As Ron dives into the world of HCQ and its potential, he encounters a web of information. From lupus patients as a key to understanding to French epidemiologist Didier Raoult's assertions, he discovers a new realm of possibilities. Yet, access to HCQ proves challenging, leading Ron to unconventional alternatives like quinine and tonic water.
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What if they held a pandemic and no one came? https://apps.nftbooks.info/urls/M3JuxT5
Vaccines vs. Antivirals: Whack-a-Mole vs. Viral Sniping
The realm of RNA viruses, and indeed virology as a whole, brims with astonishing complexity, particularly when delving into their genetic intricacies. The sheer magnitude of this complexity defies exhaustive exploration within the confines of this text. I ask for forgiveness, particularly from any virologists among our readership, as I embark on a layman's expedition through the annals of history—a journey that risks oversimplification. My aim, in this whirlwind tour, is to furnish essential insights into their discovery, their profound influence on our existence, and the diverse arsenal of strategies devised to combat their relentless replication. With an eye towards forthcoming chapters exploring innovative approaches to curtail their proliferation, I trust this narrative will serve as a compass, guiding us through the labyrinth of RNA viruses and towards the frontier of virological advancement.
Early Theories and Discovery
In the 1800s, early researchers wrestled with theories concerning the genetic essence of these diminutive adversaries. The epochal unearthing of the inaugural RNA virus emerged in the late 1800s with the revelation of the Tobacco Mosaic Virus (TMV). Tobacco, a linchpin commodity for many economies, faced a dire contagion, prompting significant investments of both capital and labor to discern its root cause.
Through astute means, such as refining plant sap via specialized filtration to excise bacteria, scientists discerned that the purified sap still retained infectious potency against other tobacco plants. This validation unveiled a pathogen even more minuscule than the single-celled bacteria initially chronicled by Antoni van Leeuwenhoek in 1675, often hailed as the "Father of Microbiology." Leeuwenhoek's seminal insights notwithstanding, his revelations proved inadequate in elucidating these enigmatic and indiscernible pathogens, which eluded detection beneath the lenses of contemporary microscopes.
Impact on Epidemiological Understanding
The study of bacteria had long underpinned epidemiological discourse, yet the emergence of TMV posed a formidable challenge to prevailing epidemiological tenets. This watershed moment underscored the imperative for a paradigmatic evolution, heralding an era of heightened comprehension regarding viral maladies and marking an epochal juncture in the annals of microbiological inquiry.
The Spanish Flu Pandemic: A Turning Point
The path towards unraveling the enigma of RNA viruses surged forward significantly during the cataclysmic Spanish Flu pandemic of 1918-20, hailed as the deadliest epidemic in human history. Across that harrowing two-year span, an estimated five hundred million individuals, roughly 33% of the global populace at the time, fell prey to its grasp. The toll of mortality ranged between 17 to 50 million souls, with countless others enduring protracted bouts of incapacitating afflictions lasting months to years.
Factors Aggravating the Spanish Flu's Impact
It has been conjectured that deficiencies in hospital care amplified the toll, exacerbated by the widespread employment of aspirin, hailed as a "miracle drug," albeit administered in dosages now acknowledged as perilously toxic. Compounding this, the utilization of cloth masks, often reused, purportedly fostered the onset of bacterial pneumonia, as microbes accumulated on the fabric, poised to be inhaled anew, potentially augmenting the already staggering death toll.
Influence on World War I
Furthermore, the Spanish Flu pandemic purportedly wielded a direct influence in hastening the cessation of World War I, as soldiers from all fronts succumbed to illness in staggering numbers. Within the battle- scarred trenches, the ranks were decimated as soldiers fell ill en masse, inundating military infirmaries ill-equipped to contend with the unknown scourge. It has been alleged, for instance, that the U.S. Army suffered more casualties in 1918 from the Spanish Flu than from actual combat engagements. Unrelenting and indiscriminate, the Spanish Flu emerged as an unseen adversary that spared no faction, prompting all belligerents to veil the extent of their losses, in a bid to conceal potential vulnerabilities from adversaries.
