The Notorious NoV

One of the problems virologists, microbiologists, and other germ theory defenders have when challenged with providing proof of the purification/isolation of any “virus”directly from a human is the complete lack of this proof in any of the original “virus” papers. They can not provide this evidence as it simply does not exist. Virologists have never purified and isolated the particles they assume are the “virus” and then prove these particles are pathogenic in a natural way. It has never happened once in the history of virology. So those defending the lie are left in a precarious position. They can either accept that this evidence does not exist or they can try to wiggle around the utter lack of evidence by citing various INDIRECT studies involving cell culture experiments, genomes, antibodies, genetically-modified animal studies, etc. suggesting “virus.” Take a guess which option they choose every time. As the defenders of the lie can not share DIRECT scientific proof that the particles claimed to be “viruses” actually exist inside humans and cause disease, they share INDIRECT evidence suggesting these entities may exist and may cause disease…pending further research.

Recently, there is one original “virus” paper that some of these defenders seem to believe is the holy grail of evidence fulfilling the request for proof of purified/isolated “viruses.”

Enter the “Norovirus.”

This lovely figment of the imagination stems entirely from the study of particles found in human feces. The defenders of Germ Theory claim this evidence meets the burden of proof as the particles are coming directly from a human since the “virus” was found directly in the poop juice of those “infected” and it does not need to be cultured in cells in order to be visualized. While they are technically correct in that the poop does come from humans, they always seem to forget the two most important criteria needed to be satisfied in order to prove the particles are in fact “viruses:”

  1. PURIFICATION: free from foreign materials as well as anything that contaminates, pollutes, debases, and/or adulterates the sample
  2. ISOLATION: separated from everything else (other similar and identical particles) within the sample

In the original 1972 study, not only were the methods used to aquire and maintain the sample mostly undefined, the researchers admitted to adding phosphate buffered saline to the samples as well as serum from “infected” patients. They also admit to other materials and particles being present within the sample, thus necessitating the use of IEM techniques to try and distinguish the various particles from each other. Obviously, this negates any purification and isolation claim. Regarding pathogeniticity, it would seem fairly obvious that drinking the poop juice from anyone will most likely make one sick irregardless of any assumed “virus.” However even then, not everyone who drank the poop juice became ill and to date, animal models recreating the disease are considered unsatisfactory. These points can be seen from a few brief highlights in a 2015 paper about the “norovirus” and the many limitations still existing nearly 40 years after it’s supposed discovery:

BASIC VIROLOGY AND VIRAL DIVERSITY

“The Norwalk virus agent (the original prototype virus is referred to as Norwalk virus in this review) was originally visualized by using immunoelectron microscopy (1), revealing 27-nm virus-like particles (Fig. 1). Efforts to cultivate the pathogen in cell culture and to develop an animal model were unsuccessful (8); therefore, the evolving literature focused on describing the physical characteristics of this small, round-structured virus in clinical specimens and on the serologic response to infection (910).”

“Norovirus has been likened to a “shape-shifter” (18), a mythical creature that can change form or being. This description refers to its diversity, with, as determined by the VP1 amino acid sequence, at least 6 genogroups (genogroup I [GI] to GVI) and >40 genotypes (1819), together with its continued evolution, apparently in response to the selective pressure exerted by the human immune system (20).”

NOROVIRUS IMMUNOLOGY

“An inability to cultivate norovirus in vitro until very recently and the absence of an animal model that closely resembles human disease, together with viral and human host diversity, have represented major obstacles to our understanding of the pathogenesis of and immune response to norovirus infection. As a consequence, much of our knowledge of the immunology of this highly species-specific virus revolves around studies of MNV and the use of virus-like particles (VLPs) of human norovirus. VLPs are the product of self-assembling viral structures derived from the expression of recombinant VP1. They are structurally and antigenically similar to their corresponding wild virions but lack genomic material.

Animal Models

Although no animal model to date has been entirely satisfactory, it has been demonstrated that chimpanzees can be successfully infected with GI.1 norovirus (269), while gnotobiotic pigs (270) and gnotobiotic calves (271) can be successfully infected with GII.4 norovirus.”

“While the inability to culture the virus in vitro precludes the ability to detect neutralizing antibody by classical methods, the prevention of binding of norovirus-derived VLPs or P particles to HBGA (blocking antibody) is believed to be an accurate surrogate of neutralization (324325).”

“Several advances into understanding the relationship among the viral strain, the host human blood group antigen type, and disease susceptibility have recently been elucidated, but this work has not yet been extended to clinical practice. The interplay of norovirus and host immunity still poses many unanswered questions. Areas of future research may overcome technical limitations, such as the inability to cultivate norovirus in vitro, and may elucidate a way to directly measure neutralizing antibodies, which could pave the way for vaccine development.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284304/

CGI: The only way you will ever see these particles in humans.

As can be seen from the above source, it is stated that the “norovirus” can not be cultured, does not have a suitable animal model, and that neutralizing antibodies can not be directly detected. In fact, they claim that the inability to culture the “virus” precludes (i.e. prevent from happening, make impossible) the ability to detect neutralizing antibodies. So what does that say about the original 1972 evidence claiming the detection of “norovirus” when it was based entirely on antibody detection?

Another source also highlights these glaring challenges related to the study of the “norovirus:”

“Noroviruses are classified as members of a category of viruses known as the Calicivirus family. The caliciviruses consist of four groups, of which the noroviruses are the most important human pathogen. Caliciviruses are single-stranded, positive-sense RNA viruses. The caliciviruses have been difficult to study due to their inability to grow in a cell culture system and the lack of a good animal model system.”

“The challenges in norovirus research are to develop models in which to study the viruses, to develop methods to more easily detect the viruses, and to develop ways to treat and prevent norovirus infection.

