Viewer Question on The Nature of Viruses & Transmission

Emmett asks,

Hi Jeff, Thanks for your talks and articles over the last few years. In 2020 you awakened me to the simple cause of illness such as a flu and the natural good function of those little particles commonly known as viruses. I was so happy to learn this, and forever grateful to you.

However I'm now confused about your present motives and intentions, with your potential attacks on the no-virus crowd. So to clear things up, could you please answer 3 simple questions for me:

1. Do you claim that viruses are a potential cause of illness or disease?

2. Do you claim that viruses are materially transmissible by any natural means?

3. What is your preferred biological definition of a virus?

Thanks in advance. No rush.

Do Viruses Cause Disease Directly?

I contend that viruses primarily arise as a consequence of the disease state rather than being direct causative agents. The disease state manifests across a wide spectrum, ranging from very minor illness to extremely severe levels of disease. My perspective challenges the conventional view that portrays viruses as malevolent invaders with the sole purpose of causing harm. Instead, it emphasizes the complex and symbiotic relationship between viruses and their host cells—this is an incredibly important distinction to make.

In a healthy body, cells maintain a state of homeostasis, functioning optimally and efficiently managing waste products, cellular debris, and minor toxins. However, when a body undergoes stress, whether due to environmental factors, genetic predispositions, or lifestyle choices, or encountering toxins which the body cannot easily sequester, the body can accumulate degenerated and dysfunctional cells over time. In many of these cases, cells no longer operate optimally, leading to an internal environment conducive to further cellular degradation and accumulation of toxic substances.

Viruses, in this context, can be seen as opportunistic entities that ‘exploit’ these weakened and degenerated cells. They possess enzymatic capabilities that allow them to degrade compromised cells, breaking down their components and releasing toxic cellular substances into the extracellular matrix, diluting toxins via hydrolysis, making it easier for cells to clean. This degradation process, while contributing to the overall toxic load within the body, is a natural method of indirect cellular cleanup, wherein viruses ‘assist’ in the removal of cellular debris that the body's own mechanisms have failed to manage effectively.

I contend that viruses themselves do not directly induce disease. Their ability to infect cells is contingent upon the presence of compatible receptors on the cell’s membrane surface. These receptors are not ubiquitously expressed; they typically appear when cells are in a state of distress and degeneration. The accumulation of toxic compounds within cells triggers the expression of these receptors, effectively marking these cells as targets for viral entry. In this manner, viruses do not indiscriminately attack healthy cells; they are drawn to those that are already compromised.

I assert that all viruses at one point originate within cells, and that cells possess the necessary functions to produce viral proteins independently of external infection. If this were not true, viruses could never be replicated by cells because cells would not contain the necessary functions to synthesize and replicate viruses. However, I now acknowledge that external viruses may play a role in the process of imparting cells with genetic information to code certain viruses.

Once inside a susceptible cell, the virus—serving as a genetic blueprint—imparts instructions to cells for its replication, often resulting in the death of the unstable cell as it depletes the energy of such a cell. In the case of moderately healthy cells, they can heal and thrive after viral infection. This process can release further toxic substances, which may exacerbate the symptoms of illness. However, it is important to understand that these symptoms are not caused directly by the virus itself but are a consequence of the body's attempt to manage the underlying state of cellular degeneration and the resultant toxic extracellular fluids from viral fractionation.

Thus, the role of viruses in disease can be seen as twofold. On one hand, they act as agents of cellular degradation, targeting and breaking down cells that are no longer viable. On the other hand, their presence and replication can amplify the symptoms of an existing disease state, primarily through the release of toxins from degenerated cells. This dual role underscores the complexity of the viral-host relationship and challenges the simplistic notion of viruses as mere pathogens, painting a far more accurate representation of the nuances of this complex relationship.

Therefore, the view that viruses are a consequence rather than a cause of disease shifts the focus from external pathogens to internal cellular health. It emphasizes the importance of maintaining cellular homeostasis. Understanding the conditions that make cells vulnerable to viral entry gives us information to disease prevention and management. This shift in focus moves away from unnecessary conflict and war with viruses and towards a more comprehensive view of cellular health, its influence on viral susceptibility, and the indirect role viruses play in supporting homeostasis.

Are Viruses Transmissible?

My view diverges from most contemporary scientific understanding because I recognize that viruses always start from the cell. Thus, if a particular type of virus exists, it first existed—not because it was initially transmitted—but because it was produced by a cell. This challenges the contemporary view that viruses are indiscriminate attackers, among other things. However, let me offer some nuance to my view in light of more than a decade of contemplating and learning the science behind viruses, which has culminated in this current point in time.