Origins and Naming of the Spanish Flu
The efficacy of this censorship was such that the initial reports of the burgeoning contagion surfaced not from the belligerent nations, but from neutral Spain, thereby bestowing upon the disease the misleading moniker of the "Spanish Flu." Even now, the precise origins of the disease remain shrouded in conjecture. Notably, as witnessed during the COVID outbreak, censorship amidst pandemics is not uncommon, with the full truth often withheld until decades later.
Ignorance and Misconceptions
Amidst the ravages of the Spanish Flu, a profound ignorance prevailed regarding the etiology of the plague. While some contended it stemmed from bacterial agents, owing to their detectability under contemporary microscopes and the substantial knowledge surrounding bacterial pneumonia, speculation regarding the existence and role of viruses abounded. Invisible to the microscopes of the era, viruses eluded direct observation, compelling scientists to devise intricate methodologies to filter out bacteria and thereby isolate the elusive causative agent responsible for the affliction.
Advancements in Viral Understanding
The initial revelation and definitive proof of Tobacco Mosaic Virus (TMV) had to wait until 1935, with the emergence of newly invented electron microscopy. This pivotal validation spurred scientists to speculate that
similar viruses might be the culprit behind various illnesses previously ascribed to bacterial origins. If RNA viruses found sanctuary within plants, the logical deduction was that they likely inhabited the realms of animals and humans as well.
First Human RNA Virus Discovery
However, confirmation of RNA viruses afflicting humans and other mammals remained elusive until 1964, when even more advanced electron microscopy captured the first image of an RNA Coronavirus. Dubbed for its regal "spikes," resembling a crown in Latin terminology, it swiftly became evident that these viral projections had evolved and adapted to bind with an array of protein receptors on the human cell membrane, as discussed in prior chapters.
Nature of RNA Viruses
Technically speaking, RNA viruses fall short of being categorized as "alive" due to their lack of DNA, the customary hallmark of living organisms responsible for genetic stability. Instead, they rely on the hospitable resources of a host cell for replication. Indeed, certain viruses, known as bacteriophages, target specific bacteria, many of which pose threats to human health. These phages penetrate the bacterial hosts, replicate, and ultimately rupture the bacterial cell membrane, spelling the demise of the host bacterium. Yet, our focus lies primarily on RNA viruses of a more menacing nature—highly pathogenic and lethal strains capable of precipitating dire consequences, including bacterial pneumonia and immunological hyperactivity, culminating in inflammatory distress often necessitating hospitalization, and in the most severe instances, intensive care unit interventions.
RNA vs. DNA Stability
DNA functions akin to a sacred repository housing our genetic essence and that of other pathogens, serving as a blueprint to be meticulously transcribed, replicated, and translocated by mRNA for the production of essential proteins. Its integrity is sacrosanct, as alterations therein precipitate fundamental changes in our very essence. Creatures and pathogens endowed with DNA exhibit staunch resistance to mutation, hence major genetic deviations are rare among DNA viruses like Smallpox, Chickenpox, and Herpes.
Genetic Flux in RNA Viruses
In stark contrast, RNA viruses lack the stabilizing influence of DNA, thus bereft of a genetic library to uphold their structural integrity and mitigate mutations. Their intrinsic propensity for recombination with other RNA viruses fosters the emergence of novel strains through mutation. Devoid of the proofreading prowess inherent in DNA polymerase, RNA viruses are predisposed to genetic flux. While mutations often culminate in genetic cul-de-sacs, conferring no evolutionary advantage, incessant genetic shuffling ultimately yields mutations with the potential for enhanced transmission capabilities.
