Observations Concerning My Encounter with COVID-19 (?)

 

For the last month, or so, I have been recovering from a fairly serious illness that began in late September 2021 and continued on throughout most of the month of October 2021. Many individuals -- whose understanding has been shaped and framed by sources that, for various reasons, cannot necessarily be trusted – might be likely to have assumed that the illness against which I have been struggling was nothing other than a manifestation of a viral infection caused by SARS-CoV-2. For reasons that will be made clear during the course of this book, such an assumption is not necessarily warranted.

This book has been written, for the most part, during my period of on-going recovery. It gives expression to a variety of observations that have been made concerning the whole COVID-19 narrative and what relevance, if any, that narrative has in relation to my recent bout of illness. Click on the image of the book cover for the link to the Amazon page.

Jeffrey Taubenberger's 1998 PBS Interview Concerning The 1918 Influenza Seems Strangely Familiar

 

Before being employed by National Institute of Allergy and Infectious Diseases, Jeffrey Taubenberger used to work for the Armed Forces Institute of Pathology (AFIP). The Institute has been in existence for about 130 years and began its operations during the Civil War as the result of an executive order by Lincoln which instructed the Army Surgeon General to study diseases that were connected to the battlefield.

The foregoing executive order was issued because more people were dying from various forms of pathologies that arose in conjunction with military conflicts than actually died as a result of the weapons that were being deployed during those engagements. Consequently, the Institute became a venue for collecting and studying samples taken from surgery as well as autopsies involving both human beings and animals that had roles of one kind or another within the military.

Taubenberger is a specialist in molecular pathology. This discipline develops methods for making diagnoses based on changes in genetic composition rather than -- as is the case in conjunction with traditional methods of pathology -- using microscopic examination of biological samples to do so.

Pathology samples are generally fixed in chemicals such as formaldehyde, and, then, embedded in wax. This makes the process of isolating DNA and RNA difficult to accomplish because the genetic material found within the samples that are fixed in the foregoing ways tends to become quite degraded over time.

RNA is much more fragile than DNA is. However, Taubenberger indicates that researchers have developed techniques which permit pathologists to help optimize – as much as possible – recovery efforts concerning those two molecules, and, consequently, the alleged 1918 flu virus served as an opportunity for using, exploring, and developing the kind of recovery techniques to which Taubenberger was alluding earlier that involve various kinds of molecules which are of interest to researchers.

Nevertheless, whatever the nature of the foregoing sorts of recovery techniques might be, unless one can show how those protocols are capable of zeroing in on RNA that is uniquely from alleged viral bodies rather than from other biological sources, then one is faced with a problem. More specifically, why should one suppose that whatever RNA is recovered through the foregoing sort of techniques is necessarily from viral bodies rather than from other biological components – such as tissue cells that have died and released their genetic contents into the samples that have been preserved?

Taubenberger said his recovery project was intended to “get a first direct look at the virus.” However, for a number of reasons (some of which are noted in the following discussion), one might wish to question whether, or not, his research group actually ever came in contact with the alleged virus, and, therefore, in order to investigate such a possibility, let’s take a look at various facets of Taubenberger’s research that are touched upon in the 1998 Taubenberger interview.

According to Taubenberger, there were some 70 samples that were present in the Institute’s archives that had been drawn from people who supposedly died from the influenza in 1918. These samples had been fixed in formalin and paraffin, and half of them were selected arbitrarily or randomly for purposes of study.

People died in different ways during the so-called Spanish Flu event of 1918. Some individuals died very quickly following the onset of symptoms, and this was quite different from the way people were believed to normally succumb to past cases of influenza.

Given that there were differences in the length of time that passed between, on the one hand, instances in which symptoms first began to appear, and, on the other hand, the point when life processes ceased in various patients, one query that could be explored is whether all the people who were dying in 1918 were necessarily dying from the same underlying pathology. For example, over the years, there have been a number of theories based on various kinds of evidence which suggest that whatever deaths occurred during 1918 might have been due to something other than -- or, perhaps, in addition to -- a suspected influenza virus.

Among the theories which have arisen over the years, are the following possibilities.  (1) The forms of vaccines and medical treatments that were in use in 1918 often were injurious to patients in one way or another and, as a result, people might have died from the medical treatments they received rather than from a virus; or, (2) what had been diagnosed as cases of influenza were, instead, actually due to the work of the bacteria that is responsible for tuberculosis – something that was endemic in many places during the era of the “Spanish Flu and which can give rise to symptoms that are very similar to ones that are present in cases of influenza and, consequently, medical practitioners might have improperly diagnosed the nature of the problem with which they were dealing; or, (3) many people might have been developing bacterial infections of one kind or another due to the masks that were being worn to (supposedly) protect them against the alleged virus; or, (4) the pathology that was being referred to as the Spanish Flu might, actually, have been a form of poisoning that occurs when susceptible people are exposed to excessive amounts of certain kinds of electromagnetic radiation; or, (5) conceivably some combination of the foregoing possibilities came together in a sort of perfect storm of lethality, but, subsequently, were all subsumed in an undifferentiated fashion under the category of “death due to influenza”.

To be sure, the aforementioned observed differences concerning the time intervals between symptom onset and death might have been a function of the extent to which individuals within the affected population could have possessed varying capacities of resistance to the pathology or pathologies to which they had been exposed. Nonetheless, as intimated previously, another way of accounting for the foregoing kinds of differences in temporal intervals between symptom onset and death is that an array of lethal causes might have been involved in the events of 1918, and some of those maladies might have been more lethal than others, and, if this were the case, then this might explain why some individuals died far more quickly than other individuals did.

Besides the issue of rapid rates of morbidity, another oddity concerning some of the people who became sick during 1918 had to do with the onset of pulmonary edema in which the lungs of patients would fill up with fluids generated by, among other things, the blood from hemorrhaging tissue. Such people died by drowning in their own fluids.

What was odd about the foregoing feature is there was very little, if any, inflammation that was observed prior to, or during, the rising, deadly onslaught of such bodily fluids. The presence of pulmonary edema together with the absence of inflammation was not ordinary when compared with cases of influenza that had occurred in past years.

A third, somewhat unique aspect of the patient histories that were being studied by Taubenberger in conjunction with the 1918 “Flu” had to do with the age of the individuals who were succumbing to whatever the pathology might have been that was stalking people during that time. Most of the cases he studied involved people who had been healthy and were young, rather than consisting of the sorts of elderly individuals who normally fell victim to influenza.

Therefore, in summary, there were at least three properties associated with some of the 70 cases that had been archived from 1918 that distinguished those cases from what might be considered to have been “normal” instances of influenza based on past clinical experience. First, the time interval between the onset of symptoms and the occurrence of death was extremely rapid in various cases; secondly, many of those cases involved pulmonary edema without being accompanied by any kind of inflammation, and, finally, many of the people who were dying were much younger in age than the individuals who normally were vulnerable to the ravages of influenza.

So, presumably, any explanation that proposes to account for what is transpiring in cases such as some of the ones that were occurring in 1918 will entail putting together a causal framework that might be capable of providing a degree of insight with respect to those cases that were exhibiting properties or characteristics that departed from what previous clinical experience had indicated was the normal course of events involving influenza. Such an explanation would need to answer at least the following questions – namely: Why was pulmonary edema showing up in 1918 patients without simultaneously being accompanied by inflammation, or why were some people succumbing quickly in 1918 relative to what seemed to have happened in the past with cases of influenza, and, finally, why did whatever was happening in 1918 seem to affect – in atypical fashion relative to cases of influenza in previous years -- young people rather than the elderly?

The foregoing questions will be re-visited toward the end of this article. However, let’s leave aside -- at least for the time being -- the foregoing considerations and continue on with exploring the information that is being transmitted through Taubenberger’s 1998 PBS interview.

For instance, according to Taubenberger, influenza viruses are believed to replicate very quickly. Yet, why – or how -- the foregoing characteristic is present is not addressed by Taubenberger.

What is said is the following: The process of rapid replication allegedly takes place within the cells of lung tissue, and, then, in about five day’s time, viral bodies supposedly withdraw from the foregoing cells and move on to infect other cells and/or individuals. Consequently, according to virologists, after about a week one will not find any viral bodies present in lung tissue cells that had been infected previously by those alleged viral bodies.

As a result, Taubenberger wanted to examine samples of “influenza” patients who died in 1918 that -- according to the archived medical records -- had died within one week, or less, from whatever pathology had befallen them. In theory, such samples might provide him with an opportunity to access some of the replicated RNA material before it disappeared from a cell’s interior.

One of the cases that met the foregoing conditions was accompanied by a sample that displayed strong histological features.  In other words, when one looked at the tissue sample with a microscope, one could detect evidence that was interpreted to have been the result of primary influenza pneumonia.

Virology theory contends that the influenza virus consists of eight RNA fragments. These fragments supposedly vary in length, and are believed to run from approximately 1000 to 2500 base pairs per fragment.

In his PBS interview, Taubenberger indicates that the size of the fragments that he was able to recover from the 1918 patient lung tissue sample was only about 150 to 160 base pairs long. He admits in the interview that his research project consisted largely of trying to find ways to piece together different RNA fragments that were recovered from the sample being studied and, then, eventually, he hoped to arrive at a stage of research through which he would be able to come up with a model for the entire genome of the influenza virus.

Taubenberger’s research is, to some extent, based on assumptions concerning the number and type of genes that are contained in different kinds of alleged influenza viruses. In other words, the number of genes (supposedly eight) is based on a theory about gene structure and function rather than being based on discoveries concerning the actual number, structure and function of genes “in the wild” that have been isolated, characterized, and sequenced in a rigorous methodological manner.

In the PBS interview, Taubenberger indicates that his research group first looked at segments of five different genes in order to attempt to develop a sense of what the overall genomic properties of the influenza virus might look like. However, given what has been said earlier in this article, Taubenberger and his associates weren’t necessarily looking at subsections of the actual genes of an alleged influenza virus, but, instead, might only have been looking at theoretical constructions of those genes … theoretical constructions that might, or might not, accurately reflect the structure of certain facets of the contents that could have – possibly -- originally existed within the cell tissue samples being studied.

Taubenberger states that after completing the foregoing sorts of preliminary studies, his group began to narrow its focus on what was considered to be – at least theoretically -- one of the primary surface proteins of the influenza virus. The aforementioned protein supposedly is coded for by the hemagglutinin gene, and virologists believe that the hemagglutinin protein is the means by which influenza viruses gain access to the interior of a host that is allegedly being infected by such an agent.

Nonetheless, once again, all Taubenberger -- as well as his research associates -- might have accomplished is to have engaged reality through the lenses and filters of the theoretical framework to which virology gives expression. After all, among other things, no one, yet, has been able to capture the dynamics of a virus entering a cell through the activity of a hemagglutinin surface protein.

Consequently, one cannot be certain that the aforementioned sorts of cellular access events actually take place. Alternatively, if the foregoing dynamics actually do occur, one still does not know the details of those dynamics and whether, or not, the character of that activity accurately reflects the theory which virologists have put forth concerning how they believe influenza viruses are structured and function.