A major hindrance to norovirus research has been the lack of a system in which to grow the virus. Scientists like to have a cell culture system and a small animal model system in which they can study details of how viruses cause illness and use these systems to test antiviral agents.”

https://www.bcm.edu/departments/molecular-virology-and-microbiology/emerging-infections-and-biodefense/specific-agents/norovirus

It would appear that, according to the CDC, “norovirus” is food poisoning.

So beyond the lack of purified/isolated particles assumed to be the “norovirus,” there is no cell culture system to grow any “virus” nor any animal models to prove pathogeniticity. The challenges related to “norovirus” include developing models/methods to study and detect it. One would think these things would be figured out and readily available had the “norovirus” been properly purified/isolated in 1972 but alas they are nowhere to be found.

Albert Kapikian and Co. are far too happy to looking at 💩. 

Before delving into the 1972 paper, in 2000 Albert Z. Kapikian, the lead author himself, provided insight into the “discovery” process used to find the elusive “norovirus.” I have provided a few relevant highlights:

The Discovery of the 27-nm Norwalk Virus: An Historic Perspective

“I was invited to present my reflections on the discovery of the Norwalk virus. This is a personal odyssey that chronicles the steps in making the arduous leap from the discovery of a 27-nm virus-like particle to its etiologic association with epidemic gastroenteritis. I will describe how, by necessity, we bypassed the classical tissue-culture virology approach, which relies on the ability of a virus to infect and produce a change in cells or to infect an animal model. Rather, we used a novel approach—“direct virology” or “particle virology”—in which the virus particle itself is studied directly as the “center of attention” without the benefit of an in vitro or animal model system.”

“The search for a viral etiologic agent for acute gastroenteritis began in the late 1960s and was intensified in the early 1970s. The search for a viral agent was based on the rationale that (1) the etiology of most episodes of infectious gastroenteritis among pediatric and adult populations was unknown [23]; (2) it was assumed that viruses were important in these outbreaks because bacteria were associated etiologically only infrequently [23]; (3) bacteria-free stool filtrates induced gastroenteritis in adult volunteer studies [4–12]; and (4) new techniques, such as organ culture, that might enable the cultivation of a fastidious etiologic agent had become available.”

Attempts to Detect a Virus Associated with Gastroenteritis by Tissue-Culture Techniques

“Although known infectious filtrates were available from these studies, all attempts to identify an etiologic agent using newly available tissue-culture techniques were unsuccessful. Similarly, studies of numerous outbreaks of naturally occurring gastroenteritis consistently failed to reveal an etiologic agent even during the “golden age” of virology in the 1950s and 1960s, when the use of tissue culture led to the discovery of scores of new cultivatable viruses, such as the ECHO and coxsackie-viruses, many of which grew to high titer in the enteric tract [2–3].

Attempts to Detect a Virus Associated with Gastroenteritis by Novel Organ Culture Techniques

During the late 1960s, new techniques were developed for the detection of fastidious viruses. These included the use of human embryonic nasal or tracheal organ culture, which preserved cells in their normal state of differentiation and architecture. Organ culture was used successfully for the discovery of several new respiratory coronaviruses that did not grow in conventional tissue cultures [1314]. The success in growing fastidious coronaviruses in organ culture stimulated renewed efforts to cultivate the elusive agents of “viral” gastroenteritis; human fetal intestinal organ cultures were established in an effort to find a method to support the growth of a heretofore noncultivatable gastroenteritis virus [1516]. However, the organ culture technique (as well as standard tissue-culture techniques) also failed to yield an etiologic agent [17]. Although the study specimens that were tested were derived from individuals with nonbacterial gastroenteritis, there was no practical way of knowing whether they contained infectious material that was capable of producing disease. It was possible that the inability to detect a virus resulted from the absence of an infectious agent in the test specimen. Fecal specimens of known infectivity from early volunteer studies described above could not be accessed because they were either not available at the time or had been exhausted.”

The Rationale for Using Immune Electron Microscopy (IEM) for Detection of Fastidious Viruses

“An unanticipated course of events influenced the ultimate progress of the gastroenteritis program at NIH. In 1970, I spent 6 months in Anthony Waterson’s Department of Virology at the Royal Postgraduate Medical School of the University of London to learn electron microscopy under the tutelage of June Almeida, an outstanding electron microscopist and a pioneer in the application of IEM to virology. This technique, a method defined as the direct observation of antigen-antibody interaction [23], was not new—it had been described in 1941 in studies with tobacco mosaic virus [2425]. Even with the development of electron microscopes with increased resolving power and the introduction of negative-staining techniques, which greatly enhanced contrast, thus facilitating the recognition of viruses [26], the application of IEM was underutilized. We examined human coronaviruses by IEM to visualize the formation of complement holes in the envelope following incubation with uninactivated serum, as previously described for an avian coronavirus [23]. We also examined rhinovirus preparations by IEM in an attempt to visualize these 27-nm viruses clearly because they did not grow to high titer, were of rather small size (even for a virus), and did not have a distinctive morphologic appearance [27].

The power of this technique was shown clearly in these rhinovirus studies, in which a relatively low-titered tissue-culture suspension of rhinovirus 1A was reacted with a specific goat serum or a control (PBS). The mixture was then centrifuged, and the pellet was reconstituted with distilled water and stained with phosphotungstic acid [27]. Examination of the control preparation revealed scattered, randomly distributed, 27-nm particles, some of which could not be identified conclusively as a virus (figure 1). However, in the virus-serum preparation, the 27-nm rhinovirus particles were no longer randomly distributed but appeared in the form of large and small aggregates coated with antibody and standing out clearly from the background, leaving no doubt that they were virus particles (figure 2). These observations had a major impact on the course of my future research as I realized that IEM might enable the detection of fastidious viruses that do not grow in tissue culture. Key to this concept was the realization that although hyperimmune serum would not be available for enabling the detection of a noncultivatable unknown agent, convalescent sera could be used for screening as it would provide the specificity needed to detect a putative viral agent.”