Research into RNA Virus Recombination
Recent avant-garde research delves into the intricacies of RNA virus recombination. Every cell in our corporeal vessel is susceptible to infection by myriad RNA viruses, serving as a crucible wherein genetic amalgamation transpires, spawning new mutations through RNA sharing. The most resilient and adaptable mutations ascend to dominance in a democratic contest, thereby perpetuating viral evolution. Consequently, just as the immune system marshals defenses against one viral adversary, another emerges, endowed with the capacity to infiltrate diverse cellular sanctuaries, including vital internal organs.
Mechanisms of Genetic Alteration
This phenomenon, known as recombination, epitomizes genetic mélange and selection, an evolving frontier in research with ongoing revelations. Chief among the mechanisms facilitating genetic alteration in RNA viruses is recombination with other viral strains coexisting within the same cellular milieu. When disparate RNA viruses converge within a solitary cell, their genetic fabric intertwines, engendering novel mutations that may either bolster, or hinder their ability to infect fresh hosts.
Elusive Identity of the Spanish Flu Virus
As the decades unfolded and the mortal remains of the afflicted decayed in their graves, leaving no discernible traces of the deadly pathogen, the definitive cause of the Spanish Flu remained elusive, shrouded in uncertainty. As with TMV research, experimental endeavors aimed at sieving out bacteria suggested the involvement of a smaller, unseen agent in the pathogenesis of the illness. Yet, the precise identity of this elusive culprit remained conjectural, albeit the absence of bacteria pointed towards an alternative causative factor, imperceptible yet
undeniably present. However, as mentioned previously, it wasn't until 1964 that the initial visual depiction of an RNA Coronavirus materialized, underscoring the relatively recent elucidation of RNA viruses.
Evolving Understanding of the Spanish Flu
The precise etiology of the Spanish Flu continues to elude definitive elucidation, though over time, scientific discourse gravitated towards the hypothesis of an H1N1 strain, predominantly affecting avian, porcine, and human populations. The adoption of the moniker "swine flu" stemmed from the concurrent emergence of an influenza-like ailment in pigs during the Spanish Flu era, fostering a speculative link perpetuated by subsequent literature. However, advancements in gene sequencing have led contemporary researchers to pivot towards an avian origin for the Spanish Flu, a conclusion reached as recently as 2014 through comparative genetic analysis. This underscores the perpetual evolution and refinement of virological understanding facilitated by technological advancements.
Potential for Multiple Viral Strains
And even today, there remains conjecture that the Spanish Flu was actually the result of two, or more different Influenza Avian RNA viruses, creating a novel, highly pathogenic genetically recombinant cocktail primed with a unique ability to infect humans. Ironically, in recent months, there has been convincing evidence that during the SARS-2 pandemic, we also witnessed extensive reports of highly pathogenic H7N9 and H5N1 Avian flu prevalent on poultry farm operations. H7N9 has a human mortality of approximately 33%, while H5N1 is upwards of 52%. And since the PCR-RT tests we were required to take tested only for SARS-2, it’s very possible that many of the fatalities may have been due to those completely different viral strains. It’s an intriguing possibility, with a whole host of ramifications, if discovered to be accurate, and something we will be discussing in later pages.
Legacy of H1N1
H1N1, a subtype of Influenza A, credited with the biological devastation of the Spanish Flu, persists today in a relatively subdued endemic form. The elderly population retains an enduring "imprinted" immune defense against it and its progeny, forged through past encounters. In subsequent years, H1N1 has resurfaced intermittently, notably during the tumultuous events of 1976-77 when an outbreak in Russia, attributed to a laboratory leak, engendered global trepidation reminiscent of the Spanish Flu era. This apprehension precipitated the inauguration of the first expedited vaccine program, akin to the contemporary "Operation Warp Speed" initiative aimed at countering SARS-2. However, the resultant vaccines, while forestalling the dreaded pandemic, exacted a toll in the form of serious adverse effects, sparking contentious legal battles that led to the establishment of legal immunity for vaccine manufacturers and government-managed, and funded, “Vaccine Court” for those claiming damages to file their legal claims.