Notwithstanding the foregoing considerations, Taubenberger maintains that his research group has succeeded in putting together the genetic sequence that is alleged to code for the hemagglutinin protein. The sequence is said to be about 1800 bases in length.

However, as noted earlier, all one can really say is that the research group has come up with a “possible” sequence which is highly theoretical in nature. This is because Taubenberger and his associates have never actually isolated an influenza virus but, instead, have put forth various hypotheses concerning the nature of those sequences that is based on various theoretical principles for which there is a consensus, of sorts, by a certain number of practitioners within the field of virology.

Yet, science requires more than consensus. One must be able to empirically demonstrate that the working hypothesis which is being used to explain certain kinds of phenomena can be verified independently by means of real world data that is capable of being replicated in a variety of experimental circumstances.

Unfortunately, in many respects, virology gives expression to a set of theories concerning the way its proponents believe certain dimensions of reality operate. As a result, virology doesn’t necessarily accurately capture the facet of reality to which its theories are alluding.

As an addendum to the foregoing claim, one might note in passing that despite a lot of early hype on the matter, nonetheless, virology failed miserably to come up with a defensible viral theory of cancer during the 1970s and 1980s. Moreover, as the Perth Group in Australia -- along with Peter Duesberg, Kary Mullis, and others -- has shown, through a variety of empirical venues, virology also struck out with respect to being able to provide a verifiable explanation for precisely how HIV causes AIDS, and, yet, despite such a monumental failure, many virologists continue to engage life through their best, blustery, Wizard of OZ, knob turning, lever pulling, smoke generating, pay no attention to the man behind the curtain modes of behavior.

Furthermore, since the HIV causes AIDS debacle (which led to the deaths of millions of people in Africa and elsewhere through the ill-advised use of poisonous anti-viral medicines such as AZT), many virologists have been making a very good living promoting various modalities of fear-porn as they sought to transmit their alleged concerns to fellow human beings with respect to all manner of alleged imminent viral pandemics [such as: West Nile Virus (1999), SARS (2003), Swine Flu (2009), MERS (2012), Avian Flu (2013), Zika Virus (2015-2016), and so on] that, supposedly, were, or are, invading humanity. Moreover, virologists and other researchers were not shy to recommend that everyone urgently needed to be treated by means of one brand, or another, of virology-based vaccinations and pharmaceuticals despite the fact that none of their pronouncements – either with respect to the alleged pandemics or the proposed treatments for those putative pandemics – accurately reflected what actually transpired in the real world during the aforementioned time periods.

During his PBS interview, Taubenberger stated he felt that the complete reconstruction of the entire set of genetic instructions for the influenza virus (and not just the hemagglutinin gene on which he was focused prior to 1998) is likely to take years to complete since the fragments being studied are so small that the process of reassembling them is very time intensive. One should point out once again, however, that the foregoing sorts of efforts will not necessarily involve reassembling the actual genetic sequence of some viral entity (For example, see my article: The Deadliest Flu: The Complete Story of an Influenza Pandemic (?), which is a critical reflection on a CDC paper that purports to provide an account of the subsequent work of Taubenberger and others concerning their contention that they have “discovered” the viral agent that, supposedly, was responsible for the 1918 flu).

Instead, as intimated previously, he appears to be interested in developing a theory about what he and his associates believe such a sequence might look like, and this assumes, of course, that such an entity actually exists. In short, Taubenberger’s research group is engaged in a process of interpreting certain kinds of data and, therefore, the group is not necessarily pursuing a course of research that is capable of uncovering the actual nature of the dynamics that give expression to the 1918 phenomena which they are seeking to explain.

In many respects, Taubenberger and his associates appear to have become entangled in a game of conceptual will-o’-the-wisp. If so, then the foregoing sorts of understanding which are guiding his research team could be nothing more than a series of variable glimpses into a mist of elusive data that is heavily shaped by theoretical considerations that could be distorting the nature of what actually might have happened in 1918.

According to Taubenberger, his research group believes that it can assert, with some degree of definitiveness, that the entity which they believe they have been studying is an influenza virus. More specifically, they claim that the agent they have been studying is a type A influenza and belongs to the subtype H1N1 where H and N stand for proteins that supposedly permit such an alleged virus to, respectively, be able to gain access to (i.e., infect), as well as to be able to exit, a given cell on its way to infect other cells or organisms.

Virologists maintain that there are three types of influenza viruses – namely, A, B, and C. These types of influenza are further sub-categorized according to the kind of hemagglutinin (H) and neuraminidase (N) proteins that are believed to be present on the surface of any given influenza virus.

While such influenza types and subtypes give expression to virology theory, nonetheless, no one has seen viruses entering or exiting cells via, respectively, H and N proteins. Therefore, there appears to be an absence of the requisite kinds of data which might be able to definitively verify any of the aforementioned theoretical pronouncements of virology.

Currently, virologists claim there are 14 different kinds of hemagglutinin protein subtypes and 9 different subtypes of neuraminidase proteins which differentiate one type of influenza from another type of influenza. The virus that is believed to have been present in the lung tissue samples from patients who died during 1918 is thought to be the H1N1 subtype, and this belief rests on the sorts of antibodies which were found in people who had been alive during 1918 but were able to survive whatever took place at that time.

Although there are theories within virology and immunology about how, and why, antibodies emerge, there is no reliable empirical data which actually captures the process of antibodies coming into existence. The evidence all has to do with finding antibodies at one point in time but not another, and, then, coming up with a theory for why such antibodies are found at one time but not another, or why those antibodies exist in some people but not others.

Virologists not only believe that influenza viruses infect human beings, but, as well, such individuals also are of the opinion that those presumed viral agents are able to infect chickens, ducks, and a variety of birds as well as pigs and horses. Furthermore, based on the study of serum drawn from human beings who lived during 1918 and were able to survive whatever transpired during that year, virologists maintain that the antibodies in circulation in those individuals are a closer match to alleged swine influenza bodies that virologists believe were discovered in the 1930s than the aforementioned 1918 antibodies were a match to the human influenzas that were supposedly discovered in the 1930s.

Unfortunately, during the interview, Taubenberger does not spell out what is meant by the idea that the so-called “matches” between certain types of influenza and antibodies circulating in the blood stream are a better fit when considered in conjunction with alleged swine influenza bodies of the 1930s rather than in relation to presumed human influenza bodies of the 1930s. Antibodies can be quite promiscuous with respect to the kinds of entities with which they manifest some degree of affinity, and, therefore, one cannot be certain – as some virologists seem to be -- that the reason why there is a some amount of affinity between antibodies from 1918 and swine influenza bodies from the 1930 is necessarily because the 1918 antibodies were formed due to, or response to, an encounter with some sort of swine flu entity either just prior to, or during, the events of 1918.

In fact, if -- contrary to current theories and models of virology -- one were to entertain an hypothesis that the 1918 influenza virus did not necessarily exist, then, one would have to come up with a different theory to account for why antibodies of a certain kind might exist at one time rather than another. After all, if the 1918 influenza virus did not exist, and if influenza was caused by something other than a virus, then, making the sort of claims that some virologists seem inclined to make concerning the alleged significance that is supposedly demonstrated through the presence of alleged matches between particular kinds of antibodies and certain kinds of swine viruses becomes something of a problem.

Among other things, the foregoing conceptual crisis would force one to search for some alternative reason or set of reasons to account for why antibodies of a particular kind can be found in the serum of some people but not others. In other words, one would have to ask: Why do certain antibodies arise if this is not in response to the presence of some sort of viral agent?

Notwithstanding the foregoing considerations, Taubenberger and his research associates believe that the aforementioned purported antibody-swine flu match indicates that the 1918 flu did not come directly from avian sources but, instead, arose through some sort of mammalian connection. In other words, they believe that the path of viral transmission might have started with avian organisms, and, then, emerged, at some point, within mammalian organisms -- such as swine -- and, then, somehow, got passed on to human beings.

However, at the present time, there is no detailed account that is capable of providing a viable explanation for the supposed process through which various genetic fragments might be able to make the jump from avian hosts to swine hosts, and then, subsequently, to human hosts. Although, in general terms, the foregoing sort of transition phenomenon is presumed to have transpired through some modality of recombinant DNA or RNA processes, nonetheless, this presumption is unaccompanied by any sort of account concerning a demonstrable, step-by-step dynamic that gives expression to the proposed series of transitions in genetic material that runs from avian, through swine, and, eventually to human beings.

The foregoing issue is crucial. In other words, based on antibody data (which, as previously suggested, does not necessarily mean what some researchers believe that data signifies), Taubenberger stipulates that prior to 1918, viruses had been circulating within human populations in a relatively non-lethal form except in conjunction with a small fraction of individuals who, for various reasons, might have been susceptible to those kinds of influenza agents, and, therefore, one needs to ask the following questions: How did the 1918 influenza virus acquire its alleged lethality, and what was the nature of the biological or molecular mechanism that underlies such supposed lethality?

 According to Taubenberger, viruses tend to be genetically unstable, and, as a result, undergo regular transitions with respect to certain aspects of their structure and function.  Taubenberger describes such transitions as “… presumably an adaptation of the virus, to evade the host immune response, so that the influenza virus that was circulating last year is not the same as the influenza virus that is circulating this year” and concludes by saying: “So they’re very clever in that sense.”

To be sure, changes in genetic sequences might give expression to some form of genetic instability, but determining the cause of those changes tends to be quite another matter. One cannot assume – as Taubenberger seems to -- that changes in the genetic sequence of a virus are due to some sort of, apparently, intentional or logistical viral strategy which seeks to adapt to a host’s immune response by bringing about changes that enable successive generations to evade that same kind of immune response.

Viruses are not necessarily “very clever” in the foregoing sense.” More specifically, if one were to assume that changes in genetic sequence occur among viruses, then, although some of those changes might confer a “novel” advantage of some sort, nonetheless, other changes might not necessarily confer any kind of advantage, or those changes could introduce something that is decidedly a disadvantage to the virus.

Therefore, whether or not a presumed virus acquires some sort of new “trick” that permits the immune responses of a host to be evaded will depend on the nature of the changes in genetic sequence that either do, or do not, occur. Yet, such changes do not necessarily have anything to do with some kind of adaptive strategy of ‘cleverness’ that is supposedly actively transpiring within a given viral entity.

In other words, changes in genetic sequence within a proposed virus could be a reflection of nothing more than – to use Taubenberger’s way of stating things -- the inherent genetic instability of those entities. If so, then, as previously indicated, whatever changes occur in genetic sequence do not necessarily have anything to do with cleverness or adaptive, evolutionary strategies but merely give expression to the alleged virus’s on-going susceptibility to genetic instability which arbitrarily moves the genome of the alleged virus in one direction rather than another … sometimes with felicitous results, and sometimes with problematic results, and, sometimes with the sort of variance that has no appreciable impact concerning issues of adaptability.

