The aim of this series of articles is to target, deconstruct, and dispel myths of COVID-19 “The Science ™” that have spread like wildfire. We will summarize the molecular biology and epidemiology of the SARS-CoV-2 virus and COVID-19, respectively. We will also discuss the vaccine efficacy studies, what we know about conferred immunity through prior infection, and the fate of other therapies such as monoclonal antibodies and antivirals. And of course, we will address the taboo question: “was SARS-CoV-2 made in a lab?”
The ongoing politicization of healthcare is both mind boggling and deeply concerning. A mixture of poor, equivocating communication by government officials, as well as intentional bastardization of “The Science” to advance political agendas, has led to alarmist reactions that propagate like wildfire in this meme-based generation. The result is a polarized public, content to hurl aspersions across the bipartisan line, and branding their political opponents as either “sheep” or “Marxists” (largely dependent on whether their faces remained cloth bound). Clearly, people have lost their minds. Can you blame them? Public health officials have done an extremely poor job educating the populace on how our continuously evolving understanding of the science behind the origins, pathophysiology, and epidemiology of the SARS-CoV-2 virus and COVID-19 disease have resulted in never-before-seen public policy. Don’t get me wrong, this is no easy task. Consensus within the scientific and medical communities is not something that’s achieved in an instant, and for good reason. Scientific theory is designed to be disproven, and experiments must be confirmed independently before conclusions are broadly accepted. Nor are new drug therapies and vaccines approved for use overnight. The FDA has developed a rigorous clinical trial process to validate the safety and efficacy of novel drug compounds in large and diverse patient populations. On average, it takes 10 years to advance a proof-of-concept therapy from the laboratory to the clinic. Governments have been tasked with funding research and translating the findings into real-world policy that is literal life or death. Moral of the story: do not run for office.
Mounting political and social tension within the US over the last two years has only added to the pressure to contain the virus and develop an effective vaccine, lest rampant fear tear the loosely woven social fabric completely apart. The pressure cooker started heating up as soon as the CDC confirmed the first US SARS-CoV-2 case on January 21, 2020. By February 10th, the COVID-19 death toll in China surpassed that of the SARS outbreak 17 years ago (908 v. 774), and over 10,000 cases and 200 deaths were reported worldwide. On March 11th, the World Health Organization (WHO) declared COVID-19 an international pandemic. All eyes were on the Trump Administration, the Wuhan district, Big Pharma, and the CDC.
Trump acted quickly by declaring COVID-19 a national emergency, freeing up billions of dollars in federal funding to fight the spread of the disease. On March 26, the Senate signed the CARES act which provided $2T to hospitals, businesses, and local governments. The next day, the House of Representatives approved the act, which provided direct payments to Americans and expansion of unemployment insurance. In a misguided attempt to quell mounting fear, Trump endorsed the use of hydroxychloroquine, an FDA-approved antiviral for malaria, as a first-line treatment for SARS-CoV-2 infection. The University of Minnesota launched a clinical trial on post-exposure treatment for SARS-CoV-2 on March 17, 2020 that ultimately led to the FDA issuing an Emergency Use Authorization (EUA) for hydroxychloroquine on March 30th. The American Heart Association, the American College of Cardiology, and the Heart Rhythm Society issued a joint guidance which noted severe heart complications caused by the antiviral, leading to the FDA rescinding the authorization within 1 month of approval (the FDA has been under immense scrutiny as of late). A viable treatment for COVID-19 remained elusive, and the nation would remain in various states of lockdown for the foreseeable future. The events that transpired in the next year and a half would have a lasting impact on the public’s perception of Big Pharma, the FDA, and the WHO. They would also leave an indelible smudge on our faith in the government and trust in our fellow Americans.
The aim of this series of articles is to present a high-level overview of what is known about the SARS-CoV-2 virus, the available treatment options, and to dispel myths of “The Science™” that have spread like wildfire. We will summarize what is known about the molecular biology and epidemiology of the SARS-CoV-2 virus and COVID-19, respectively. We will discuss the Big Pharma vaccine efficacy studies, what we know about conferred immunity through prior infection, and the results of other therapies such as monoclonal antibodies. We will address the controversial question, “was SARS-CoV-2 made in a lab?”
