by James Lyons-Weiler, PhD, Popular Rationalism, ©2024
(Jan. 7, 2024) — BASIC UNDERSTANDING OF THE PATHOPHYSIOLOGY OF THE SPIKE PROTEIN INFORMS US THAT THE VACCINATED SHOULD AGE FASTER AND HAVE MORE CHRONIC ILLNESS, AS SHOULD THEIR IMMUNE SYSTEMS. THIS IS A COMPLETE REFERENCE RESOURCE FOR YOURSELF, YOUR DOCTORS AND YOUR LAWYERS.
The last decade of research in immunology has led to advances in understanding how viruses can lead to accelerated aging. The relationship between persistent viral infections and accelerated aging in particular garnered significant attention in the scientific community. Considering first mechanisms by which viruses can hasten the aging process, we will then contemplate the effects of repeated exposures to SARS-CoV-2 spike proteins.
The Aging Burden of Persistent Viral Infections
Persistent viral infections, particularly those caused by herpesviruses, have been shown to exacerbate the decline of the immune system, a phenomenon termed immunosenescence. This study published in AGING RESEARCH REVIEWS highlights how these infections drive T cells into a state of exhaustion. This chronic immune activation not only strains the immune system but also accelerates its aging.
The van den Bossche effect is a different matter; his concern is evolutionary IMMUNE ESCAPE. Immune escape refers to the ability of a virus to mutate and evolve in a manner that allows it to evade the immune response. This can happen through changes in the virus’s surface proteins, which are the primary targets of the immune system’s antibodies. (See, for example In Anticipation of a Highly Virulent SARS-CoV-2 Variant (substack.com)).
Others expect only the survival and transmission of less lethal variants due to the loss of lethal variants from high morbidity and mortality given the trade-off between transmissibility and and mortality. In viral evolution, the trade-off between transmissibility and mortality (commonly referred to as the “virulence-transmission trade-off” or simply the “trade-off hypothesis”) posits that over time there is a balance between a virus’s ability to spread (transmissibility) and the severity of the disease it causes (virulence or mortality).
The trade-off hypothesis works because if a virus is too virulent and kills its hosts rapidly, it may reduce its chances of transmission, as severely ill or deceased hosts are less likely to interact with others and spread the infection. Conversely, if a virus is highly transmissible but causes less severe disease, it can spread more effectively through the population. Over time, this evolutionary pressure can lead to the emergence of strains that are more contagious but potentially less deadly, as they can sustain their transmission by not incapacitating their hosts too severely.
In a system as complex as human society, some of whom are attempting to acquire personal immunity via vaccination and others not, the adaptive immunological landscape for the virus will have two peaks – if the vaccine has positive efficacy. Once the vaccine achieves negative efficacy, fewer people will continue to accept the “booster”, and the landscape will shrink toward primarily natural immunity.
Inflammaging – Aging and Immune System Decline
As we age, our immune system gradually deteriorates. This well-characterized decline is multifaceted, involving thymus involution, cellular senescence, and chronic low-grade inflammation, known as inflammaging. A comprehensive review in Lancet Infectious Disease discusses how aging may be both a cause and a consequence of infection, with enhanced inflammation and pathogen-dependent mechanisms playing pivotal roles, one feeding back on the other.
This source of inflammation will confuse some clinicians as either “a normal part of aging” or misdirect them, for some patients toward autoimmunity (e.g., via increased C-reactive protein, or even antinuclear antibodies) toward occult disease like autoimmunity when, in fact, the repeated exposures may lead to increased inflammation with or without pathogenic priming.
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