Taubenberger maintains that while mutations do tend to occur on a regular basis, most of these changes will not lead to substantially different structural or functional forms. However, he believes that every so often, substantial changes do occur, and this takes place he supposes as the result of some sort of recombinant exchange dynamic that takes place between two different species.

As a result, he maintains that the foregoing sorts of recombinant changes could give rise to a form of virus that has not previously been encountered. Furthermore, he believes that this sort of virus might pose a threat for any species that did not have the capacity to defend against the presence of that kind of an agent.

Of course, not all changes in genetic sequence will necessarily give rise to a variant that carries potential lethal implications in conjunction with human beings. Moreover, for a virus, the essence of adaptation is a function of being able to replicate and continue on, and such a capacity is quite independent of any potential that might bring about biological mayhem in the organisms that are being engaged by the virus. 

In short, the capacity of a virus to inflict pathology on its host – or, in conjunction with some degree of vulnerability or susceptibility in a host to the properties of a virus that will generate a dynamic that results in death or disease -- is not necessarily adaptive. On the other hand, the capacity of a virus to be able to replicate is quintessentially adaptive in nature.

Although there is considerable evidence indicating that recombinant processes do occur, nonetheless, the notion that those recombinant processes will necessarily give rise, at some point, to something that is, on the one hand, capable of evading the capacity of organisms to defend against the presence of such entities, and, on the other hand, will be capable of being highly lethal in relation to its impact on a given organism is really nothing more than a conjecture. Consequently, even though Taubenberger – along with other researchers -- has put forth a hypothesis which contends that the foregoing sort of ‘substantial’ recombinant event occurred in connection with 1918, nonetheless, he has not provided evidence which demonstrates that such an event actually did occur.

In fact, during the PBS interview, he indicates that he actually is searching for the foregoing sort of evidence. Consequently, although – as noted earlier -- he does refer to a certain amount of data involving antibody titers in blood serum that had been drawn from people who lived during -- but survived – the 1918 event, nevertheless, at best, that sort of data is only suggestive – and can even be ambiguous with respect to its significance concerning the possible relationship between swine influenza viruses and human beings  -- and, therefore, the presence of the sorts of antibody data to which Taubenberger is alluding does not necessarily support his contention that the existence of those antibodies means that they came into existence as a result of earlier encounters with swine flu antigens.

During the PBS interview, Taubenberger refers to three alleged pandemics – namely, events in 1918, 1957, and 1968 – which he believes give expression to the possibility that some sort of recombinant set of events occurred which gave rise to novel viruses of one kind or another that had lethal properties in all three of those instances. However, in each case, Taubenberger fails to put forth any evidence to persuasively demonstrate that what he believes was responsible for those three events – namely, changes in genetic sequence due to recombinant dynamics – is what actually happened.

Furthermore, one might note in passing that there is a certain amount of evidence to indicate that the events of 1918, 1957, and 1968 might not have been due to a viral agent at all. For example, in the book: The Invisible Rainbow: A History of Electricity and Life, Arthur Firstenberg puts forth considerable evidence in support of the possibility that the three “pandemics” cited by Taubenberger (as well as a number of other outbreaks of “influenza” that occurred prior to 1918 and after 1968) might have been due to various kinds of changes in electromagnetic radiation that were being introduced into the Earth’s environment at those times (e.g., numerous new sources of powerful radio frequencies had come on line in many geographical locals just prior to and during 1918 and were being beamed throughout the world; or, in the case of 1957 there were many powerful radar facilities that were being deployed in various parts of the world, or, in the case of 1968, numerous communication and intelligence satellites had been, and were being, launched by various military groups as well as by an array of corporations and, as a result, such technology was bathing the Earth – and its life forms – in an array of electromagnetic radiation).

Radiation poisoning has been demonstrated to be capable of producing many of the same sorts or symptoms that are present in cases of influenza … symptoms that, for nearly a hundred years, have been attributed to a viral agent of some kind. In fact, although abundant evidence currently exists which is capable of demonstrating that electromagnetic radiation can bring about flu-like symptoms as well as many other kinds of pathological conditions (see the work of, among others, Samuel Milham, Olle Johansson, Martin Pall, and Devra Davis), nonetheless, to date, no one has been able to properly isolate an influenza virus which can be shown to be infectious or lethal (and the notion of “isolates” that appears in the virology literature is a bastardized version of the sort of rigorous methodologies that are needed to properly isolate, sequence, and demonstrate that such isolated agents actually exist as well as that they are actually infectious and lethal).

The foregoing considerations give expression to a very critical issue. If viruses, of one kind or another, cannot be shown (following proper isolation and sequencing) to be the cause of, say, influenza, then, one must look to some other sort of environmental trigger (e.g., chemical, electromagnetic, or biological) to account for the existence of those maladies.

Yet, if something other than a virus plays a role in the onset of influenza, then, the nature of the dynamic with which human beings are presently faced changes in substantial ways. For instance, instead of trying to come up with some kind of virology-based vaccine or virology-based pharmaceutical elixir, and, then, insisting that people – as a matter of public health – must become vaccinated with, or must ingest, such an anti-viral concoction, then, perhaps, the proper way of treating such maladies lies in another direction.

More specifically, if viruses do not have a causal role to play with respect to the occurrence of diseases such as influenza (and, to date, the viral theory of influenza rests on evidentially problematic grounds), and if, furthermore, viruses do not have a role to play in pathologies like SARS, MERS, Zika, and so on (and, once again, there has been no proper process of virus isolation that identifies different kinds of viruses as causing the foregoing maladies), then public health in those circumstances need not depend on discovering and mandating certain kinds of virology-based vaccines or pharmaceuticals.

Instead what is required is a shift in the nature of the paradigm through which those diseases are explored. In other words, if the nature of the problem with respect to the foregoing sorts of maladies is not a function of the role that different kinds of infectious agents of a viral nature play, then, perhaps the problems associated with, for example, influenza, might be better resolved if one were to suppose that the diseases mentioned previously might be due not to viruses but, instead, could be due to, for example, the impact that different kinds of electromagnetic and/or chemical poisoning are having on the environment along with the ecologies that reside in the environment.

If the latter possibility were the case, then the onus of responsibility for combating those pathologies would no longer be a matter of trying to foist off some sort of mandated vaccine or pharmaceutical program onto the people and, then, proceeding to try to argue that resolving those health crises requires individuals to do their civic duty and take their medicine in order to protect others. Instead, the responsibility for combating the aforementioned diseases shifts to those who are poisoning the environment through chemical, electromagnetic, or biological means, and, therefore, what must be mandated are not various kinds of vaccines or pharmaceuticals but, rather, mandates should be issued which require various environmental polluters to cease and desist with respect to the activities which are poisoning human beings.

Toward the latter part of his 1998 PBS interview, Taubenberger returns to the idea of evolutionary adaptation. For example, after mentioning how there are many bacteria which can be found on our skins and within various parts of the gastrointestinal tract that are well-adapted to the surrounding biological environment and which actually perform many useful functions for their hosts – such as generating vitamin K – he goes on to allude to different kinds of bacteria and viruses that are not well-adapted to their hosts and, as a result, those entities take on what Taubenberger believes to be is an adversarial relationship with their hosts.

Taubenberger does not explain how bacteria and their hosts came to work out adaptive solutions which serve their mutual interests – or how they discover ways that, at least, do not adversely affect one another. Furthermore, he does not mention the fact that there are many different kinds of agents that have been found on, say, human skin – such as staphylococcus aureus – that, under the right circumstances, are potentially harmful but which, for unknown reasons, are not always active, and, therefore, contrary to what Taubenberger claims, do not automatically take on an adversarial relationship with their hosts.

In any event, Taubenberger indicates that if an agent -- virus ‘x’ -- were to behave in an overly aggressively manner with respect to their hosts, then, the infected individuals will die too quickly. As a result, this sort of aggressive activity would tend to prevent that virus from being able to move on to other hosts.

Taubenberger alludes to the idea that the alleged 1918 virus seems to have avoided the foregoing sort of problem and, instead, was able to work out a good evolutionary strategy. In other words, although he believes that the virus killed a lot of people, nevertheless, it somehow managed to constrain its activities in ways that only lethally affected somewhere between 2 and 5 percent of the population.

According to Taubenberger, by behaving in the foregoing manner, such a strategy provided the virus with an opportunity to move from host to host and, thereby, spread all over the world since only a relatively small percentage of the host population succumbed to the alleged onslaught of that virus. One wonders, however, whether the aforementioned 2-5% solution is the product of an evolutionary strategy that emerged in some inexplicable manner or whether that percentage merely reflects the possibility that 2-5% of the population is, for whatever reasons, vulnerable to the presence of certain kinds of agents and, therefore, the 2-5% figure might have nothing to do with some sort of viral evolutionary strategy but, instead, just gives expression to the manner in which viral agents with certain kinds of properties interact with susceptible biological systems in a given set of contingent circumstances and, in certain instances, leads to a series of complex interactions that result in the demise of some of those organisms.

Taubenberger maintains that as a virus is transmitted from locale to locale in different regions of the world, people eventually would have developed an effective immune response to the virus. He further contends that such a state of affairs of general immunity would have placed the virus under “enormous pressure” to undergo mutation so that it could change some facet of its genetic composition – such as the part of the genome that gave expression to one or another protein on its surface – in order to be able to find new ways of infecting human hosts.

Notwithstanding Taubenberger’s foregoing account, one might suppose that mutations either occur, or they don’t. One does not need to assume that there is some sort of “pressure” that is present which induces a given virus to mutate.

Taubenberger’s use of the term “pressure” might merely be his way of framing the discussion by means of a theory which seeks to advance the possibility that there is some kind of “force” in existence which is capable of inducing organisms to move in – or mutate in -- new directions that will prove to be adaptive. However, over a period of several billion years, the primary lesson of life on Earth would seem to be that, sooner or later, almost all species tend toward extinction irrespective of whatever changes might, or might not, take place with respect to their genomes.

As far as we know, to whatever extent viruses exist, they consist only of a glycoprotein coating which houses either an RNA or DNA-based genomic reservoir which codes for a small number of genes that, under the right circumstances, supposedly enable those viruses to go about the business of replicating themselves by hijacking the machinery of a host cell or organism. Whether the foregoing entities can be considered to be alive in some sense is a debatable issue, but irrespective of their existential status, there is nothing in their molecular or genetic composition which would seem to suggest that there is some underlying force or pressure within them, or working through them, that requires mutations of a certain kind to emerge … namely, mutations that would allow those entities to find new ways to infect and/or inflict damage on a host.

However, Taubenberger resorts to the idea of viruses operating under an ‘extreme pressure’ to bring about adaptive mutations of certain kinds in order to account for why, after 1918, the alleged pandemic did not continue on but, eventually, petered out. Presumably, the virus had undergone some sort of mutation that would permit it to continue to circulate within the human population but, in the process, had – due, perhaps, to the immune responses of host organisms – lost the ability to have anything more than a limited capacity for lethality with respect to all but a small percentage of human beings who were somehow vulnerable to such a viral presence.