Initially, my position was that viruses were not contagious in totality due to specific RNA key interactions; however, I have determined that this was an oversimplification, and years later, I now recognize that viruses can molecularly change their binding capabilities to fit the lock. The concept of contagion requires precise delineation—it is often misconstrued as implying indiscriminate pathogenicity, but the reality is more nuanced.
As another reader in the past noted: “What does contagious really mean anyway?”—that is an apt question to pose. I believe the term should be understood as far more complex than the black and white issue is tends to be.
Viruses exhibit selectivity in infection, targeting only cells with compatible receptors. As previously noted, one of their biological functions includes the breakdown of unstable, degenerated cells, which indirectly facilitates the removal of toxic cellular debris—gene transfer is another. Viruses, like microorganisms, can be transmitted as all bodily fluids can be. Again, however, for a virus to infect a cell, it must be compatible with the cell’s molecular receptors and must normally originate from a cell type that has produced it. For instance, hepatitis viruses are specialized to infect liver cells because they have evolved to bind to receptors present on those cells, which is why they generally cannot infect lung cells.

My revised hypothesis acknowledges that cells may indeed recognize and replicate a virus produced by another organism if it provides beneficial instructions that susceptible cells can utilize. This replication process enables viruses to exit the host cell and body of one person, and infect other unstable cells in someone else, but only if those cells are susceptible to that particular virus. On the surface, you may surmise that I am merely claiming viruses are contagious and deadly, but that is not the entire case—context is highly important.
For example, bacteria similarly require specific conditions to thrive and multiply within the human body. Tissues in a particular state of decay can provide an environment conducive for certain bacteria to flourish, highlighting the balance between host health and bacterial presence—the same is true for fungi. External sources, including raw foods, serve as natural reservoirs of bacteria that can be introduced into the body. Through consumption or contact with these sources, a diverse array of bacteria can integrate into the body, contributing to the body's microbiome and aiding in various physiological processes that support overall health. The integration of bacteria from external sources into the body represents a harmonious coexistence between the host and the microbial community. These bacteria can play essential roles in regulating immune responses, aiding in digestion, and producing beneficial compounds that support cellular functions and overall well-being.

Viruses operate similarly, though they are not alive. I initially overlooked this aspect because I viewed things in a binary fashion, interpreting contagiousness as a rigid concept, which was and remains incorrect.

But you may ask: Why would the body not simply produce its own virus every time? The answer is multifaceted. One reason is that it may not be able to.

Because external viruses provide a novel stimulus to the immune system, triggering a response that further aids in the clearance of degenerated cells and toxic cellular debris. The introduction of external viruses can activate immune cells and signaling pathways that amplify the body's natural protective and cleansing mechanisms, leading to a more robust and comprehensive cellular cleansing process.
External viruses bring a diverse array of genetic information and enzymatic capabilities that cells in one body may not possess internally. These external viruses may contain specialized components or functionalities that can target specific cellular structures or pathways involved in the breakdown of compromised cells that current cells in one body may have trouble synthesizing on their own. By introducing external viruses to unstable cells, these viruses can synergize with the cellular machinery to enhance the process of cellular cleanup and removal of toxic substances.
How do we know this to be true? Because oncolytic viruses and other viruses are successfully employed to target and destroy cancer cells. These external viruses are introduced into the body specifically to infect and fractionate cancer cells. Albeit, these viruses are modified to be more selective to cancer cells, the same principles apply to non-modified, natural viruses and the cell types that created them.

When considering the scenario where viruses originate from cells within one individual and are subsequently transmitted to another individual for the purpose of facilitating cellular cleansing, we must examine the mechanisms of the unique cellular environments of each individual. While both individuals may have the capacity to produce viruses internally, the specific genetic makeup, cellular conditions, and environmental factors within each person's body can influence the production and efficacy of certain viruses for cellular cleansing.
Thus, it is possible that the individual who initially produces a particular viral mutation may have a cellular environment that is particularly conducive to generating viruses that have a higher affinity in cellular cleansing of certain proteins. This may be attributed to genetic factors, immune response mechanisms, or cellular processes that are primed for producing viruses with specific capabilities.

The cellular machinery involved in virus replication can differ between individuals. Factors such as the presence of specific enzymes, the availability of nucleotides, and the overall metabolic state of the cell can influence viral mutation rates and the nature of these mutations. Viral protein mutations have the added benefit of maintaining an elevated immune response in order to continue detoxification. Some cellular environments might be more prone to producing viral particles that contribute positively to cellular maintenance or cleansing​. As such, an individual with a compromised state of health may have a different cellular context that does not inherently support the production of certain viruses for cleansing purposes.