“Because of the failure to cultivate virus from infectious stool material from ill volunteers from the Norwalk outbreak, I extended the IEM studies [30] and examined the Norwalk agent stool filtrates, using a volunteer’s convalescent serum as the source of antibody [31]. In June 1972, almost 20 months after beginning such studies, I examined a Norwalk agent stool filtrate (designated 8FIIa) derived from a volunteer who became ill after oral administration of the Norwalk agent [31]. This filtrate was known to contain an infectious agent because it had induced a diarrheal illness in 6 of 10 volunteers. Following incubation of the stool filtrate with a volunteer’s convalescent serum and further preparation for electron microscopy, glistening aggregates of nonenveloped, antibody-coated 27-nm, virus-like particles, which resembled rhinoviruses, were visualized. A characteristic aggregate observed in early experiments is shown in figure 3A. The visualization of virus-like particles was very promising, but it was clear that further studies were needed to determine the significance of this finding. Had the incubation of the Norwalk agent stool filtrate with convalescent serum merely facilitated the detection by IEM of an adventitious virus that had no relationship to the Norwalk outbreak?”

“Although these findings moved us closer to an etiologic association, another step in establishing causation was necessary. Could the 27-nm virus-like particle be an adventitious virus that was present in the Norwalk stool filtrate and, thus, had merely infected each volunteer nonspecifically and was unrelated to the illness? The adventitious virus could have been a contaminant in the original rectal swab specimen (along with the real Norwalk virus) or could have been picked up during passage in volunteers.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7110248/

It is clear from Kapikian’s words that they went in believing (i.e. assuming) a “virus” was responsible for the the non-bacterial cases of gastrointestinal disease and that they had no way of determining whether this was true or not as they were unable to culture any “virus.” Thus, he set out to use the same IEM technique he had utilized previously to find 27 mm particles in tissue culture he claimed to be “rhinoviruses” in order to find 27 mm particles in stool samples from the Norwalk outbreak which…just so happened to resemble “rhinoviruses.” In other words, he found the exact same particles using the exact same methods yet claimed they were two different “viruses.”

Yep.

If you desjre to throw yourself further into this fraudulemt feces fantasy, presented below is Kapikian’s full “norovirus” paper from 1972:

Visualization by Immune Electron Microscopy of a 27-nm Part’icle Associated with Acute Infectious
Nonbacterial Gastroenteritis

A 27-nm particle was observed by immune electron microscopy in an infectious stool filtrate derived from an outbreak in Norwalk, Ohio, of acute infectious nonbacterial gastroenteritis. Both experimentally and naturally infected individuals developed serological evidence of infection; this along with other evidence suggested that the particle was the etiological agent of Norwalk gastroenteritis.

In spite of intensive efforts, an etiological agent has not been found for acute infectious nonbacterial gastroenteritis-a usually self-limited disease characterized by a spectrum of clinical symptoms which may include vomiting, diarrhea, abdominal pain, or a combination thereof (5, 10, 16). This syndrome affects a broad segment of the population and was the second most common disease experience in a 10-year family study (8, 9). The disease, which has been given various descriptive names, was transmitted to volunteers in the 1940’s and 1950’s and again more recently in 1971 and 1972, but all attempts to definitively cultivate and characterize an etiological agent in vitro have failed (5, 6, 11-17, 19, 21, 22). In the 1971 study, a filtrate from a rectal swab specimen from an adult who developed a secondary case of acute nonbacterial gastroenteritis during an outbreak in Norwalk, Ohio, induced the typical illness in two of three volunteers; it was serially passaged two additional times in volunteers and again induced the typical illness (1, 5, 11, 12). Characterization studies in volunteers revealed that the infectious agent in Norwalk outbreak-derived filtrates was less than 66 nm in diameter and probably less than 36 nm and, in addition, was not inactivated by ether, acid, or heating at 60C for30 min (11).

In an attempt to detect these fastidious, presumably viral, gastroenteritis agents, we adapted the technique of immune electron microscopy to the study of stool filtrates derived from the Norwalk outbreak. Previously, this method had been employed in serological or antigenic studies, or both, of various viruses, and was used for the successful observation of rubella virus (3, 4).

Recently, this technique had facilitated the detection of Australia antigen and permitted the observation of rhinoviruses in semipurified suspensions (18, 23). Furthermore, immune electron microscopy has been employed successfully for the detection of an antigenic inner component of the Dane particle associated with hepatitis virus B and enabled the detection of a new coronavirus strain (2, 7, A. Z. Kapikian, H. D. James, Jr., S. J. Kelly, and A. L. Vaughn, Infect. Immunity 7, 1973, in press). The present studies which resulted in the detection of small “picorna or parvovirus-like” particles to which certain volunteers and naturally infected individuals developed significant antibody increases are described below.