Yet, to suppose, as Taubenberger does, that a virus must mutate if it is to continue on is not necessarily true. Indeed, until one knows why some people are either more vulnerable than others -- or vulnerable at all -- to the presence of a viral agent, one cannot necessarily suppose that the virus will have to mutate in order to continue to be able to infect a host.

Thus, irrespective of whether, or not, antibodies arise in conjunction with the presence of a given viral agent -- and leaving aside the issue of whether, or not, the presence of those antibodies helps confer sufficient immunity to prevent all of a virus’s genetic potential from being able to express themselves -- it might be that some small percentage of a previous viral population will continue to exist even if such entities were to have lost their capacity to act in a lethal manner with respect to most individuals within a host population. A virus – to whatever extent it exists – has certain capabilities that (given the right opportunity) will be expressed, but in other circumstances might just remain inactive.

If the right kind of conducive circumstances do not arise, then, even if the virus was not able to fully express itself, nonetheless, it might continue to exist for an indeterminate or indefinite period of time quite independently of whether, or not, a host actively engages – or is engaged by -- such an agent. The entity just wouldn’t replicate, and since viruses – to whatever extent they exist – are not necessarily “alive,” then whether or not replication continues to occur is not necessarily a matter of “life and death” for such an entity.

The life cycle of a virus – to whatever extent it exists -- is digital in nature. It is either on or off … that is, it either replicates or it doesn’t.

Whatever else happens with respect to such an entity – in the way of lethality or infectivity or pathology – will be a matter of the particular manner in which a given virus and a given host interact with one another during the time in which the two are in contact. Conceivably, a virus could remain inactive or dormant even though the circumstances that are necessary for replication are not present, and, yet, such a body might still continue to inhabit a host just as bacteria like staphylococcus aureus can be found in human beings in a non-active or non-problematic state.

Consequently, Taubenberger’s notion that viruses must mutate in order to continue their existence is little more than a conjecture. While the possibility that he mentions is consistent with the theory of viruses as well as an evolutionary framework, there is not any evidence which is capable of definitively demonstrating the truth of the conceptual thrust of his conjecture concerning the existence of some sort of pressure that induces a virus to continue to mutate in ways that are increasingly adaptive in some sense of the word.

Indeed, one might suppose that developing some sort of capacity for lethality is actually counterproductive for a virus’s continued viability. Viruses appear to complete their life-cycle via replication and not through inflicting pathology.

There is no evident evolutionary purpose that appears to be served by enhancing the capacity of a virus to inflict pathology. Being able to gain access to the interior of a cell or to be able to find a way out of that cell or to be able to borrow some of a cell’s potential to replicate does not necessarily require the virus to be able to “infect” that cell in pathological manner and, thereby, cause some sort of disease anymore than DNA or RNA needs to inflict damage on a cell in order to be able to replicate.

Taubenberger’s 1998 PBS account of the 1918 pandemic leaves unanswered a number of questions. For example, what was the specific nature of the recombinant event(s) involving -- at least, possibly, initially -- birds and mammals (such as swine) and, then, how did the process of species jumping continue on by, allegedly, making the transition from the foregoing sorts of mammals to human beings? One also would like to know the precise character of the dynamics of lethality that supposedly arose in an unknown manner, and, therefore, one might ask whether the lethality came from birds, or mammals, or, in some unanticipated way, emerged during the time when the jump was made to human beings? Finally, one might also ask why and how such a lethal agent suddenly appeared to vanish.

Apparently, Taubenberger is putting forth nothing more than a narrative which has been woven from various assumptions and conjectures based on a hermeneutical engagement of different kinds of empirical data. Indeed, in many respects, virology – and any discipline (for instance, molecular pathology) that has a potential for contributing to the development of virology -- appears to be nothing more than a theoretical narrative which seems to be masquerading as a set of scientific discoveries.

Taubenberger states that: “Historically, it seems that most new influenza viruses emerge in Asia, in the Far East, which is another thing that’s unusual about the 1918 virus because everything we know historically suggested that it actually originated in the United States.” One might wonder, however, about why different kinds of influenza supposedly have such an inclination to begin in Asia.

Could the foregoing sort of asymmetry in racial or ethnic susceptibility be a function of certain kinds of environmental conditions (e.g., electromagnetic, chemical, as well as biological)? Or, could such a racial or ethnic asymmetry be due to some sort of genetic vulnerability that is more pronounced in Asians relative to other racial and ethnic groups? Or, perhaps such an asymmetry might be due to some sort of systemic iatrogenic issue in which various kinds of pneumonia and respiratory diseases are being misdiagnosed as, or confused with, influenza, and, as a result, one is being given a distorted impression of what is actually taking place or whether there is any actual kind of asymmetry in susceptibility to influenza that is present.

Nonetheless, notwithstanding the foregoing sorts of considerations, Taubenberger’s claim that the 1918 event started in the United States is not necessarily capable of being verified. More specifically, there is a considerable body of evidence (e.g., see Virus Mania by Torsten Engelbrecht and Claus Köhnlein, as well as The Invisible Rainbow by Arthur Firstenberg) indicating that large numbers of people were dying all over the Earth from influenza-like maladies at roughly the same time in 1918, and, indeed, even Taubenberger states during the PBS interview that the spread of influenza took place with an incredible rapidity that occurred “within a period of a month or so in the fall of” that year.  

Consequently influenza-like deaths were taking place in many locations around the world in a fashion that seemed to be faster than could be accounted for by any possible route of surface transmission that was available at that time (e.g., horses, automobiles, trains, or ships). On the other hand, the seemingly inexplicable rapidity of disease transmission in 1918 would be quite consistent with the possibility that the deaths being attributed to the “Spanish Flu” were actually due to the generation of electromagnetic frequencies that were poisoning people all over the world in a, more or less, simultaneous fashion at roughly the speed of light.

The explanation which Taubenberger offers as a way of trying to account for why influenza tends to emerge in Asian societies rather than in Western nations is zoonotic in nature. In other words, he contends that the cultural eating habits of many Asians involves going to so-called wet markets where various exotic life forms are available for purchase and consumption.

Presumably, somewhere along the line -- during or following the aforementioned visits to the so-called wet markets -- influenzas supposedly made a species jump from birds to mammals of one kind or another, or, a species jump allegedly transpired between mammals of one kind to other mammals such as human beings. Yet, as intimated previously, Taubenberger really doesn’t appear to have any concrete evidence that is capable of demonstrating the validity of his zoonotic hypothesis.

Taubenberger goes on to indicate that during the 1950s “influenza viruses could be cultured and characterized in the laboratory.” Technically speaking, however, viruses are not living and, therefore, do not need to be cultured. Indeed, short of a fully functioning host, there is no medium in which one could place a virus in order to help it grow and replicate.

In fact, if a given virus is functional, then, one does not need to place such a virus in some sort of medium culture. All one has to do is take a virus that has been properly isolated – and, therefore, separated from everything else including a culture medium of some kind – then, expose a potential host to that isolated virus and, finally, just wait to see what takes place.

This is what transpires in the wild, so to speak. Introducing cultured mediums into the research process merely obfuscates the character of whatever dynamics might follow.

According to Taubenberger, various attempts were made to exhume bodies of individuals in Alaska and elsewhere who supposedly died of influenza during 1918. However, while those exploratory expeditions were able to bring forth live bacteria through the use of various kinds of culture mediums, no one had been able to induce influenza viruses to surface.

In passing, Taubenberger mentions the work of a Canadian researcher, Dr. Kirsty Duncan, who has been attempting to locate the bodies of individuals who had died from influenza in 1918 but who had been buried in very cold – i.e., frozen – conditions. He notes that she is hoping to be able to uncover functional viruses from the foregoing sorts of cold storage exhumations.

Taubenberger contends that he feels the aforementioned research venture is not likely to succeed.  He goes on to indicate that influenza viruses are quite fragile and that although bodies frozen in permafrost might retain some fragments of viral RNA, nonetheless, those samples would be unlikely to contain “live” or viable viral entities because of – as previously noted -- the fragile character of the influenza virus.

While Taubenberger mentions the extremely fragile nature of influenza viruses in the foregoing overview, nonetheless, he doesn’t actually go into any sort of detail about the kind of environmental conditions that are necessary in order for a virus to be able to “survive” – i.e., be in a position to replicate when conditions are right. Presumably, the understanding which the aforementioned sort of missing information might help engender would be of value if one wanted to try to figure out the nature of the dynamic through which influenza viruses and human beings tend to engage one another, and, furthermore, such information also would be of value if wished to determine what kinds of conditions might be more conducive or less conducive to such alleged viruses becoming active within a host – human or otherwise.

Taubenberger believes that, generally speaking, societies in 1998 are in a much better position than they were in 1918 to be able to deal with potential pandemics. He feels this is the case because, among other things, “…we know that influenza viruses exist, and we can analyze them and watch their emergence and evolution.” In addition, Taubenberger maintains that societies also are better prepared to deal with potential forthcoming pandemics due to (1) advancements in medical treatment such as drugs that, supposedly, are able to thwart the capacity of influenza viruses to, for example, replicate, as well as due to (2) the emergence of influenza vaccines which Taubenberger claims “are obviously the most important factor of our current armamentarium against influenza viruses.”

However, as noted previously, neither Taubenberger, nor anyone else, has actually gone through the necessary set of rigorous procedures which are capable of properly isolating, characterizing, or sequencing the alleged1918 influenza virus, nor, in addition, has he or other researchers also been able to go on to reliably demonstrate that such isolated virus are both infectious as well as lethal [See my article: “The Deadliest Flu: The Complete Story of a Virus Influenza Pandemic (?)”]. Moreover, the antiviral treatments that are used to treat various viruses have proven, quite frequently, to be quite hazardous in their own right (for example, consider the deadly impact that the use of AZT had on the treatment of alleged cases of HIV).

Finally, notwithstanding Taubenberger’s foregoing claim to the contrary concerning the alleged essential role of vaccines, there is considerable evidence that flu vaccines (e.g., see Jabbed by Brett Wilcox; The Vaccine Court by Wayne Rohde; Dissolving Illusions: Disease, Vaccines, and the Forgotten History by Dr. Suzanne Humphries and Roman Bystrianyk; Vaccines: A Reappraisal by Dr. Richard Moskowitz, Vaccine Epidemic, edited by Louise Kuo Habakus and Mary Holland, as well as What Really Makes You Ill? – Why Everything You Thought You Knew About Disease Is Wrong by Dawn Lester and David Parker) are neither safe nor effective. In this respect, one might consider, among other possibilities, the fiasco that arose in 1976 with respect to so-called swine flu in which hundreds of cases were documented in which human beings suffered from Guillain-Barré Syndrome, instances of transverse myelitus, or death as a result of the flu vaccines that were given in 1976.