You may ask: Since viruses are highly specific, and utilize an RNA lock-and-key system, how then would an external virus potentially infect another person's cells?
As previously noted, viruses exhibit a high degree of specificity in their interactions with host cells, often relying on a precise molecular recognition process to infect and replicate within a cellular environment. The RNA lock-and-key system refers to the specific binding interactions between viral RNA sequences and cellular receptors, allowing the virus to gain entry into a receptive cell and initiate the infection process.

I hypothesize that when a virus is transmitted from one individual to another, the key factor in the infection process lies in the compatibility between the viral RNA sequences of the transmitted virus and the cellular receptors present on the recipient's cells. Despite the specificity of viral interactions, viruses can exhibit a degree of adaptability and variability that may allow them to infect susceptible individuals, albeit with varying efficiency.
In short: viruses are highly specific and highly selective—subcellular conditions must be in a certain state to allow for this to occur.
When a virus is transmitted from one individual to another, carrying different RNA sequences, the process of viral entry into the recipient's cells involves complex processes of viral adaptability and host cell receptor recognition. Despite the variations in viral RNA between individuals, viruses can exhibit a degree of plasticity that enables them to adapt to new host environments and engage with cellular receptors in different individuals.

One mechanism through which viruses adapt to new host environments is through genetic diversification of their surface proteins, a previous area of study that I did not fully account for. These genetic variations can enhance the virus's ability to recognize and bind to a wider range of cellular receptors in different individuals, fostering a harmonious interaction between the virus and host cells for efficient entry and infection. Previously, I held that RNA differences would prevent this from happening. However, if that were the case, injected viruses would not trigger an immune response capable of producing similar types of viral replication. Thus, I had to revisit my hypothesis in an ongoing process of the scientific method.

Essentially, the spikes of viruses are like intricate keys that must fit precisely into the locks of cellular receptors to gain entry into host cells. Through genetic modifications and diversification, viruses can fine-tune their spikes to better match the unique molecular configurations of cellular receptors present in diverse host environments. This adaptability allows viruses to optimize their binding affinity and efficiency in interacting with host cells, promoting a harmonious and effective process of entry and infection.

Therefore, if viruses are indeed transmittable on some level, they must first bypass the many bodily protection mechanisms in place, and then encounter a specific cell in a specific manner, and if so, the body must be able to replicate the virus effectively. Without the necessary cellular receptors, and molecular interactions, viruses will fail to infect another person effectively. Under the right conditions, it is plausible that this can occur and is merely a part of the natural functions of nature playing out. One must also consider the effects of environmental factors such as temperature, humidity, and barometric pressure on the susceptibility of cells, as well as their regulation of detoxification pathways and susceptibility to infection.

What are Viruses in Basic Terms? + Conclusion

Viruses are obligate intracellular parasites, requiring host cells for replication. They come in many different shapes and sizes—from spherical to icosahedral, and beyond, and from enveloped to non-enveloped. They possess either RNA or DNA as their genomic material and rely entirely on host cellular machinery for their creation. This relationship suggests that the origin of viruses is inherently linked to that of cells. It is hypothesized that viruses initially emerged as proteinaceous entities from primordial cells, indicating a co-evolutionary trajectory. Consequently, while viruses and cells are inextricably linked and mutually dependent, the cellular form predates the viral form.

With this understanding, my hypothesis is that viruses primarily arise from cellular conditions, whether due to natural distress or more severe stress induced by modern factors. Considering this, and acknowledging that viruses need to encounter susceptible cells to propagate, presents a more realistic perspective than asserting that there is no influence of external viruses on human biology whatsoever. This viewpoint addresses several gaps in my previous hypothesis, which too narrowly viewed the totality of circumstances.
Essentially, my revised hypothesis is that viruses result from specific cellular environments and conditions and play indirect roles in cellular detoxification. It recognizes that viruses, rather than existing as independent entities, are intrinsically linked to the cell itself. It also acknowledges that all living things are interconnected, recognizing the potential for shared genetic information to instruct cells with respect to their biological survival and function. This perspective integrates the idea that the cellular state—whether due to inherent biological factors or external stressors—plays an important role in virus emergence and propagation.

Finally, it recognizes that fearing viruses is futile, as they are inevitable components of the human condition and life on Earth. Instead, viruses should be understood as fundamental players in the grand scheme of life, rather than being viewed solely through their often exaggerated associations with disease and death, which fails to recognize their ubiquitous and beneficial roles in nature and disease.

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Thanks for reading,

Jeff Green