The 2% second human passage stool filtrate (8FIIa) used in these immune electron microscopy studies was derived from a stool specimen of a
volunteer who developed gastroenteritis after oral administration of a stool filtrate derived from one of the two volunteers who became ill after receiving the original inoculum from the Norwalk outbreak (1, 11, 12). The 8FIIa pool, which had been filtered through a 1,200- and a 450-nm membrane filter (Millipore Corp.) and prepared by previously described methods, was known to contain an infectious agent; it had induced gastroenteritis in 6 of 10 volunteers, but extensive attempts to recover or detect an etiological agent by conventional techniques were unsuccessful (11, 12; R. Dolin et al., unpublished studies). Therefore, we examined this filtrate for the presence of virus particles by immune electron microscopy utilizing inactivated convalescent serum from experimentally infected volunteers as the source of specific antibody as previously described in our
coronavirus studies (A. Kapikian et al., Infect. Immunity 7, 1973, in press). This approach was taken in the hope that virus particles would appear in the form of aggregates, thereby enabling the observation of a small virus, possibly present in low titer. The serum-stool filtrate mixtures (and at various times, 0.85% phosphate-buffered [pH 7.4] saline [PBS]-stool filtrate mixtures) were incubated at room temperature for 1 hr routinely. PBS was then added, if necessary, to make a final pre-centrifugation volume of 1.0 ml for each mixture. The mixtures were then centrifuged at 17,000 rev/min for 90 min in a Sorvall RC2B centrifuge with an SS34 fixed-angle rotor. The supernatant fluid was carefully discarded; the pellet or sediment was suspended with a few drops of distilled water, stained with 3% phosphotungstic acid (PTA), pH 7.2, placed on a 400-mesh Formvar-carbon coated grid, with the excess fluid being removed with the edge of a filter paper disc, and the grid examined at a magnification of 40,000 with a Siemens Elmiskop 1A electron microscope (3, 18).

In the initial experiment, reaction of 0.4 mnl of the 8FIIa stool filtrate with 0.1 ml of a 1:10 dilution of convalescent serum from volunteer A who developed the typical illness after challenge with an 8FII stool filtrate (see Table 1) resulted in the appearance of aggregates similar to the one shown in Fig. 1. The particles which were heavily coated with antibody were not randomly distributed but were present as groups which stood out clearly from the surrounding matter and appeared to resemble the picorna or parvoviruses.

In stool filtrate-PBS control preparations, occasional particles or groups of particles without apparent antibody were seen, and Fig. 2 shows a particularly favorable orientation of six such particles. The significance of these particles would have been difficult to evaluate without the previous experience acquired from examining similar, but heavily coated, particles which had been aggregated by antibody. These particles appeared to have cubic symmetry and there was a suggestion of surface substructure, but a definite pattern could not be ascertained (Fig. 2). They measured approximately 27 nm in their shortest diameter and 32 nm in their longest and again resembled both the picornaviruses and the parvoviruses morphologically.

These studies were then extended to include both prechallenge and convalescent sera in an attempt to detect serological evidence of infection by immune electron microscopy. A 0.2-ml amount of a 1:5 dilution of uninactivated serum was mixed with 0.8 ml of the 8FIIa stool filtrate since in preliminary studies 0.1 ml of a higher dilution of serum plus 0.4 ml of the 8FIIa stool filtrate resulted in variable staining with PTA. In these
serological studies, the grids were read without prior knowledge of the specimen being examined in order to eliminate the possibility of biased interpretation. Routinely, five squares on each grid were examined in a median time of approximately 1 hr, and the preparation was then rated for the quantity of antibody as follows: 0 = no aggregates (3 or more particles in a group were considered to constitute an aggregate); 1+ = m glistening aggregates, lightly covered with antibody; 2+ = moderately glistening aggregates, moderately covered with antibody; 3+ nonglistening aggregates, heavily coated with antibody; 4+ = nonglistening aggregates so heavily coated with antibody that they were almost obscured. A 1 + difference was considered to be a significant change in the amount of antibody present. An example of an aggregate scored as 1 + is shown in Fig. 3, and another scored as 4+ is shown in Fig. 4.

The paired sera from volunteer A were tested as noted above with the 8FIIa stool filtrate. The pre-illness serum mixture yielded one aggregate which was lightly covered with antibody, whereas with the convalescent serum specimen approximately 15 very heavily coated aggregates were observed. As shown in Table 1, these pre-and postsera were rated as 1 + and 4+, respectively; no aggregates were observed in a PBS control in which 0.2 ml of PBS was incubated with 0.8 ml of the 8FIIa stool filtrate.

Volunteer B, who developed the typical experimental illness, also demonstrated an increase in antibody by immune electron microscopy from 2 + to 4 + with 4 and 10 aggregates, respectively (Table 1). Similar increases in antibody were seen with volunteers C and D who also became ill after challenge with the 8FIIa stool filtrate, whereas volunteer E, who did not develop illness, did not have a significant change in antibody titer (Fig. 5 and 6, and Tables 1 and 2). No aggregates were observed in PBS-8FIIa stool filtrate mixtures.

Although all four volunteers who developed illness after challenge with the 8FIIa stool filtrate developed serological evidence of infection, it was possible that the observed particles might represent a virus not related to the etiological agent of the Norwalk outbreak; it was conceivable that an adventitious virus could either have been present in the stool of the patient from the original Norwalk outbreak or could have been acquired during passage through volunteers. We examined this possibility by testing paired sera from six individuals from the Norwalk outbreak; four were primary cases, one a secondary case and one a contact who did not become ill (1). Serum samples were kindly supplied by Milford H. Hatch, Jonathan L. Adler, and Raymond Zickl. As shown in Table 1, three of the five persons
with naturally acquired Norwalk gastroenteritis developed an increase in antibody to the 27-nm particles during convalescence from disease, whereas the two who did not show such an increase demonstrated a high degree of antibody in both their acute and convalescent sera. The acute-phase sera were not collected until several days after the onset of disease, and this may explain our failure to detect a response in two of the patients. The contact who did not become ill similarly did not exhibit a serum response (Table 1); one of the aggregates observed with the contact’s early serum was comprised not only of the usual “full” particles but with two “empties” as well (Fig. 7). It is of interest that among the seroresponders was the donor (J) of the original rectal swab specimen
which had induced illness in two of three volunteers in the 1971 study (1, 12). We examined by immune electron microscopy the prechallenge and convalescent sera of these two volunteers (L and M) and found that one developed an increase in antibody whereas the other did not (Table 1). The development of an increase in antibody by three of the five naturally ill individuals suggests that the 27-nm particle was not acquired during passage in volunteers. Furthermore, these serum responses suggest that the virus-like particles had infected patients during the Norwalk outbreak.