The human immune system is equipped with two defensive strategies: innate immunity and adaptive immunity. As the name suggests, innate immunity is pre-programmed into our genetic code, having been honed over an evolutionary time scale and trained to fight off a plethora of foreign pathogens (e.g., bacteria, viruses, cancer cells, etc.) with a rapid response (minutes to hours after exposure). Innate immunity is described as “antigen-independent,” referring to its non-specific mechanism of action. Contrast this with the adaptive immune system, which is “antigen-dependent,” referring to its ability to recognize specific antigens present on foreign pathogens (an antigen is a molecule, often a protein or peptide, that is found on the surface of a pathogen and reacts with our antibodies and immune cells). Exposure of antigens to the adaptive immune system creates a “memory” effect, allowing the system to mount a stronger response upon subsequent exposure to the same antigen. The innate and adaptive immune systems work synergistically, and are carefully tuned to prevent autoimmune (i.e., a hyperactive immune response, as in rheumatoid arthritis) or immunodeficiency (i.e., a hypoactive immune response as in AIDS) disorders.
Upon initial infection, the innate immune system responds by recruiting many different types of immune cells through the release of signaling molecules called cytokines. Cytokines are small proteins that signal to specific classes of immune cells to release antibodies and other proteins that activate the complement system, a cascade that marks pathogens for destruction via phagocytosis (a process by which specific classes of immune cells, called phagocytes, to engulf and digest the pathogen). The innate immune system relies on many cell types to mount a quick response, such as phagocytes (macrophages and neutrophils), natural killer (NK) cells, lymphocytes (T cells), and other white blood cells (eosinophils, basophils, and mast cells). Importantly, it also interacts with and activates the adaptive immune system via “antigen presentation” performed by dendritic cells and macrophages. Macrophages and dendritic cells phagocytose pathogens to clear them from the site of infection. They also “present” pieces of the digested pathogen (i.e., antigens) to members of the adaptive immune system to catalogue and “memorize” for later.
Antigen-presenting cells activate the T cells that are a part of the adaptive immune system, generating pathogen-specific pathways that identify and eliminate specific pathogens upon a subsequent infection. Once activated, T cells differentiate into cytotoxic T cells (CD8+ cells) or T-helper cells (CD4+ cells). Cytotoxic T cells are equipped with a T cell receptor (TCR) that recognizes a singular, specific antigen present on the surface of pathogen-infected cells. T cells do not target the pathogen directly. Instead, they are involved in the destruction of pathogen-infected human cells through the release of chemical agents such as perforin, granzymes, and granulysin, which induce a form of cell death known as apoptosis. Interestingly, the genes that code for the TCRs are not consistent across the entire population of T cells in the body. Instead, they are programmed by a random process of “shuffling” that produces a population of heterogeneous T cells with unique receptors capable of binding to millions of different antigens. Molecular biologists call this a stochastic process, and it is one of the ingenious ways that the human body copes with the plethora of pathogens that exist in nature. Since TCR recognition of antigens is somewhat left to fate, there is always the chance that the TCR might target tissues in the body itself. To prevent this autoimmune recognition, the budding T cells are exposed to “self-antigens” in the thymus (the organ in which they are produced), and the T cells that bind to the self-antigens undergo apoptosis (programmed cell death).
Most of the cytotoxic T cells die off when the infection subsides, but a few remain and are retrained as “memory” cells that can quickly transform back into cytotoxic CD8+ T cells upon subsequent infection. These CD8+ T cells are complemented by CD4+ T-helper cells that modulate the strength of the immune response. Although they are not cytotoxic (i.e., they can’t kill infected human cells) nor phagocytic (i.e., they can’t digest free-floating pathogens), T-helper cells activate B cells, mast cells, and eosinophils through the release of cytokines. Once activated, B cells begin producing antibodies that target the antigens through direct interaction with the pathogen. Lastly, regulatory T cells (T reg) are critical for managing the strength and duration of the overall immune response. T reg cells function like a thermostat, constantly monitoring the immune system activity and tweaking it so that it stays within an acceptable range.
