nih.gov), A mutation in the prion protein gene in Creutzfeldt-Jakob disease in Jewish patients of Libyan, Greek, and Tunisian origin - PubMed (nih.gov), Mutation of the Prion Protein in Libyan Jews with Creutzfeldt–Jakob Disease | NEJM, 1109.full.pdf (bmj.com), 1109.full.pdf (bmj.com)

[42] SciELO - Brazil - Prions: the danger of biochemical weapons Prions: the danger of biochemical weapons, Prions as Bioweapons? | Defence IQ, Prion-based nanomaterials and their emerging applications (nih.gov), What are Biological Weapons? – UNODA, UNICRI 2012 Security Implications of Synthetic Biology and Nanobiotechnology_0.pdf, The Next Plague: Prions are Tiny, Mysterious and Frightening | American Council on Science and Health (acsh.org), Prion theory: Induction of Prion Diseases by Nanoparticles Conversion (Prpc To Prpsc) Related to Electromagnetic Field (juniperpublishers.com)

[43] Fantasy of a Virus.pdf (science-connections.com)

[44] (PDF) TMPRSS2 expression dictates the entry route used by SARS‐CoV‐2 to infect host cells (researchgate.net), Why does SARS-CoV-2 hit in different ways? Host genetic factors can influence the acquisition or the course of COVID-19 (binasss.sa.cr)

[45] A common TMPRSS2 variant protects against severe COVID-19 | medRxiv

[46] A genetic variant of TMPRSS2 may confer protection against severe COVID-19 (news-medical.net)

[47] TMPRSS2 expression dictates the entry route used by SARS‐CoV‐2 to infect host cells | The EMBO Journal (embopress.org), Expression of SARS-CoV-2 receptor ACE2 and TMPRSS2 in human primary conjunctival and pterygium cell lines and in mouse cornea (nih.gov)

[48] The transmissible amyloidoses: Genetical control of spontaneous generation of infectious amyloid proteins by nucleation of configurational change in host precursors: Kuru-CJD-GSS-Scrapie-BSE | SpringerLink

[49] Protein amplification technology: New advances in human prion disease diagnosis - ScienceDirect, Frontiers | Biomarkers and Immune Repertoire Metrics Identified by Peripheral Blood Transcriptomic Sequencing Reveal the Pathogenesis of COVID-19 | Immunology (frontiersin.org), The optimal diagnostic methods for COVID-19 (degruyter.com), Covid-19 diagnosis by combining RT-PCR and pseudo-convolutional machines to characterize virus sequences | Scientific Reports (nature.com)

[50] History Repeats Itself: Viral pandemics offer clues to neurodegenerative disorders (colostate.edu), Viruses & nervous system disorders: insights from other pandemics (neurex.org)

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