One might also note in closing – and as was intimated to be a topic that would resurface toward the beginning of this article -- that early in the PBS interview Taubenberger listed a number of features that were atypical with respect to cases of influenza that had been encountered prior to the 1918 event. More specifically, he indicated that: (1) the death of many individuals took place very rapidly following the onset of symptoms; (2) a substantial number of the cases that occurred in 1918 exhibited signs of pneumonia edema without any accompanying inflammation; (3) a large proportion of the cases he studied involved individuals who had been healthy and were young, rather than the sort of elderly people who, in the past, normally fell victim to influenza; (4) the “influenza” that occurred in 1918 seemed to emerge, more or less, simultaneously in different parts of the world rather than following some sort of epidemiological path that moved from one location to the next via individuals who were traveling by foot, or via horses, trains, or ships.

Nothing which Taubenberger stated in the 1998 PBS interview is capable of providing an answer to any of the foregoing anomalies that he, himself, introduced into the discussion and which seemed to differentiate the 1918 event from previous bouts of influenza. While he offers a lot of conjectures during his interview, nevertheless, he does not provide much in the way of substantive, definitive information that is capable of addressing the four aforementioned anomalies that apparently were uniquely characteristic of the 1918 “influenza” event and do so in a satisfactory manner.

Finally, as indicated earlier in this article, during the 1998 PBS interview, Taubenberger attempted to describe some of his research concerning the hemagglutinin gene and, in the process, sought to link that work to the events of the 1918 “Flu”. However, at best, his research only appears to advance a theoretical narrative, of sorts, concerning what he believes transpired in 1918 rather than giving expression to a fully delineated account of the 1918 phenomenon that is capable of being empirically substantiated.   

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If you would like to download a PDF edition of the foregoing article please go to: Taubenberger

The Deadliest Flu: The Complete Story of a Virus Influenza Pandemic (?)

 

The CDC article: “The Deadliest Flu: The Complete Story of a Virus Pandemic Influenza” – minus the parenthetical question mark which I have added for the title of this essay -- begins with a Transmission Electron Micrograph of the alleged virus that, supposedly, caused the 1918 pandemic known generally as “the Spanish Flu” despite not necessarily having its origins in that country. However, the micrograph does not constitute proof that the bodies depicted in the image are either infectious or lethal.

A micrograph, after all, is a static rather than a dynamic depiction of something about which claims are being made. This remains the case even if one were to concede that the bodies being depicted in the micrograph actually constitute a virus or even if one were to concede that the entities in the image constituted the same virus that many individuals believe was so lethal in 1918, and this latter contention is not necessarily a foregone conclusion. 

The CDC article operates on the assumption that the proper explanation for the 1918 phenomenon is that it involved a viral agent that was both highly infectious and highly lethal. As a result, the CDC article argues that the 1918 event provides valuable data and insights concerning how to prepare for future viral pandemics, and this assertion is also not necessarily tenable.

Early on, the CDC article maintains that “an unusual characteristic of this virus was the high death rate it caused among healthy adults 15 to 34 years of age.” Such a statement makes a number of assumptions.

For example, the foregoing statement presupposes – but does not prove -- that the people who died in 1918 all died from the Spanish flu virus (and there is considerable evidence to indicate that this might not be the case). Moreover, the aforementioned claim also operates on the assumption that the people who died were actually healthy individuals … as opposed to individuals who were outwardly apparently healthy but who might actually have had underlying health problems of one kind or another which had not, yet, shown up in the form of symptoms, and, therefore, while a viral agent of some kind might have played some role in the demise of certain individuals,  there may have been a number of factors aside from the presence of a given virus which was responsible for the death of various people. 

According to the CDC article, a dedicated group of researchers were able to: “ … search for the lost 1918 virus, sequence its genome, recreate the virus in a highly safe and regulated laboratory setting at CDC, and ultimately study its secrets to better prepare for future pandemics.” The CDC article purports to be a “complete” account of the history to which the foregoing process of research gives expression. 

The story being provided through the CDC paper begins with a small, ocean-side Alaskan village known as Brevig Mission. In 1918, the village contained approximately 80 adults, consisting mostly of Inuit indigenous people.

The article goes on to say that there has been some degree of controversy concerning just how the inhabitants of that village became infected. Some individuals believe that the virus was transmitted by a local member of the postal service, while others contend that the virus arrived in the village via one, or another, trader who travelled to Brevig Mission via dog sled.

Notwithstanding the foregoing considerations, if one doesn’t know how the virus was introduced into a community, then, one can’t necessarily be sure that the virus is what killed those individuals. All one can say is that something happened in 1918 which resulted in the death of 72 of the 80 inhabitants of that village, and one does not necessarily know why the 72 individuals who died were vulnerable to whatever happened, or why 8 people were able to survive.

One also one does not know if the latter eight individuals got sick and, then, recovered, or whether they ever became ill. Furthermore, if the latter possibility is the case, then, why didn’t they get sick?

What one does know is that all of the deaths took place within a six day period, lasting from November 15th to November 20th in 1918. The bodies were all buried in a mass grave near the village and remained that way until 1951.

In 1951, Johan Hultin, a Swede, was doing doctoral research in microbiology at the University of Iowa. He sought, and received, permission from village elders in Brevig Mission to excavate the bodies from 1918 because he believed that he might be able to find remnants of the 1918 flu in tissues of the bodies that had been buried and preserved in a frozen state while having been entombed in the permafrost for more than three decades. 

Hultin was able to procure lung tissue samples from five of the excavated bodies. Nonetheless, back in his laboratory at the University of Iowa, he was unable to induce what he believed were viral entities to become active when he injected his collected lung tissue samples into chicken eggs in order to try to get the virus to grow. 

In 1997, nearly a half century later, Hultin read an article by Jeffrey Taubenberger, and others, that appeared in the journal Science. The article was entitled: “Initial Genetic Characterization of the 1918 ‘Spanish’ Influenza Virus.”

Taubenberger is a molecular pathologist who, at that time, was working within the Armed Forces Institute of Pathology in Washington, D.C. . He, together with other members of his research team, had been able to obtain a lung tissue sample from an apparent victim of the 1918 flu who had been stationed in Fort Jackson, South Carolina at the time of the alleged pandemic. 

The soldier had been hospitalized on September 20, 1918 with a diagnosis of influenza and pneumonia. He died less than a week later on September 26, 1918, and a sample of lung tissue had been taken from him and stored for possible subsequent examination. 

Before proceeding further, perhaps, the following observation would not be inappropriate. More specifically, making a clinical diagnosis of influenza gives expression to a judgment that is made by a physician with respect to various symptoms that are being observed.

What is causing those symptoms is a separate, although, obviously, not an unrelated issue. However, electron micrographs that were capable of capturing images of possible viral-like entities would not be possible for nearly another two decades, and, consequently, to maintain in 1918 that symptoms of influenza or pneumonia were caused by a viral infection would be an entirely speculative perspective (This is a point that is touched upon in passing toward the latter part of the CDC article being discussed here.) . 

Physicians treat the clinical presentation of symptoms. The cause of those symptoms might not ever be known until an autopsy is performed, and, perhaps, not even then.

Furthermore, the issue of autopsy findings is somewhat of a moot point in 1918. Very few autopsies were performed in conjunction with determining the cause of whatever might be causing the deaths that transpired in 1918.

Putting the foregoing considerations aside for the moment, Taubenberger’s research group had been able to sequence nine relatively small remnants of single-stranded RNA chains from the aforementioned soldier’s lung tissue sample. Those nine fragments were alleged to be from four of the purported eight gene segments that were theorized to make up the genome of the 1918 influenza. 

One problem with the foregoing account is that since human cells – including samples from the lungs – often contain single-stranded RNA sequences of many different kinds, one cannot necessarily be sure that any given RNA fragment which one is able to acquire from a human cell is necessarily from a virus. Moreover, even if the single-stranded RNA sequence were from a virus, there is no guarantee that the segment will be from one particular kind of virus (i.e., 1918 Influenza) rather than from some other virus that might have been in the lung tissue of the soldier who died in 1918. 

Virologists contend that the Influenza A viral genome consists of eight, single negative-strand RNAs that can range between 890 and 2340 nucleotides long. Each RNA segment is believed to encode one to two proteins … including the glycoproteins -- hemagglutinin and neuraminidase – which is where the ‘H’ and the ‘N’ come from in the H1N1 subtype that is believed by many virologists to constitute the 1918 influenza virus.

There are thousands, if not millions, of RNA fragments that are to be found within the cultures that supposedly contain the foregoing sort of virus. So, the question becomes, how does one know that the “nine relatively small remnants of single-stranded RNA chains from the aforementioned soldier’s lung tissue sample” actually constitute fragments from the 1918 influenza?

Notwithstanding the foregoing issues, Taubenberger’s research group maintained that the RNA which it had sequenced constituted a novel form of influenza A – namely, H1N1. This virus was alleged to belong to a subgroup of viruses that tended to inhabit pigs and human beings rather than birds.

After reading the Taubenberger article in Science, Johan Hultin, wrote to Taubenberger and inquired about whether, or not, Taubenberger would be interested in what might be discovered if Hultin returned to Brevig Mission and, once again, tried to obtain some lung-tissue samples from the interred bodies that had died during the 1918 phenomenon. Taubenberger said he would be interested in such a venture, and, consequently, Hultin returned to the village which he had visited in 1951. 

During this return journey, and after, once again, receiving permission from village elders, Hultin unearthed the body of an Inuit woman who was buried some 7 feet deep in the mass grave. Her lungs had been extremely well-preserved due to the permafrost in which they had been entombed.

After placing the lungs in an appropriate kind of preserving fluid, Hultin later sent the excavated biological materials to Taubenberger. Word subsequently came back to Hultin from Taubenberger “that positive 1918 virus genetic material had indeed been obtained from” the lung tissues that had been sent.” 

Nothing is said in the CDC article at this point about what made the RNA sequences from the Inuit woman’s lungs positive with respect to the 1918 virus. In other words, one does not know what the RNA sequences from the Inuit woman’s lung tissue cells were being compared against in order to permit someone to be able to conclude that, in fact, some of her RNA had come from the 1918 Influenza virus that supposedly had caused the woman’s death. 

Putting aside the foregoing sorts of issues, the CDC article proceeds to state that in February of 1999, a paper entitled: “Origin and evolution of the 1918 ‘Spanish’ influenza virus hemagglutinin gene” appeared in the Proceedings of the National Academy of Sciences. The article was written by, among others, Anne Reid, who was part of Taubenberger’s team of researchers and Johan Hultin had been given credit as being one of the co-authors of the article. 

The Hemagglutinin gene is hypothesized to help make possible the entry of the influenza virus into the interior of a healthy cell within the respiratory system of a human being and, thereafter, go about replicating itself. The foregoing claim is actually only a theory about how a virus gains access to the interior of a cell since no one has actually seen or proven how the breeching process take place, just as once a virus is alleged to have gained entry to the interior of a cell – no one has seen, or knows how the virus is able to take control of the cell’s replication machinery or how it sets in motion a series of events that lead to death. Everything which is said about such a virus – or viruses in general -- is part of an elaborate theoretical framework that is based, in part, on data, and, in to a large degree, on speculations concerning how to interpret that data.

At this point, the CDC article offers an illustration of what virologists believe the influenza virus looks like. One needs to understand that the illustration in the CDC article is someone’s rendition of the virus since there are no electron micrographs that are capable of verifying that such an illustration is accurate.  