The immune system is incredibly complex, and we have barely touched on all the cell types and functions. However, the overall defensive strategy is fairly simple, and can be broken into 3 core concepts:
Once the innate immune system has sounded the alarm via the release of cytokines, the pathogen-hungry phagocytes digest the foreign invader and present the adaptive immune system with pictures of their meal. Call it culinary reconnaissance. Impressed with the work of the innate system, the adaptive system distributes the picture of the chewed-up pathogen like a wanted ad. A posse of cytotoxic T cells forms to root out human cells that are infected with the pathogen, while the B cells make sure that the pathogen will be recognized if it decides to invade again by producing unique antibodies that will result in direct elimination of the pathogen by phagocytosis. Antibody-mediated immunity is very important during the early stages of an infection when the pathogen has infected (relatively) few human cells, but a complete immune response relies on the activity of cytotoxic CD8+ T cells that can target and eliminate infected human cells without antibody targeting.
Viruses are confusing lifeforms. Their status as “living” organisms is contentious within the scientific community, and any discussion of the topic will eventually encroach upon the existential quandary, “What is life?” Our current, carbon-based definition of life is much more stringent than the Aristotelian concept of spontaneous generation, the theory that life spontaneously arose from inanimate elements. Clearly, living things arise from other living things. Life as we know it requires two fundamental elements: reproduction and metabolism. Every high school student knows that DNA is the building block of life, as it is capable of encoding information that is passed on to its descendants. The dogma of molecular biology states that double-stranded DNA is transcribed into single-stranded RNA, which is then translated into proteins. In order for a cell to replicate, it must duplicate its entire genome using specialized enzymes. The Catch 22 is that DNA on its own is not capable of its own replication (DNA polymerases are the only enzymes capable of duplicating the genetic information stored in the nucleic acid DNA - Learn more). We are left with a classic chicken-or-egg conundrum: Which came first, the DNA or the enzyme? Perhaps these enzymes arose first, in the form of proteins? Possible, but proteins are not capable of encoding information like nucleic acids. This dilemma may be solved by the existence of RNA, which stores genetic information and has enzymatic function due to its three-dimensional conformations. RNA may truly be the fundamental building block of life, originating as a precursor to both DNA and proteins.
Viruses, unlike mammalian cells, can rely on either DNA or RNA to create copies of themselves. They also lack their own replicative enzymes and require the molecular machinery of a host cell to duplicate their genetic information. In this sense, viruses are inert before they enter an organism, and only become alive once they have successfully infiltrated a host cell. RNA viruses can bypass the transcription step and immediately express their viral proteins through translation. These proteins assemble into complete virions by forming a capsid around the viral RNA, which is replicated using the host cell's polymerase enzymes. RNA polymerases are more error-prone than DNA polymerases, resulting in a higher mutation rate of RNA viruses than DNA viruses, an essential characteristic of the novel SARS-CoV-2 virus.
Severe Acute respiratory Syndrome (SARS) viruses are not exactly new. In fact, SARS-CoV-2 is the seventh coronavirus to infect humans (SARS-CoV, SARS-CoV-2, MERS-CoV, HKU1, NC63, OC43, and 229E). But for some reason this one hit differently. The high rate of infection and severe respiratory symptoms of the disease, combined with media-driven panic, thrust the world into a state of emergency. Luckily, scientists now have a good understanding of how the virus works and results in the upper respiratory disease known as COVID-19. Coronaviruses are enveloped, positive-sense single stranded RNA viruses, affecting the respiratory systems of humans and animals alike. Since the discovery of the first coronavirus in the 1930s (avian) and the first human coronavirus in the 1960s, significant progress has been made towards understanding their mechanisms of replication and pathogenesis.