The specter of H1N1 resurfaced in the 2009-10 "Swine Flu" epidemic, characterized by heightened infectivity among younger demographics. Despite official assertions attributing its source to a mutated animal strain, speculation regarding a potential laboratory leak scenario lingered but was swiftly dismissed by authoritative bodies. While the epidemic's toll paled in comparison to its Spanish Flu predecessor, virologists caution that the specter of mutation looms, necessitating sustained research efforts and accompanying funding.
In the aftermath of the Spanish Flu, the burgeoning vaccination industry increasingly pivoted its focus towards RNA viruses, recognizing their pivotal role in pandemics. This paradigm shift, propelled by the inherent mutability of RNA viruses, engendered a surge in private and governmental research funding aimed at averting the recurrence of a catastrophic RNA viral pandemic. Over the past century, highly transmissible RNA viruses have emerged as a formidable threat to humanity, prompting speculation regarding the underlying factors driving their prevalence. Among its historical milestones, Dr. Jonas Salk's development of the Poliovirus vaccine stands as a testament to the pivotal role of vaccination in combating viral scourges. Polio is also an RNA virus. And as we will relate to the reader, PROTOCOL-Z can also play a role in its prevention, without the danger of experimental inoculations.
This condensed history of the H1N1 "Spanish Flu" pandemic, alongside its recurrent mutations, serves to elucidate the cognitive lens through which the world viewed the unfolding events of 2020. RNA viruses, formidable in their potency, wield the capacity for substantial human toll and economic upheaval, while also serving as effective instruments of terror. However, over time, they inevitably evolve towards decreased lethality, prioritizing replication and transmission to new hosts—a testament to nature's relentless adaptability.
The emergence of H1N1 and other viral outbreaks has catalyzed a century-long collaboration between governments and corporate entities—some dubbing it a "cabal"—focused on identifying new RNA viral mutations with the potential to leap from animal hosts to humans. This partnership, purportedly aimed at pre-empting such zoonotic spillovers, includes initiatives like Gain of Function research, which attempts to anticipate and model potential mutations to prepare potential vaccine formulations. Yet, regardless of speculation, RNA viruses remain astonishing in their adaptability, enabling them to evade immune defenses and propagate with remarkable efficacy. With each genetic roll of the dice, a new opportunity arises for the genesis of a virulent mutation capable of infecting novel hosts. Thus, a trillion-dollar industry has emerged, dedicated to researching vaccines, antiviral therapeutics, and, more recently, gene-therapy solutions, in the form of mRNA “vaccines” to combat these viral menaces.
Vaccines epitomize a time-honored strategy predicated on the principle of acquainting our adaptive immunity with attenuated, or inactivated, pathogens, thereby priming it to discern and fortify natural defenses against such invaders. Initially, this approach seemed rational, affording our immune systems a proactive advantage by furnishing ample viral protein data and temporal leeway to develop robust defenses. Historically, vaccines proved adept at staving off a plethora of viral pathogens, or curtailing their severity in human populations.
Yet, this method was not devoid of risks, as each individual's response to these foreign formulations varies. This discrepancy is particularly pronounced considering that RNA viruses predominantly target our lungs—a natural barrier—raising questions about the rationale behind administering vaccine concoctions into our shoulders, where cellular composition differs markedly from pulmonary tissues. Additionally, with each passing year, traditional vaccines appear to exhibit diminishing efficacy. Researchers unearthed evidence suggesting that recurrent vaccination induces a phenomenon termed "immune imprinting," elucidated with an excerpt from an April 2023 paper:
Immunological Imprinting: Understanding COVID-19 Link to the paper
"In experiments conducted in the 1930s, young geese demonstrated an inclination towards attaching to moving objects encountered shortly after hatching, be it their mother, the experimenter, or inanimate entities. This behavior, termed imprinting, mirrors the learning of behaviors through exposure during a critical period in early life."