The hemagglutinin – HA – protein that was the subject matter of the aforementioned Reid article is a surface protein which is believed to aid the virus to gain access to the interior of a human cell. Once inside a cell, the virus proceeds to infect a healthy respiratory tract, but, so far, nothing has been said in article to indicate how this infection process takes place or why it can be so lethal. 

The fact that an entity of some kind might be able to gain entry into the interior of a human cell doesn’t, in and of itself, prove anything. One needs to understand the dynamics taking place within human cells, but this is difficult to do in conjunction with objects that are the size that viruses are said to be, and, therefore, such accounts tend to be heavily theory-laden.

The aforementioned HA component is one of the features of the virus that is believed to be targeted and tagged by antibodies. One theory underlying flu vaccines is built around the idea of finding a way to target, and, then, neutralize, the HA surface protein of that virus, and, in the process, undermine the putative means by which such viruses are believed to gain access to the interior of human cells.. 

The CDC article goes on to indicate that the 1999 Reid – et. al. – study was able to put together a proposed sequence structure for the hemagglutinin surface protein. This structure was based on combining fragments from the lung tissue samples drawn from the woman unearthed in Brevig Mission, as well as from the soldier who had died at Fort Jackson, along with remnants from a service member who had been stationed – and who died -- at Camp Upton in New York in 1918. 

The foregoing amalgamation of data constitutes a theoretical construction. The aforementioned study did not isolate such a protein in any of the bodies, but, instead, inferred its existence on the basis of genetic data drawn from three different people. 

According to Reid and others, the 1918 virus had initially invaded human beings sometime between 1900 and 1915. Since the HA gene was believed to have various mammalian – as opposed to avian – adaptations, and, therefore, was more human-like or swine-like --“depending on the method of analysis” -- the virus was placed within a mammalian clade. 

More specifically, Reid and Taubenberger maintain that the purported 1918 virus sequence that had been constructed is most closely related to the oldest classical strain of swine influenza – namely, “A/sw/Iowa/30. Moreover, they note that the former viral sequence seems to be quite different from current avian influenzas but, also add that no one is certain about what avian influenza viruses might have looked like back in 1918. 

How closely related the purported 1918 virus sequence is to the oldest classical strain of swine influenza is not specified. Furthermore, precisely what the considerable differences are that differentiate current avian influenzas from the alleged 1918 viral sequence that was constructed is also not spelled out in the CDC article.

Nonetheless, Reid and Taubenberger believe that the HA component of the virus originated from an avian viral source. However, they are uncertain about the extent to which the virus might have been undergoing changes within a mammalian evolutionary framework before it assumed the form that led to a pandemic. 

There are a number of points to note with respect to the foregoing claims.  First, one might highlight the acknowledgment by Reid and Taubenberger that whether a researcher considered the HA component to be swine-like or human-like depended on the nature of the method of analysis which was used, and, therefore, one needs to recognize that conclusions concerning the precise mammalian nature of the HA protein might be more a reflection of a given method of analysis than any intrinsic feature of the HA protein.

Secondly, because Taubenberger and Reid are uncertain about how long the HA component of the virus might have been undergoing evolutionary changes within a mammalian environment before emerging as something capable of bringing about a pandemic, they are not certain about how the virus came to possess its – alleged -- lethal qualities … or what the nature of such lethality actually involves. In fact, they can’t even be certain if the virus is what was actually responsible for the deaths of so many people.

In addition, although they believe that the HA component of the virus ultimately came from an avian source, they have no data to demonstrate how the virus component might have been able to jump species. The alleged link between an avian source and a mammalian version of the virus is entirely speculative. 

Finally, the so-called mammalian adaptations to which Reid and her associate authors allude are not necessarily expressions of evolutionary change. Those differences might be nothing more than artifacts of the computer program that is used to construct the theoretical version of the HA protein. In other words, as the computer programs that are used in such research is run a number of different times, the available base pairs and fragments that have been detected in a given culture are put together according to an underlying pre-fabricated template for – in this case – a given protein, but, nonetheless, differences will show up during each run as a function of the program and, therefore, one cannot suppose that differences which show up in a constructed model of a protein are due to evolutionary changes over time rather than being expressions of the way the computer program constructs things on any given occasion. 

Reid and her fellow authors also indicate that the alleged 1918 virus’ HA1 protein exhibited four glycosylation sites. Virologists believe that glycosylation sites play a critical role in influenza viral functioning, but one should probably keep in mind that the foregoing belief is part of a theoretical framework in which the notion of “an influenza virus” is embedded rather than being an expression of experimentally observed performance involving those glycosylation sites. 

Current HA proteins associated with human beings exhibit anywhere up to five additional glycosylation sites when compared with the alleged 1918 virus’s HA1 protein. These extra sites are believed to be the result of a process of “antigenic drift” which constitute small changes that are introduced into a component – in this case a protein – that occur as a result of errors that occur during the process of being copied to form the next generation version of that component. 

These instances of antigenic drift are believed to be adaptive in nature as a given kind of virus adjusts to its animal hosts. However, the foregoing perspective is somewhat presumptuous because one cannot automatically assume that any particular copying error that might occur will necessarily give rise to a functional adaptation. 

Such instances of antigenic drift are cited as being one of the reasons why there is a new flu season every year or why someone might be able to become infected with an influenza virus on more than one occasion. Nonetheless, once again, this is like putting the cart before the horse because one cannot be certain that any given case of influenza that might occur in the future is necessarily infectious as a result of such changes. 

Perhaps, somewhat more importantly, Reid and the other authors of the aforementioned article did not come across any sequence changes for the HA protein that might account for why the 1918 influenza virus was, supposedly, so virulent. For example, unlike modern avian influenza A viruses involving H5 or H7 variants which exhibit “cleavage site” mutations that are associated with added virulence due, allegedly, to the way in which such sites supposedly permit a virus to grow in tissues outside of its usual host cells through the insertion of amino acids in the aforementioned cleavage sites, the 1918 virus did not contain any sequences that coded for amino acids which could become inserted into the cleavage sites in its HA proteins. \

Because Dr. Reid and her associate researchers could not identify any biological markers associated with the HA protein that might have been capable of generating the sort of enhanced virulence that supposedly was exhibited by the 1918 influenza virus, the researchers maintained that there were probably an number of factors which might have synergistically interacted with one another to give expression to enhanced virulence, and, therefore, lethality during the 1918 pandemic. However, the foregoing claim concerning the multifaceted nature of virulence really amounts to little more than an admission that the researchers actually have no idea why the 1918 influenza was capable of doing the damage that it was perceived to have done, and whether, or not, that virus was even responsible for what took place in 1918. 

The aforementioned research group wrote a second paper in June of 2000. This article focused on the neuraminidase gene which codes for a surface protein known as NA and was entitled: “Characterization of the 1918 ‘Spanish’ Influenza Virus Neuraminidase Gene.”

The NA protein is believed to enable a virus to escape from an infected cell, and, therefore, helps the virus to spread to other cells. According to immunologists, antibodies arise in conjunction with the NA surface proteins of viruses, and while such antibodies do not prevent infection, such antibodies are believed to help stem the tide of viral spread from taking place within human beings. 

Unlike the genetic sequence for the hemagglutinin surface protein (HA) which needed to be pieced together using data from tissue samples that came from three different human bodies, the research group that was working with the tissue samples that had been sent to them by Hultin which had been obtained from excavated cadavers in Alaska, the researchers were able to work out a genetic sequence for the neuraminidase using tissue samples from just one body. Nonetheless, whether one is working with tissue samples from three bodies or one body, the process of generating a genetic sequence from such samples is pretty much the same and, consequently, such a process depends on using a computer program (set of algorithms) involving a theoretical template for whatever viral component in which one is interested in order to be able to make educated guesses about whether the RNA fragments that are present in a given tissue sample contain a sufficient number of the right kind of fragment sequences that might have underwritten the expression of a certain kind of surface protein … in this case, the neuraminidase protein. 

In short, the hypothesized genetic sequence for the neuraminidase protein that many virologists believe to have been present in the 1918 influenza virus – along with the genetic sequence for the hemagglutinin (HA) viral surface protein -- is a theoretical construct. Neither the protein nor its purported genetic sequence was not found intact inside of a virus that had been properly isolated but was, instead, put together by running a variety of RNA fragments that were present in tissue samples through a computer program to see whether, or not, such fragments could be put together in a way that was capable of matching -- to varying degrees – the theoretical template being used in the underlying program. 

This is like taking the scattered letters of an alphabet that are within a sample of some sort and, then, running those letters -- along with various fragmented, short combinations of those letters -- through a computer program containing templates of certain words – say hemagglutinin and neuraminidase – in order to see whether, or not, one might be able to come up with a set of possible alphabet sequences that were capable of matching up with the program templates. One’s understanding is being filtered through the lenses of a theoretical framework, and, as a result, one might, or might not, be introducing some degree of obfuscation into the process of trying to understand whether such words were actually present in the sample or one merely had discovered a way to come up with such words using the alphabetic fragments that were available in a given sample.

To claim that such words actually were present in the original sample -- but simply had degraded over a period of time -- is a problematic contention. After all, such words were not actually found intact in the sample one was studying but, rather, those words had to be constructed as possibilities based on what is known about the presence of various kinds of exemplars from an alphabet that were found in a given sample that contained both single instances of the alphabet along with various fragments of combined components of that alphabet. 

In any event, once again, just as was true in conjunction with the constructed hemagglutinin gene sequence in which Dr. Reid and her fellow researchers were not able to identify anything in that  sequence which might have enabled the proposed 1918 flu virus to be especially virulent, so too, the researchers came to the conclusion that their constructed sequence of the neuraminidase gene did not exhibit any properties that might suggest, or were known to be associated with, a capacity for enhanced virulence or lethality that was assumed to exist in the 1918 influenza virus. 

For instance, there is a certain amount of evidence to indicate that the loss of a glycosylation site in the neuraminidase gene at amino acid 146 is associated with an increase of virulence in certain current influenza viruses. However, nothing of this kind was detected in the gene sequence of the neuraminidase surface protein from the 1918 tissue samples from Alaska, and, in passing, one also might note that correlating certain features in gene sequence with enhanced virulence is not the same as demonstrating that such gene sequence features are the cause behind observed increases in virulence. 

According to the phylogenetic analysis conducted by the aforementioned research group, the neuraminidase gene sequence from the 1918 tissue sample was classified as being intermediate between mammals and birds. What exactly is entailed by the notion of “intermediacy” is not spelled out, but such considerations notwithstanding, the researchers contend that the intermediary status of the neuraminidase viral protein indicates that the virus was, most probably, introduced into human beings at some point just prior to the 1918 pandemic and that the source of the change in virulence is most likely rooted in an avian source of some kind.  Yet, the CDC article also goes on to note that the research group was not able to trace the precise nature of the pathway that led to increased virulence.