Viruses have co-evolved with humans to locate “doorways” into our cells, which they pass through like Trojan Horses, wreaking havoc once inside. For SARS-CoV-2, this doorway is the ACE2 receptor that functions as a bridge between the exterior of a cell and the interior cytoplasm (where the molecular machinery needed for RNA replication is located). The ACE2 receptor is highly concentrated in the lungs, which is why COVID-19 is primarily an upper respiratory disease that hinders lung function and impairs oxygen transport. Binding of the virus to the ACE2 receptor sets off a cascade of molecular signaling that results in internalization of the viral particles within the host human cell. Once inside, the virus releases its DNA or RNA (as in the case of SARS-CoV-2) and hijacks the cell’s replicative machinery to produce copies of itself. A massive study conducted by 49 collaborating institutions in the US determined that there are over 300 potential coronavirus-host protein interactions. Further investigation of those proteins revealed 69 FDA drug compounds that are already FDA approved or in clinical trials and could target these interacting proteins necessary for SARS-CoV-2 replication .
SARS-CoV-2 does a fantastic job of cloaking its elicit activities within the host cell by hiding its RNA-synthesis, which would normally be recognized by the host cell and trigger an antiviral response through interferon signaling . The virus also has a mechanism to counteract this innate immune response by releasing a protein (nsp1) to modify the host cell’s translational activity to favor expression of the viruses’ mRNAs over the cells’ mRNA. This is particularly clever because even if the cell does recognize the production of viral mRNA, it is incapable of synthesizing and releasing the cytokines (interferons type 1 and 2) necessary to trigger an innate immune response. It is this rapid replication and evasion of antiviral mechanisms that leads to a dysregulated immune response and the pro-inflammatory signaling that destroys lung tissue in COVID-19 patients. Counterintuitively, it is the hyperactive, aberrant recruitment of cytokine-driven immune cells, such as macrophages and cytotoxic T cells, to the site of infection that induces the damage .
Eventually, the virus exhausts the cell’s replicative resources and exits the cell via exocytosis . Interestingly, a group of molecular biologists at the NIH published findings that suggest that SARS-CoV-2 actually escapes the cells via a different mechanism (lysosome egress) that disrupts proper antigen presentation by macrophages. This may explain the poor immune responses seen in COVID-19 patients , . Once free of their cellular confines, the viruses (also known as virions) spread to other cells in exponential fashion.
Understanding how SARS-CoV-2 enters the human cell and replicates is critical to developing effective treatments. There may be ways to render the virus impotent by targeting its internalization and replication mechanism before the immune system even needs to get involved. More attention should be turned towards blocking the binding of the virus to the ACE-2 receptor, preventing the virus from internalization after binding, and hindering replication after internalization. These ideas have been deprioritized by the scientific community as the pressure to develop vaccines consumes everyone’s attention. Due to the high mutation rate of SARS-CoV-2, it is unlikely that a single vaccine alone will be the solution to treating COVID-19. This is certainly how it is playing out.
SARS-CoV-2 is an upper respiratory disease, inducing pneumonia and applying stress to the immune system (a disorder known as "lymphopenia" wherein lymphocyte levels are reduced). The immune system identifies the virus by detecting certain viral antigens, such as the spike (S) glycoprotein, small envelope (E) glycoprotein, membrane (M) glycoprotein, and nucleocapsid (N) protein (see explanation in section below). As we have learned, the immune response is mediated by B cells, which produce the antibodies against specific viral antigens, and T cells, resulting in cytokine secretion and cytotoxic activity. Researchers have found that in the acute phase of infection, B cells elicit a quick response against the N protein, and later develop antibodies against the S protein (which has been the focus of all the vaccination efforts to date) . These antibodies persist in the body for different amounts of times, and distinct types of antibodies (called "isotypes," of which there are 5 main classes: IgG, IgE, IgD, IgM, and IgA) are responsible for the immune response at different points at time. In general, IgG and IgM antibodies are the most important for viral recognition and destruction. It may seem counterintuitive, but a robust antibody response is actually associated with disease severity, and a weaker response is associated with elimination of the virus .