Finally, we investigated the possibility that gastrointestinal disease might stimulate the observed antibody responses by a nonspecific mechanism. In another study to be reported in detail later, volunteers were first administered either a stool filtrate containing an infectious agent from a secondary case of gastroenteritis which had occurred in Honolulu, Hawaii, or from a secondary case which had occurred in Montgomery County, Md., (R. G. Wyatt et al., unpublished studies). Those volunteers who became ill after primary challenge were later rechallenged with the same agent, and homologous immunity was demonstrated. Subsequently, challenge with a filtrate derived from the Norwalk outbreak produced disease, indicating that the filtrates derived from the Hawaii and Maryland cases differed from that of Norwalk. Sequential sera from two volunteers (C and D described previously) who underwent the sequence of three challenges just described were studied by immune electron microscopy with the 8FIIa pool as antigen. The volunteer administered the filtrate derived from the Hawaii case failed to develop an increase in antibody following gastroenteritis induced by the primary challenge, but did develop a significant response after illness induced by the Norwalk filtrate, suggesting that the immune electron microscopy seroresponse was specific (Table 2). The other volunteer developed an increase in antibody after gastroenteritis induced by primary challenge and a further increase after illness induced by the Norwalk filtrate, suggesting that the infectious agents in the Maryland and the Norwalk filtrates may have been antigenically related (Table 2).

It was noteworthy that each of the 13 individuals demonstrated the presence of antibody in pre-, acute-phase, or early sera, suggesting that infection with the agent derived from the Norwalk outbreak, or a related agent (or agents), was quite common. Possibly, the agents of nonbacterial gastroenteritis may resemble certain respiratory viruses in their capacity to reinfect with facility.

We have presented data suggesting that the 27-nm particle was the etiological agent of Norwalk gastroenteritis. Although it is conceivable that the 27-nm particle induced infection which was not related to the disease, it is unlikely. In any case, additional laboratory and epidemiological studies are needed to confirm the postulated etiological relationship.

https://lm.facebook.com/l.php?u=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC356579%2Fpdf%2Fjvirol00275-0197.pdf%3Ffbclid%3DIwAR1e_AsbtWV2vH3RUWNT81iq1z7IWHmE0FoT2BXQm9PVD7wBs9lcmw2MpYI&h=AT1rgTprmF3WsLyWwOEjDOX48rdtoZoqv49td3B52-76kMV3IcPXA4m6dRTRs3RlbOVWQOcmnLnx0Z63lC0hEp9UCzm9yq50ui8N4Kjm2pCvD1REGpdMZ5VR1imPN_SEkFmwgwkmP9-cmk2m5TiLnA

In Summary:

  • Efforts to cultivate “norovirus” in cell culture and to develop an animal model were unsuccessful
  • The evolving literature focused on describing the physical characteristics of this small, round-structured “virus” in clinical specimens and on the serologic response to infection
  • “Norovirus” has been likened to a “shape-shifter,” a mythical creature that can change form or being due to its continued evolution
  • An inability to cultivate “norovirus” in vitro until very recently and the absence of an animal model that closely resembles human disease, together with “viral” and human host diversity, have represented major obstacles to understanding of the pathogenesis of and immune response to “norovirus” infection
  • Much of our knowledge of the immunology of this highly species-specific “virus” revolves around studies of MNV (a mouse “virus”) and the use of “virus-like” particles (VLPs) of human “norovirus”
  • VLPs are the product of self-assembling “viral” structures derived from the expression of recombinant VP1 (i.e. synthetic creations)
  • No animal model to date has been entirely satisfactory
  • The inability to culture the “virus” in vitro precludes the ability to detect neutralizing antibody by classical methods
  • Several advances into understanding the relationship among the “viral” strain, the host human blood group antigen type, and disease susceptibility have recently been elucidated, but this work has not yet been extended to clinical practice
  • The interplay of “norovirus” and host immunity still poses many unanswered questions
  • Areas of future research may overcome technical limitations, such as the inability to cultivate “norovirus” in vitro, and may elucidate a way to directly measure neutralizing antibodies
  • “Noroviruses” are classified as members of a category of “viruses” known as the “Calicivirus” family
  • The “caliciviruses” have been difficult to study due to their inability to grow in a cell culture system and the lack of a good animal model system
  • The challenges in “norovirus” research are:
    1. To develop models in which to study the “viruses”
    2. To develop methods to more easily detect the “viruses”
    3. To develop ways to treat and prevent “norovirus” infection
  • A major hindrance to “norovirus” research has been the lack of a system in which to grow the “virus”
  • Kapikian described how, by necessity, they bypassed the classical tissue-culture virology approach, which relies on the ability of a “virus” to infect and produce a change in cells (i.e. CPE) or to infect an animal model
  • Instead, they used a novel approach—“direct virology” or “particle virology”—in which the “virus” particle itself was studied directly as the “center of attention” without the benefit of an in vitro or animal model system
  • The search for a “viral” agent was based on the rationale that:
    1. The etiology of most episodes of infectious gastroenteritis among pediatric and adult populations was unknown
    2. It was assumed that “viruses” were important in these outbreaks because bacteria were associated etiologically only infrequently
    3. Bacteria-free stool filtrates induced gastroenteritis in adult volunteer studies
    4. New techniques, such as organ culture, that might enable the cultivation of a fastidious etiologic agent had become available
  • All attempts to identify an etiologic agent using newly available tissue-culture techniques were unsuccessful
  • Similarly, studies of numerous outbreaks of naturally occurring gastroenteritis consistently failed to reveal an etiologic agent even during the “golden age” of virology in the 1950s and 1960s
  • The success in growing fastidious “coronaviruses” in organ culture stimulated renewed efforts to cultivate the elusive agents of “viral” gastroenteritis; human fetal intestinal organ cultures were established in an effort to find a method to support the growth of a noncultivatable gastroenteritis “virus”
  • However, the organ culture technique (as well as standard tissue-culture techniques) also failed to yield an etiologic agent
  • There was no practical way of knowing whether samples contained infectious material that was capable of producing disease
  • It was possible that the inability to detect a “virus” resulted from the absence of an infectious agent in the test specimen
  • Kapikian studied under June Almeida, of “coronavirus” fame, and utilized Immunoelectron Microscopy (IEM) for virology
  • This technique, a method defined as the direct observation of antigen-antibody interaction, was not new—it had been described in 1941 in studies with tobacco mosaic “virus”
  • They examined “rhinovirus” preparations by IEM in an attempt to visualize these 27-nm “viruses” clearly because they did not grow to high titer, were of rather small size (even for a “virus”), and did not have a distinctive morphologic appearance
  • In “rhinovirus” studies, a relatively low-titered tissue-culture suspension of “rhinovirus” 1A was reacted with a specific goat serum or a control (PBS)
  • The mixture was then centrifuged, and the pellet was reconstituted with distilled water and stained with phosphotungstic acid
  • Examination of the control preparation revealed scattered, randomly distributed, 27-nm particles, some of which could not be identified conclusively as a “virus”
  • However, in the “virus-serum” preparation, the 27-nm “rhinovirus” particles were no longer randomly distributed but appeared in the form of large and small aggregates coated with antibody and standing out clearly from the background, leaving no doubt that they were “virus” particles
  • Key to this concept was the realization that although hyperimmune serum would not be available for enabling the detection of a noncultivatable unknown agent, convalescent sera could be used for screening as it would provide the “specificity” needed to detect a putative “viral” agent
  • Because of the failure to cultivate “virus” from infectious stool material from ill volunteers from the Norwalk outbreak, Kapikian extended the IEM studies and examined the Norwalk agent stool filtrates, using a volunteer’s convalescent serum as the source of antibody (assumed to be specific to the invisible “virus” never discovered to be in the poop sample in the first place)
  • In June 1972, almost 20 months after beginning such studies, he examined a Norwalk agent stool filtrate (designated 8FIIa) derived from a volunteer who became ill after oral administration of the Norwalk agent (the volunteer got sick after drinking poop juice…shocking…)
  • This filtrate was known to contain an infectious agent because it had induced a diarrheal illness in 6 of 10 volunteers
  • Following incubation of the stool filtrate with a volunteer’s convalescent serum and further preparation for electron microscopy, glistening aggregates of nonenveloped, antibody-coated 27-nm, “virus-like particles,” which resembled “rhinoviruses,” were visualized
  • In other words, they found the exact same particles as “rhinoviruses” using the exact same methods for “rhinoviruses” but later claimed they were “norovirus”
  • While Kapikian felt that the visualization of “virus-like” particles was very promising, it was clear that further studies were needed to determine the significance of this finding
  • Kapikian even pondered whether the 27-nm “virus-like” particle could be an adventitious “virus” that was present in the Norwalk stool filtrate and had merely infected each volunteer nonspecifically and was unrelated to the illness
  • He also wondered whether the adventitious “virus” could have been a contaminant in the original rectal swab specimen (along with the real Norwalk “virus”) or could have been picked up during passage in volunteers
  • Both experimentally and naturally infected individuals developed serological evidence of infection
  • This paper starts off shooting itself in the foot as beyond the fact that they are entirely theoretical, specific serological antibody responses would be impossible to determine without purifying/isolating the particles believed to be a “virus” first
  • In spite of intensive efforts, an etiological agent had not been found for acute infectious nonbacterial gastroenteritis
  • The disease, which had been given various descriptive names, was transmitted to volunteers in the 1940’s and 1950’s and again more recently in 1971 and 1972, but all attempts to definitively cultivate and characterize an etiological agent in vitro have failed
  • In the 1971 study, a filtrate from a rectal swab specimen from an adult who developed a secondary case of acute nonbacterial gastroenteritis during an outbreak in Norwalk, Ohio, induced the typical illness in two of three volunteers; it was serially passaged two additional times in volunteers and again induced the typical illness
  • In other words, they took poop juice from one man, fed it to 3 others which caused 2 of them to have upset stomachs (shocking) and then did it again by using poop juice from other volunteers
  • In an attempt to detect these fastidious, presumably “viral,” gastroenteritis agents, they adapted the technique of immune electron microscopy to the study of stool filtrates derived from the Norwalk outbreak
  • This technique was said to have facilitated the detection of Australia antigen and permitted the observation of “rhinoviruses” in semipurified (i.e. not purified) suspensions
  • The 2% second human passage stool filtrate (8FIIa) used in these immune electron microscopy studies was derived from a stool specimen of a volunteer who developed gastroenteritis after oral administration of a stool filtrate derived from one of the two volunteers who became ill after receiving the original inoculum from the Norwalk outbreak
  • Once again, a person drank another person’s poop juice and got an upset stomach…mind-blowing work here…
  • The 8FIIa pool, which had been filtered through a 1,200- and a 450-nm membrane filter and prepared by previously described methods, (not detailed) was known to contain an infectious agent; it had induced gastroenteritis in 6 of 10 volunteers, but extensive attempts to recover or detect an etiological agent by conventional techniques were unsuccessful
  • Of course, what is in the poop juice mixture is hidden behind PREVIOUSLY DESCRIBED METHODS
  • This approach was taken in the hope that “virus” particles would appear in the form of aggregates, thereby enabling the observation of a small “virus,” possibly present in low titer
  • The serum-stool filtrate mixtures (and at various times, 0.85% phosphate-buffered [pH 7.4] saline [PBS]-stool filtrate mixtures) were incubated at room temperature for 1 hr routinely
  • PBS was then added, if necessary, to make a final pre-centrifugation volume of 1.0 ml for each mixture
  • The particles which were heavily coated with antibody were not randomly distributed but were present as groups which stood out clearly from the surrounding matter (i.e. not purified) and appeared to resemble the picorna or “parvoviruses”
  • In stool filtrate-PBS control preparations, occasional particles or groups of particles without apparent antibody were seen
  • The significance of these particles would have been difficult to evaluate without the previous experience acquired from examining similar, but heavily coated, particles which had been aggregated by antibody
  • They measured approximately 27 nm in their shortest diameter and 32 nm in their longest and again resembled both the “picornaviruses” and the “parvoviruses” morphologically
  • In other words, the control sample had the exact same particles and the only way they would know these particles were different from any other particles in the mixture was due to staining by antibodies in the prior experiment
  • Routinely, five squares on each grid were examined in a median time of approximately 1 hr, and the preparation was then rated for the quantity of antibody as follows:
    • 0 = no aggregates (3 or more particles in a group were considered to constitute an aggregate)
    • 1+ = m glistening aggregates, lightly covered with antibody
    • 2+ = moderately glistening aggregates, moderately covered with antibody
    • 3+ nonglistening aggregates, heavily coated with antibody
    • 4+ = nonglistening aggregates so heavily coated with antibody that they were almost obscured.
  • A 1 + difference was considered to be a significant change in the amount of antibody present
  • Nothing subjective about this highly subjective rating scale at all…
  • Volunteer B, who developed the typical experimental illness, also demonstrated an increase in antibody by immune electron microscopy from 2 + to 4 + with 4 and 10 aggregates, respectively
  • Although all four volunteers who developed illness after challenge with the 8FIIa stool filtrate developed serological evidence of infection, it was possible that the observed particles might represent a “virus” not related to the etiological agent of the Norwalk outbreak
  • It was conceivable that an adventitious “virus” could either have been present in the stool of the patient from the original Norwalk outbreak or could have been acquired during passage through volunteers
  • Only three of the five persons with naturally acquired Norwalk gastroenteritis developed an increase in antibody to the 27-nm particles during convalescence from disease
  • The development of an increase in antibody by three of the five naturally ill individuals suggested that the 27-nm particle was not acquired during passage in volunteers
  • They investigated the possibility that gastrointestinal disease might stimulate the observed antibody responses by a nonspecific mechanism
  • One volunteer administered the filtrate derived from the Hawaii case failed to develop an increase in antibody following gastroenteritis induced by the primary challenge, but did develop a significant response after illness induced by the Norwalk filtrate, suggesting that the immune electron microscopy seroresponse was specific
  • The other volunteer developed an increase in antibody after gastroenteritis induced by primary challenge and a further increase after illness induced by the Norwalk filtrate, suggesting that the infectious agents in the Maryland and the Norwalk filtrates may have been antigenically related
  • In other words, if a stool filtrate from a different outbreak did not produce the same antibody results, then their results were considered specific. However, when acquiring the same results with a filtrate from another outbreak, instead of claiming the results were proven not to be specific, Kapikian decided the two different filtrates must be related thus still claiming specificity. See the trick?
  • It was noteworthy that each of the 13 individuals demonstrated the presence of antibody in pre-, acute-phase, or early sera, suggesting that infection with the agent derived from the Norwalk outbreak, or a related agent (or agents), was quite common
  • This could also suggest that the antibody response ISN’T SPECIFIC if it could relate to agents other than “norovirus”…
  • Kapikian claimed to have presented data suggesting that the 27-nm particle was the etiological agent of Norwalk gastroenteritis
  • He then admitted that it was conceivable that the 27-nm particle induced infection which was not related to the disease, but claimed it was unlikely
  • He concluded that additional laboratory and epidemiological studies were needed to confirm the postulated etiological relationship
Not so notorious.