So, once again, one is talking about theories of virulence and phylogenetic transitions that are bereft of the sort of evidence which is necessary to be able to demonstrate that such a theory has credible empirical legs. Correlational possibilities and plausibilities are not the same thing as empirically demonstrated causality.

The CDC article proceeds to mention further facets of the 1918 influenza research project that led to the appearance of articles focusing on six more of the eight genes that are believed to be present in the 1918. Thus, in 2001, a paper published in the Proceedings of the National Academy of Sciences was authored by Christopher Basier and others which provided an account of a nonstructural gene (NS) that was believed to be present in the 1918 influenza virus, and this was followed, in 2002, by a paper from an Ann Reid led research group which appeared in the Journal of Virology and dealt with the matrix gene that was alleged to be present in that same virus.

In 2004, a further study was published in the Journal of Virology that put forth an account of the nucleoprotein – NP gene – which is believed to have been present in the 1918 influenza virus. Finally, a year later, Taubenberger et. al. wrote an article that was published in Nature and focused on different polymerase genes which are considered to have been a part of the 1918 influenza virus.

All eight of the genes that are believed to make up the genome of the 1918 influenza virus are theoretical constructs. None of those genes were actually discovered by examining the sequences of a genome that had been located within a virus that had been isolated from all other aspects of the tissues and cultures that served as the basis for the research that was being carried out by Basier, Reid, Taubenberger and their associates … research that was being published in a variety of prestigious scientific journals. 

Following the publication of the foregoing papers, a program was set in motion that was intended to create a live version of the 1918 virus. The first step in this process of going “live” involved the creation of plasmids, and this was done through the work of microbiologists Peter Palese and Adolfo Garcia-Sastre, both of whom worked at the Mount Sinai School of Medicine in New York City. 

A plasmid consists of a tiny, circular strand of DNA. Such strands are capable of being amplified through means of laboratory controlled forms of replication. 

The plasmids that were generated by Palese and Garcia-Sastre would be utilized in a process of reverse genetics that researchers hoped might enable them to study the possible relationships between viral structure and function. In turn, the foregoing sort of studies could help lay the basis for moving to the next phase of producing viable forms of viruses which will be discussed shortly.

Once the foregoing plasmids had been created, they were shipped to the CDC. Because researchers at the CDC were going to use those plasmids during the process of generating live versions of the 1918 influenza virus, the CDC instituted what it considered to be rigorous protocols for ensuring that such research would take place within an environment that exhibited the necessary qualities of biosecurity and biosafety … and these enhanced set of protocols turned out to constitute what is known as BSL-3, one level lower than the maximum conditions for biosecurity and biosafety that have been established in conjunction with BSL-4.

Dr. Julie Gerberding -- who is now the executive vice-president for strategic communications, global public policy & population health, as well as the chief patent officer, for Merck & Co., Inc. but at the time of the proposed 1918 influenza reconstruction project was the Director of the CDC -- appointed a microbiologist, Terrence Tumpey, to be the individual who would be solely responsible for working within the BSL-3 containment facility in conjunction with the attempt to recreate a live viral version of the alleged cause of the 1918 influenza pandemic. The foregoing proposal also had been approved by the National Institute of Allergy and Infectious Disease under the authority of Anthony Fauci.

The project actually got under way in the summer of 2005. The plasmids which had been sent to the CDC -- and, previously, had been constructed by Dr. Palese for each of the eight genes that were theorized to constitute the 1918 Influenza virus and -- were introduced into human kidney cells by Terrance Tumpey. Once inserted into the kidney cells, the plasmids induced those cells to generate what the members of the reconstruction project believed were a complete set of RNA sequences for the 1918 virus. 

There is some question, however, as to whether, or not, the RNA sequences that are being alluded to in the foregoing claim actually captured the structural and functional properties that might have been present in the alleged agent of the 1918 pandemic. After all, Taubenberger and Reid -- together with their associate researchers who had been involved with the various studies that produced the 8 genes that, supposedly, made up the composition of the 1918 influenza virus -- had acknowledged, as noted earlier, that they saw nothing in the 8 genes that might be considered to be a possible causal source of the virulence that was thought to be present in the 1918 influenza virus. 

If the reconstructed edition of the 1918 influenza virus had no obvious capacity for inducing infectious lethality in its hosts, then perhaps, something is missing from the reconstructed, alleged version of the 1918 influenza. Indeed, one should keep in mind that each of the 8 genes that had been created by Taubenberger, Reid and others were, actually, all constructs that were based on various kinds of computer programs, algorithms, templates and the like in order to produce what was presumed -- on the basis of an array of theoretical considerations, assumptions, and calculations – to be an accurate re-creation of the 1918 influenza virus. However, absent the presence of a causal mechanism for infectious lethality in such a model, then, perhaps, the researchers should have exercised some degree of scientific caution concerning precisely what it is that had been created and whether, or not, such a creation has anything to do with the agent that supposedly led to a pandemic in 1918. 

An article, entitled: “Characterization of the Reconstructed 1918 Spanish Influenza Pandemic Virus” appeared in the October 7, 2005 edition of Science. Following the publication of the foregoing article, the researchers undertook a series of experiments which was conducted in order to assess the pathogenicity of the reconstructed entity. 

In other words, the researchers wanted to evaluate the capacity of their creation to infect and disrupt the healthy functioning of organisms into which their reconstructed agent was going to be introduced. This process of evaluation involved conducting a number of experiments involving mice. 

The CDC article proceeds to give an overview of the experimental procedures that were used and, in the process, indicates that one set of mice were infected with the reconstructed agent, while other sets of mice were exposed to various combinations of the eight genes that constituted the reconstructed agent that had been combined with various strains of influenza A viruses (H1N1) that affect human beings on a seasonal basis. These latter concoctions are referred to as “recombinant viruses.” 

There might, or might not, be problems surrounding the character of the foregoing experimental setup. For example, nothing is specifically mentioned in the CDC article about how the different sets of mice were infected or just what it was that constituted the vector that was being introduced into those mice. 

To begin with, living organisms come into contact with potentially infectious agents by interacting with the surrounding environment. Therefore, unless the various experimental sets of mice were being exposed to a possible infectious agent via air, water, food, or through their physical interaction with the environment, then, one is using a mode of vector introduction into the test subjects which is of questionable scientific value. 

Secondly, there are a number of questions that should be raised in conjunction with the nature of the precise contents of the potential infectious agent to which the test animals were being exposed. For instance, since the CDC reconstruction project supposedly had succeeded in generating the RNA sequences for the complete genome of the purported 1918 virus, then shouldn’t they have been able to produce completely isolated versions of the entities to which such RNA sequences give expression  … versions that would be uncontaminated or unadulterated by the presence of any other components such as would happen if one were to embed the reconstructed virus in some sort of culture which, supposedly contains said agents  but, in addition, also often tend to involve a number of other components, as well, that are considered by researchers to be necessary to maintain a viable culture. 

The term “viable” in the foregoing means something that serves the purposes of a group of researchers rather than something that necessarily reflects what is likely to happen outside of a laboratory. If the potentially infectious vector which is being introduced to experimental groups of mice consists of anything except a purified compilation of the reconstructed virus, or anything but a purified amalgamation of various kinds of recombinant viruses in control groups, then whatever other components are being mixed in with the reconstructed virus or mixed in with recombinant viruses that are being used as control groups might have the capacity to obfuscate the character of the biological dynamics that are taking place within organisms in conjunction with the possibly infectious agents to which they are being exposed?  

According to the account provided by the CDC article concerning the foregoing experiments, there was a marked difference between the impact of the reconstructed version of the 1918 influenza virus on mice and the nature of the impact which the recombinant viruses had when they were introduced to various control groups of mice. For instance, mice that had been given the reconstructed version of the 1918 influenza virus contained quantities of the replicated virus that were 39,000 times higher than were produced through one of the recombinant viruses.

One question that might be asked in conjunction with the aforementioned claim in the CDC article is the following possibility. Given the claim that mice which, somehow, had been exposed to the reconstructed version of the 1918 influenza contained 39,000 times the amount of that reconstructed version than mice which were not exposed to the reconstructed version, how does one know that all the entities which are being claimed to be exemplars of the reconstructed version (some 39,000 times some given amount) are what they are said to be? In other words, have samples from the set of entities that arose in conjunction with the fully reconstructed edition of the 1918 influenza virus been properly isolated, opened up, and shown to contain an intact RNA genome that is the same as the reconstructed version from which the large quantity of replicated entities supposedly arose and which also can be shown, when re-introduced to other mice, to produce the same kind of patterns of replication?

According to the CDC report concerning the reconstruction project for the 1918 influenza virus, another indicator of the virulence of their reconstructed agent -- beside the degree of replication that is observed -- concerned the possible lethality of that agent. More specifically, the reconstructed edition of the 1918 influenza virus was said to be 100 times more lethal than “one of the other recombinant viruses tested.” 

Does the foregoing claim mean that the recombinant viruses were also lethal but 100 times less so than the fully reconstructed edition of the 1918 influenza virus, and, if this is the case, then why would such a recombinant virus be lethal? Furthermore, one might entertain various questions in relation to the extent of the lethality to which the article seems to be alluding in conjunction with the recombinant viruses which are not specified, as well have questions about the nature of the mechanism of lethal pathogenicity that might be involved in those deaths. 

In other words, if one accepts the premise that the fully reconstructed edition of the 1918 virus was 100 times more lethal than “one of the other recombinant viruses tested,” then just how lethal was the latter recombinant virus? How many mice in this group died, and what was the cause of death?

Moreover, there is a certain amount of ambiguity present in the CDC article with respect to experiments involving the reconstructed virus when the article indicates that the fully reconstructed version was 100 times more lethal than “one of the other recombinant viruses tested”. In other words, does the foregoing claim in the CDC article mean that other versions of the recombinant viruses were associated with higher degrees of lethality than the one recombinant virus, in particular, that was tested and which, apparently is being referenced in the quoted statement. Or, alternatively, were the other recombinant viruses found to be more lethal than one of the recombinant viruses that was tested but were, to varying degrees, less lethal than the reconstructed edition of the 1918 influenza virus, and, if the latter is the case, then, once again, what is the extent to which such recombinant viruses are associated with dead mice and why do such deaths occur at all? 

The CDC article does indicate that the HA or hemagglutinin gene from the fully reconstructed edition of the purported 1918 flu virus seems to play a critical role in rendering the virus to be lethal. The evidence for such a claim rests with an experiment in which the gene from the fully reconstructed edition of the 1918 gene was removed, while the seven other genes from the reconstructed virus were combined with a seasonal influenza virus labeled as: “A/Texas/36/91” or in more abbreviated form: “Tx/91.”

The latter recombinant virus did not result in the death of any mice. Furthermore, such mice did not undergo any sort of weight loss, whereas many mice exposed to the supposedly fully reconstructed rendition of the 1918 virus not only died but, as well, some number of the latter group of mice lost up to 13% of body weight within two days of being exposed. 