Analogous to juvenile geese, the naïve immune system, upon primary viral exposure, undergoes "imprinting," acquiring the ability to discern antigenic determinants in the virus and engendering memory cells that react to antigenically related strains in subsequent encounters. Humans maintain a perpetual pattern of heightened antibody reactivity towards influenza viruses encountered during childhood. Further expounding on this theory, the paper states:
"Individuals across all age brackets exhibited the highest antibody titers against strains encountered during childhood, while certain individuals displayed robust immune memory recall responses towards historically circulating influenza A strains absent from contemporary vaccines. This phenomenon was exclusive to individuals born around the era of circulation of the historical strain, absent in younger cohorts untouched by its prevalence. These observations prompted Francis to posit that the inaugural strain encountered during childhood imparts a lifelong antigenic predisposition. Though subsequent exposures broaden reactivity to encompass newer strains, immunity towards the original strain persists at elevated levels relative to recent strains."
The research sourced above delves into immunological imprinting, an ongoing endeavor marked by diverse interpretations. Nevertheless, the irrefutable reality is that traditional vaccines are progressively faltering against evolving RNA viral strains, a fact widely acknowledged.
Thus, with each exposure to a natural virus, or its attenuated form via vaccination, immunity inclines towards past strains, rendering it less responsive to emergent viral variants encountered in nature. Consequently, the efficacy of successive vaccine iterations targeting new mutated outbreaks wanes—a sobering reality encapsulated in the chapter's title, symbolizing a futile game of viral "whack-a-mole." This necessitates incessant research to prognosticate the next viral strain, akin to predicting the forthcoming flu season. Despite the profitability of vaccine schemes, the industry siphons vast resources from more productive pursuits, prompting reflection on the wisdom of targeting such elusive, mutable foes with our primary defense strategy.
mRNA Gene Therapies... Err...I mean, “Vaccines”
A clarification is in order: mRNA vaccines represent a form of gene therapy repackaged to sidestep potential legal liabilities. Allow me a brief
digression on this matter. Traditional vaccines are based upon taking a wild viral strain and weakening, or inactivating it, while preserving its complete protein envelope, hoping that it will elicit an immune response against it. This will create a “memory” that our bodies can rely upon to fight a future infection by the “wild” virus. In fighting infections, the sooner our bodies respond to destroy the quickly replicating virus, the less hyper-reactive that response will become. It’s when viruses replicate in excess, building up such an extreme viral load, that our immune systems go into an over-reactive cascade of inflammatory immune responses. With SARS-2, this was evident when infected patients were hospitalized with COVID.
The Pfizer and Moderna mRNA “vaccines” focus only on one of those proteins, in the case of SARS-2, the Spike protein that binds to our ACE2 receptor, to create this immune response. Its intent is to spur an immune antibody response against the protein that primarily binds to our cellular receptors. In the case of SARS-2, this was the ACE2 receptor, found primarily in our vascular system, as its functional role is to assist in regulating blood pressure.
RNA-Dependent RNA Polymerase (RdRP) Inhibitors
Replicase inhibitors represent a distinctive approach compared to vaccines, or conventional antiviral therapeutics. They are also sometimes referred to as “broad-spectrum small molecule” therapeutic drugs, or protocols. PROTOCOL-Z is also grounded within this realm. Such formulas seek to target a singular viral vulnerability latent within all RNA viruses. That vulnerability is RdRP. Remember this acronym. Its critical function will be examined and explored throughout the remainder of this work.
To illustrate this disparity, envision your cell as your home, surrounded by vigilant, yet lethargic, guard dogs representing your innate immune antibody response, poised to thwart viral intruders attempting to breach your home's defenses. In nature, these guard dogs require full genetic details of the intruder to react effectively—its appearance, characteristics, and even attire. Should the intruder mutate any of these protein features, the guard dogs will only respond aggressively when the intruder attempts to breach the cellular locks and gain entry.