During infection, T cells become activated against viral antigens resulting in cytokine release (a pro-inflammatory response) and cytotoxic activity (remember those CD8+ T cells?). Researchers have identified the S protein as the most immuno-reactive, meaning that CD8+ T cells respond most strongly when they "see" this antigen . Circulating CD4+ T cells ("helper" T cells) have been identified in COVID-19 convalescent patients (i.e., patients recovering from the disease), and SARS-CoV-2-reactive CD4+ T cells were identified in ~50% of unexposed individuals, which suggests a cross-reactive "memory" effect in T cell activity between other coronaviruses and SARS-CoV-2 . As previously described, CD4+ memory T cells, upon re-stimulation by a subsequent infection, trigger B and immune cell activation by cytokine production, while cytotoxic memory CD8+ T cells are ready to fight upon reinfection. An analysis of patients who recovered from the 2003 SARS virus revealed that both CD4+ and CD8+ memory T cells were capable of inducing an immune response from 3 months to 6 years after initial infection . This T cell response has been largely ignored by the media due to its relative complexity when compared to antibodies, but T cells clearly have a powerful, long-lasting response to the virus.
A heightened cytokine response is a well-known consequence of SARS-CoV-2 infection (the "cytokine storm"), and numerous studies have identified dysregulated cytokine production from innate and adaptive immune cells. The production heavily favors pro-inflammatory cytokines (e.g., TNF-α, IL-6, and IFN-α/-γ) over their anti-inflammatory brethren . Elevated cytokine levels can lead to Multi-Organ Dysfunctional Syndrome (MODS) and Acute Respiratory Disease (ARDS) due to the recruitment of other immune cells (macrophages, dendritic cells, neutrophils, etc) by the cytokines in upper respiratory tissues. Controlling the "cytokine storm" is a worthy scientific pursuit, but so far no anti-inflammatory has been approved to this effect.
Viruses, like cancer, have co-evolved with humans over revolutionary timescales. This has resulted in an accumulation of clever genetic modifications that allow these invaders to "escape" the immune system. The virus's evasive tactics interfere with the innate immune system's ability to obstruct the proliferation of neighboring infected cells through interferon secretion. SARS-CoV-2 uses several techniques to induce lymphopenia (reduction in lymphocytes, like B and T cells), as well as "exhaust" CD8+ T cells through cytokine signaling .
To begin a discussion of the origins of SARS-CoV-2, we must understand the protein structure of the virus and genetic variants between CoV-2 and the coronaviruses of the past. SARS-CoV-2 has four main structural proteins: spike (S) glycoprotein, small envelope (E) glycoprotein, membrane (M) glycoprotein, and nucleocapsid (N) protein. The S protein spans the viral membrane and is responsible for binding to host cells through angiotensin-converting enzyme 2 (ACE2), which is prevalent in the respiratory tract. A series of enzymatic reactions cleaves the S protein into two subunits, S1 and S2. S1 contains the receptor binding domain (RBD) that is unique for the ACE2 receptor, and S2 is important for the fusion of the viral membrane with the host cell.
SARS-CoV-2’s unique RBD on the S protein allows scientists to study the evolution of viruses by comparing the DNA coding for the RBD to other SARS viruses. One of the first research papers to present a theory on the origins of the novel coronavirus was published to Nature in March of 2020 .The investigation was a collaborative effort between The Scripps Research Institute (La Jolla, CA, USA), Institute of Evolutionary Biology (University of Edinburgh, UK, Columbia University (NY, USA), the University of Sydney (AU), Tulane University (New Orleans, LA, USA), and Zalgen Labs (Germantown, MD, USA). Of all the contributing parties, only Zalgen Labs may have a conflict of interest, as they develop countermeasures to emerging viruses. The research syndicate noted that RBD of the S protein is the most variable part of the coronavirus genome, with the rest of the genome exhibiting ~96% similarity between SARS-CoV-2 and the bat coronavirus RaTG13. There are six amino acids within the RBD that are critical for binding to the ACE2 receptor, and variations in this small sequence determines which host organisms that the virus can infect. Just how many amino acid variations within the RBD could there be (keep in mind that there are a total of 20 amino acids found in Nature)? A bit of back-of-the-envelope math reveals 6^20 = 3.65 * 10^15 combinations. Wow.