Kapikian’s 1972 paper amounts to using EM to pick random particles from poop which resemble preconceived ideas of what a “virus” should look like and seeing if they clump together when serum is added to them. The antibody staining is assumed to be specific and marking only the “virus” and none of the other similar/identical particles within the sample. Kapikan and Co. then infer meaning behind the subjective analysis of the clumping based on a scale they created themselves. Meanwhile, no purified/isolated “virus” is ever shown nor are these unpurified/unisolated particles ever proven pathogenic. It all boils down to one completely subjective shitty experiment (pun somewhat intended).

While the unpurified IEM images of random particles stained with non-specific antibodies is enough to call into question the claims made in the 1972 paper, there is another factor which disproves the particles assumed to be “norovirus” as pathogenic. This is the fact that there are many (30-40%) asymptomatic (i.e. HEALTHY) cases of “norovirus:”

“Assuming that all norovirus outbreaks (n = 55) were the result of random sampling from an identical distribution and ignoring genogroup and genotype specificities, the asymptomatic ratio was estimated AT 32.1% (95% confidence interval [CI], 27.7–36.7). Although not significant, separate estimation of the asymptomatic ratio of the GII.4 genotype appeared to be greater than other genotypes and was estimated at 40.7% (95% CI, 32.8–49.0).”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6111106/

“Asymptomatic” is considered if a person is a carrier for a disease or infection but experiences no symptoms. There was no consensus among the studies on this definition. Some studies defined “asymptomatic” as healthy person’s with no symptoms of gastroenteritis (diarrhea, vomiting, or fever, etc.). Others included people without symptoms of gastroenteritis for at least 1 week prior and more than 3 weeks after the day of stool collection. Finally, in some studies, norovirus was detected in nondiarrheal stool specimens collected from healthy persons, but it was unknown if they had vomiting or other symptoms.”