In the event that the viral intruder eludes recognition by the guard dogs, various antiviral drugs intervene by obstructing the cellular locks, impeding the intruder's efforts to breach security. They essentially obstruct the cellular receptors, or modify the cellular membrane surface, hindering viral entry into cells. However, this intervention entails a delayed response. Consider that this scenario unfolds concurrently in thousands to millions of cells, with any delay increasing the likelihood of successful viral invasion and replication, proliferating the intruder's presence.
A delay in this response could determine whether the intrusion is thwarted, or necessitates the intervention of "police" killer T-cells, which may inadvertently damage cellular homes in the process. Yet, akin to real-life law enforcement, these "police" are often tardy or absent altogether, leaving individuals prone to succumb to the viral onslaught.
Enter RNA-dependent RNA polymerase (RdRP) inhibitors, a different breed of antiviral therapeutics that disrupt viral replication regardless of intruder entry. In the crime-fighting analogy, they embody the homeowner equipped with a weapon to inhibit the intruder's ability to replicate. Instead of focusing solely on preventing viral entry, RdRP inhibitors target the core of the problem—viral replication within cells. And furthering the analogy, RdRP inhibitors represent the cellular “homeowner” lurking within, armed with an antiviral .44 magnum prepared to hold at bay the invading virus’ ability to loot cellular resources, stolen for the purpose of self-replication.
Imagine if there existed RdRP inhibitors potent enough to incapacitate these viral intruders, halting their replication until the body's immune "police" could finally respond to identify and neutralize this formidable invasion force. Wouldn't it be more efficacious to obstruct viral replication outright rather than engage in a perpetual game of whack-a-mole, or hide-and-seek with ever-mutating viral adversaries? PROTOCOL-Z represents that .44 magnum.
Our immune systems engage in a perpetual battle against viral and bacterial invaders, requiring adequate ammunition to mount a defense. Deficiencies in critical nutrients compromise our immune terrain, undermining any enhancement strategy.
As previously mentioned, traditional vaccine tactics, akin to those used against DNA viruses like Smallpox, rely on inactivated, or weakened viruses to provoke immune recognition and reaction. However, the constantly mutating nature of RNA viruses, such as Coronaviruses, presents a challenge. These mutations alter the viral protein "image" perceived by our immunological “guard dogs,” leading to delays in the immune response until sufficient virus replication prompts recognition.
Consequently, existing vaccine technologies, including mRNA vaccines, perpetuate a game of "whack-a-mole" against ever-changing viral strains. Traditional vaccines offer a complete picture of viral protein structure, akin to assembling a jigsaw puzzle to reveal its complete likeness. Yet, their diminishing efficacy against mutating strains underscores the need for alternatives. The use of synthetic mRNA to replicate a chimeric viral antigenic particle to spur that immune response has emerged as a gene-therapy technique amid the SARS-2 pandemic. However, concerns persist over its safety and efficacy, prompting the exploration of alternative solutions.
In the quest to combat RNA viruses, various protective measures have been explored, including nutritional supplements, protective masks, and decontamination methods. However, unanswered questions and political distractions hinder progress toward effective solutions. Instead, focus should be directed toward understanding and neutralizing viral threats at their most vulnerable points, ensuring victory over fear and uncertainty. The pursuit of truth regarding the virus's origin must not overshadow efforts to develop effective countermeasures. By prioritizing solutions over debates, victory against viral adversaries becomes attainable. Through collaboration and focused research, the secrets of defeating RNA viruses can be uncovered, empowering individuals and safeguarding communities. This will be the focus of PROTOCOL-Z.
But first, we must explore the life of one of the most renowned and controversial microbiologists on the planet, Dr. Ralph Baric. Strap yourselves in; this is where the viral journey will require your utmost attention. The author will endeavor to, figuratively speaking, hold your hand along the path to understanding.
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De Oppresso Liber