The foregoing experiment involving “TX/91” is described in a somewhat ambiguous manner. Presumably, the only difference between, on the one hand, the recombinant virus that combined seven genes from the fully reconstructed version of the 1918 virus with the “Tx/91” control virus would have centered around the absence of the HA gene. However, since nothing was said in the CDC article about the number or kinds of genes that might have been present in the “TX/91” to which the seven genes from the fully reconstructed version were being added, one is not really certain if the only difference between the fully reconstructed virus and the recombinant “Tx/91” virus is the presence or absence of the HA gene, or whether there are other differences in genomic structure as well.

Furthermore, the phrase: “lost up to 13% of body weight” which appears in the CDC article sounds like a lot of television advertisements which indicate that if one buys a certain product, then, one can save up to “x” amount, or if one uses a certain product, then one’s condition can improve by “x” amount, but, in reality, the amount which can be saved, or the benefit that actually accrues, turns out, in most instances, to be substantially less than whatever the indicated “x” amount might be, and, yet, the original statement would not constitute a lie because there were some cases in which “x” amount was saved or “x”  benefit accrued. Consequently, to say that some mice “lost up to 13% of body weight” doesn’t necessarily provide one with much information or provide any insight into what the nature of the dynamic that might have caused such a loss in body weight. 

One would like to know how many experimental mice exhibited the foregoing loss in body weight.  One also would like to know how many mice in the experimental group exhibited little, if no, weight loss, as well as how many mice in the control group exhibited some degree of weight loss, even if not substantial. 

Aside from the issue of numbers involving various kinds of weight loss, one might also like to know something about the causal issues underlying such weight loss. Why did some mice experience more weight loss than others, and what factors might have affected how much weight, if any, was lost? 

Apparently, according to the CDC account of the reconstruction project, the presence or absence of the HA gene had a marked effect on the symptoms that arise. However, exactly what role the HA gene plays in the nature of the symptoms that arise, or do not arise, is not actually spelled out.

The CDC article describing the experiments involving the fully reconstructed gene version of the purported 1918 influenza virus also indicates that within four days of being exposed to the aforementioned reconstructed edition, mice displayed various forms of inflammation in their lungs that were reminiscent of, or similar to, the sorts of lung tissue inflammation that had been observed in conjunction with many human beings during the alleged 1918 pandemic. In other words, apparently, the lungs of the exposed mice filled up with fluids, or exhibited signs of pneumonia, or had some other kind of lung inflammation.

However, the term “similar” that appears in the CDC article is somewhat open-ended. As a result, one remains unsure as to the extent or degree of similarity between the sorts of lung complications that emerged in conjunction with the mice that were exposed to the fully reconstructed version of the purported 1918 virus and the kind of lung complications that were fairly common among the human beings who were said to be infected with the 1918 virus.

The CDC article also describes a set of experiments that were run using a human lung cell line referred to as “Calu-3 cells”. More specifically, measurements were taken at 12 hours, 16 hours, and 24 hours following exposure of those cells to the alleged fully reconstructed edition of the 1918 virus, and, then, these measurements were compared with measurements that were made following the exposure of the human lung cell line to various forms of recombinant viruses involving different arrangements of certain genes from the fully reconstructed form and various kinds of seasonal flu viruses that supposedly affect human beings. 

According to the CDC article, the reconstructed version replicated rapidly within the human lung cell line into which they had been introduced. In fact, the reconstructed virus produced “as much as 50 times” the amount of virus as various forms of the recombinant viruses did.

Once again, the notion that one virus produces “as much as 50 times more” of that virus than does another kind of virus doesn’t really explain how frequently this maximum of 50 times greater production actually occurred. Rather, the statement only indicates that there were some cases in which this sort of rate of multiplication was observed, but there also were other instances in which this kind of differential in production was not observed, but no details are given concerning the latter sorts of cases.

The CDC article goes on to state that one of the conclusions drawn from the aforementioned sorts of experiments is that the polymerase genes that were present in the reconstructed viral form also appeared to play a significant role in the pathogenicity (i.e., virulence and capacity for infectivity) that was observed when human lung tissue was exposed to the fully reconstructed edition of the alleged 1918 virus. Nonetheless, what the nature of that enhanced role might be is not really spelled out.

In addition, what takes place in a laboratory Petri dish is not necessarily an accurate reflection of what takes place in the much more complex environment of a living organism. Do the dynamics occurring within a laboratory point to certain possibilities in conjunction with life? Possibly … however, there is a potential for many a slip twixt experimental cup and living lip. 

As noted earlier, Taubenberger and Reid were of the opinion that the 1918 influenza virus might have derived certain gain of function properties from an avian source … properties that were theorized to have made a species jump at some point prior to the onset of the pandemic. The researchers had reached the foregoing point of view because they felt that the reconstructed influenza virus had segments in its genetic sequence that seemed to be much closer to avian influenza A viruses (H1N1) than they were to various kinds of H1N1 mammalian influenza viruses, but what precisely was entailed by the notion of appearing to be “closer” to avian influenza A H1N1 viruses than to H1N1 mammalian editions of such viruses was not really specified or explained.

In order to test the foregoing thesis concerning the possible origins of the alleged 1918 influenza virus, 10-day old fertilized chicken eggs were exposed to the CDC reconstructed virus and, then, compared with results from experiments that exposed the same kind of eggs to various editions of a modern human influenza A virus that contained different combinations of the two, five, and seven gene recombinant viruses that had been created by Dr. Tumpey during earlier stages of the series of experiments that were being run through the CDC concerning the alleged 1918 influenza. 

According to the CDC article, the fertilized chicken egg experiments indicted that the reconstructed version of what was assumed to be the virus at the heart of the 1918 pandemic had a much more lethal effect upon the chicken egg embryos than did any of the recombinant versions of the human influenza virus. In fact, none of the recombinant viruses seemed to have the same degree of lethality in conjunction with the fertilized egg embryos as the fully reconstructed version did, but the CDC article is unclear about whether, or not, the presence of any of the recombinant viruses led to symptoms of one kind or another in the fertilized chicken embryos. 

Furthermore, the pathogenicity of the fully reconstructed edition of the 1918 influenza virus in relation to fertilized chicken eggs was said to be “similar” to the kind of pathogenicity that was observed when fertilized chicken eggs were exposed to various kinds of current H1N1 editions of avian flu viruses. However, the nature of the alleged ‘similarity’ between, on the one hand, the fully reconstructed edition of the putative 1918 virus and, on the other hand, contemporary versions of avian flu viruses was not specified, nor was there any discussion in the CDC article concerning whether, or not, similar sorts of pathogenetic outcomes might have been produced in more than one way. Yet,  if there were multiple possible paths to similar sorts of effects in the chicken embryos, then, one couldn’t necessarily conclude that the reason for such similar outcomes is necessarily due to the role that avian flu viruses might have played in the theorized gain of function that supposedly showed up in the virus that is alleged to have caused the 1918 pandemic. 

In addition, although the researchers believe that the foregoing experiments with chicken egg embryos showed – as the researchers also had concluded with respect to the human lung cell line experiments – that both the HA, or hemagglutinin gene, as well as the polymerase genes of the reconstructed influenza virus played significant roles in enhancing the virulence of the alleged 1918 influenza virus, once again there was an absence of details in the CDC article concerning just what the nature of those roles might have been, or how such capabilities actually came into being (rather than theoretically might have come into being in such a fashion), and why such features would have generated the kind of pathogenicity that had been observed in 1918. 

Although much speculation within the CDC article, as well as elsewhere, has been focused on the possible mechanisms of pathogenicity to be found in conjunction with any given form of influenza virus, one should keep in mind that not all mice died in the CDC experiments when they were exposed to such viruses, nor did all mice lose 13 % of their body weight within a couple of days following that exposure. Consequently, one must also take into consideration the characteristics of the organisms that are being exposed to a putative virus in order to try to account for the differential outcomes that occurred in such experiments despite being exposed to precisely the same reconstructed virus. 

Death, like life, involves a dance between environment and organism. Why, despite being exposed to the same set of environmental features, some organisms die, while other organisms live, is an issue that cannot be reduced down to only questions of pathogenicity concerning a given virus, but, as well, one must take into consideration the degree of vulnerability, if any, that exists in various organisms and just what is entailed by such vulnerability. In short, one can’t talk about the lethality of a viral agent or entity without simultaneously exploring the susceptibility of an organism to certain kinds of difficulties that might arise when engaged in various ways by various elements within a given environment. 

In fact, given the foregoing considerations, one might ask: Is the pathogenicity that is observed in such circumstances a function of the virus or is it a function of the organism? Where is the locus of causality to be set? 

If an organism is immune to the presence of a certain entity (say, some sort of viral agent), then, in reality, the latter entity has absolutely no pathogenicity relative to such an organism. So, if another organism of the same kind displays various kinds of biological difficulties when exposed to the same sort of environmental agent, can one really say that it is the entity’s pathogenicity that causes such difficulties or is the causal dynamic much more complex than assigning pathogenicity to a entity such as a virus? 

Perhaps, the reason why researchers have had such difficulty in delineating the causal process with respect to the 1918 pandemic is because their analysis should have been looking for something beyond the idea of an agent or entity that has some sort of capacity for generating pathogenicity in an organism. In other words, perhaps, they should have been looking into the complexities of how organisms interact with the environment and what both sides of the dynamic bring to the life, death, and well-being equation.

Finally, the research conducted by Taubenberger, Reid, Tumpey, and others that is, to a degree, delineated in the CDC article and which has been the focus of the present essay, hasn’t actually demonstrated that the reconstructed genome that arose through their efforts was the same as the viral agent that supposedly played such a devastating role in the events of 1918. Although they believe they have demonstrated that their reconstructed version is correlated with certain kinds of results in various sorts of experimental contexts, nonetheless, by their own admission, they acknowledge that their reconstructed genome does not seem to display any features which have been empirically demonstrated to be capable of generating the sort of virulence or pathogenicity that is believed to have been characteristic of whatever transpired in 1918. 

They talk about a possible mechanism for entry into a cell (e.g., hemagglutinin – HA gene) as well as a possible means of being able to exit from cells (e.g., neuraminidase – NA gene). In addition, they allude to the possible role that various polymerase genes in their reconstructed entity might have had in conjunction with the process of successful replication as well as possibly enhancing, in some way, the virulence of the alleged 1918 virus, but the capacity to enter, exit, and replicate do not necessarily give expression to a causal account of how such a virus generates its lethality within a human host 

Consequently, the foregoing lacks causal concreteness. They cite experiments that were conducted at the CDC concerning the potential pathogenicity of their reconstructed creation, but none of those experiments demonstrate that their re-created entity is identical to what supposedly was at the heart of events in 1918, and, in fact, only indicate that in some fashion their reconstructed genome can be correlated with certain kinds of experimental results without being able to spell out what the precise causal dynamics were which underlay those experimental results. 

Once can agree with the authors of the CDC article when she, he, or they conclude: “… that more work needs to be done.” Whether the future work to which the article is alluding will be able to demonstrate that researchers will be able to causally prove that their constructions constitute accurate recreations of the agent that, supposedly, was responsible for the public health crisis that occurred in 1918 remains to be seen. 

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The Deadliest Flu