https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(18)30026-9/fulltext

So with all of this information taken into consideration, how does the evidence for “norovirus” stack up? Let’s look to Koch’s Postulates, the basic logical requirements needed to be fulfilled in order to prove a pathogen causes disease, and see if the “norovirus” is the home run the defenders believe it to be:

  1. The pathogen must be found in diseased but not healthy individuals
    • FAIL: It is estimated that there are anywhere from 30-40% asymptomatic healthy cases
  2. The pathogen must be cultured from the diseased individual in a pure form
    • FAIL: It can not be cultured at all in any form
  3. Inoculation of a healthy individual with the cultured pathogen must recreate the disease
    • FAIL: Not everyone came down with symptoms of disease and no satisfactory animal model exists recreating the disease
  4. The pathogen must be re-isolated from the inoculated, diseased individual and matched identically to the original pathogen
    • FAIL: It was never purified/isolated originally nor were any purified/isolated particles ever shown to be pathogenic

It would seem that the “norovirus” evidence is not the bases loaded grand slam people thought it was. It is more akin to bottom of the ninth, down by 10 runs with 2 outs, and the weakest batter is at bat with no balls and 2 strikes.

Swing and a miss.

You’re out!

Game over.

10 comments

  1. This is classic. If you’re hired as a virologist and get to investigate a disease that could have multiple causes, you will find viruses.
    It’s just like the church who used to be in charge of “medicine” who would declare it the devil needing an exorcism.

    Such a fucking joke. Scientific method goes out the window with this nonsense “specialization” crapitalist system of compartmentalization.

    Liked by 1 person

  2. Me and some of my family got this 3-day illness they call “novovirus” some years ago, one family member after another. This was in Central America after I ate some unwashed fruit.

    Seemed like a cut and dried case of contagion, and maybe it was, but we were all eating at the same places, plus I had it again a few weeks later back in my home country. Also, my girlfriend and I were making out heavily for hours a day that whole time and she never got sick at all.

    But there’s one obvious aspect to this: me and the family member who got sick were hitting the junk food uncharacteristically hard and eating tons of local cheap&unhealthy snacks (it was Christmas season). I was feeling like I was not doing so well already, so I decided to eat something healthier and immediately got “noro.”

    I’m pretty sure it’s a bowel detox for times when one has really gone too far with bad food, or could just be food poisoning, but the family had two separate stories of “one immediately after another” illness rather than simultaneous, so that may nix the food poisoning possibility.

    The apparent transmissability suggests it’s something the body takes some discretionary cues as to when to perform. It kind of makes sense the body is reluctant to screw you over by making you a barfing, diarrhea-spurting 12-times-a-day pariah if no one else is doing a similar process, but if someone else is…golden opportunity for radical removal of this junk.

    The fact that I got it again so soon after, back in my home country, though, suggests no transmission is needed. The body will do it if it really needs to. The odds of “catching noro” twice in 3 weeks in two different countries seem very small.

    Liked by 2 people

    1. I agree. I believe it is nothing more than a detox process from unhealthy nutrition/lifestyle. There are probably cases where it is food poisoning as well. Same symptoms either way. They just love to claim different illnesses by giving the same symptoms different names and causative agents. This way they can sell more toxins as cures and nobody blames the quality of the food.

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  3. Big pharma has been striking out for decades. Their entire drug empire is based on fear, paranoia, legerdemain and aiding and abetting by multiple thousands of conflicting interests. Destroy the virus illusion and a whole lot of people go broke. Researchers and scientists need income to live so why not create a whole new branch of fake science? The greenies are following the same script.

    I wonder how humanity managed to survive and thrive during the previous 5,000 years before “modern” drugs came along? Seems like their was little in the way of anti-germ systems, sanitary systems, and useful medical knowledge provided by doctors. But they had healthier foods and purer water and knowledge of natural remedies like herbs and spices. Using those make much more sense to me as a means of healthy survival.

    Liked by 1 person

    1. The narrative dismisses the past 5,000 years with janky arguments about life expectency, which neglects things like malnutrition (due to poverty), famines, wars, security issues, slavery, dangerous work, predators, child sacrifice, abandonment of the elderly, general hard lives with more injury, high infant mortality due to having many children and other non-pharma factors, and notably there’s no accounting for quality of life and aesthetics (so many crooked faces due to vaccine-induced microstrokes (see the work of Forrest Maready and Andrew Moulden)). And probably more I’m forgetting.

      Liked by 2 people

    2. Yes, I believe the idea that people were unhealthier and/or dying younger in the past is a myth. We are unhealthier today due to the numerous sources of toxins we encounter, both physically and mentally. Those who lived in unsanitary conditions died younger of course, much like they do today. However, those who lived away from these toxins (i.e. native Americans) thrived until they were forced into a different way of life when conquered by outside invaders.

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  4. I always love the specificty of statements like “27 to 32 nm in diameter”. Can something this small actually be measured, even using electron microscopy? I also wondered, how is a norovirus infection diagnosed? Yep, our old friend, the notorious PCR based on a genomic sequence. “Diagnostic methods for norovirus focus on detecting viral RNA (genetic material) or viral antigen. Diagnostic tests are available at all public health laboratories and many clinical laboratories, and most use reverse transcription- real-time polymerase chain reaction (RT-qPCR) assays to detect norovirus.” Thanks Mike, you blew the lid off another “virus” story.

    Liked by 1 person

    1. Thanks Lynn! I highly doubt that anything they do with particles that small can be considered accurate. And yes, once it is clear that PCR is involved, we know we are being conned. 😉

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