Computational analyses of the binding interaction between the virus and the host human cell have revealed that SARS-CoV-2 is statistically more inefficient at entering cells than previous strains, casting doubt on the notion that the virus was engineered in a Wuhan lab. Why would a scientist create a subpar virus, after all? Genomic analysis of the S protein’s subunits, S1 and S2, revealed the presence of a unique ("furin") cleavage site that is absent in related coronaviruses. The importance of this cleavage site is still not completely understood, but the researchers note that this unique furin cleavage site gene sequence pops up in avian influenza viruses due to rapid replication and transmission. Furthermore, efficient cleavage of the MERS-CoV spike proteins is known to enable transmission of the MERS coronavirus from bats to humans. Taken together, this data seems to support the theory that SARS-CoV-2 emerged as a consequence of natural evolution and is not the direct result of human engineering . It is very important to note that this evolution could have occurred within a laboratory because experimenting with viruses involves allowing them to replicate and infect host cells just like they would in the wild. The authors conclude it is improbable that SARS-CoV-2 emerged by direct manipulation.
"Never attribute to malice that which can be adequately explained by stupidity."
It is unlikely that SARS-CoV-2 was released on purpose, but it could very well have leaked out of a lab. Scenario 3. Which lab, exactly? The Wuhan Institute of Virology (WIV). Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases within the NIH, confirmed that the NIH had granted $600,000 over five years to the WIV through EcoHealth Alliance, a global nonprofit . Just what, exactly, were they spending the money on? According to a declassified intelligence document released by the State Department on January 15, 2021, the Chinese Communist Party (CCP) has made investigation into the WIV’s work nearly impossible. Recently, the US Department of State declassified a document that summarizes what the Western nations know about the Wuhan Institute of Virology.
Illnesses inside the Wuhan Institute of Virology (WIV):
Research at the WIV:
Secret military activity at the WIV:
The theory that the virus leaked from the Wuhan lab is supported by several independent academic groups. The Lawrence Livermore National Laboratory report (May 2020) provided early evidence of the lab leak hypothesis and was made available to Capitol Hill during a time when that notion was still politically taboo. Have you heard of it? Neither have I. The document was far from a smoking gun, but Republican lawmakers use it as evidence that the Biden administration has been burying any evidence that points to China as the culprit. A couple of research papers published in 2020 suggest that the SARS-CoV-2 virus could have arisen from handling cell cultures in a lab (remember Scenario 3 - evolution of SARS-CoV-2 in a laboratory through multiple “passaging” of the cells in a petri dish) [15, 16].
Recently, the Office of the Director of National Intelligence declassified their assessment on whether the SARS-CoV-2 virus originated from animal-to-human (zoonotic) transmission or was created in a lab. The consensus is that both hypotheses are plausible, but it is unlikely to have been engineered as a biological weapon; an extremely equivocal and unsatisfying conclusion (see below).
"China’s cooperation most likely would be needed to reach a conclusive assessment of the origins of COVID-19. Beijing, however, continues to hinder the global investigation, resist sharing information and blame other countries, including the United States. These actions reflect, in part, China’s government’s own uncertainty about where an investigation could lead as well as its frustration the international community is using the issue to exert political pressure on China."
Without conclusive evidence that the Wuhan scientists never engaged in "gain of function" research we cannot be sure that the virus wasn't intentionally engineered to be highly virulent.
The WIV needs to provide the scientific community with the exact gene sequences they were experimenting with to compare to the original SARS-CoV-2 genome that appeared in late 2019 and was sequenced in January 2020.
A complete audit of the Wuhan research is long overdue.
The CCP will never let that happen.
Note: a previous version of this article stated that the series would be divided into two parts. Due to the overwhelming pandemic news flow and recent clinical data publications, we have decided to segment the article into a three part series, and will provide updates as the story unfolds.
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