Sofra, Xanya Ph.D (2021). Checkmate by a Protean Invisible Enemy. Book. Lambert Publishing)

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Sofra, Xanya Ph.D (2021). Checkmate by a Protean Invisible Enemy. Book.  Lambert Publishing)

Book Summary:

COVID-19 appears to use mutations adaptively to escape immune exposure and expand its transmissibility. It circumvents the errors accumulated by random amino acid switches that previously eradicated other coronaviruses. The infectiousness of this pandemic is exponentially increasing, evolving into even more elusive pernicious variants. By apprehending the ACE2 receptors to contaminate human cells, COVID-19 neutralizes our primary anti-inflammatory and anti-fibrotic defences. The body counterattacks by unleashing chemokines, interleukins, leukocytes, TNF, CSF; but COVID-19 has a strategy: First, it overwhelms the innate response; then, it manoeuvres to avoid exposure by inhibiting the adaptive mechanisms of viral recognition. Undetected, COVID- 19 multiplies, while the immune system is blindly shooting in the dark, ravaging the vital organs of the host who is fatally injured by the cytokine storm.  Vaccines’ safety and effectiveness is evaluated along with new therapeutics. The focus is on COVID-19 susceptibility factors, hormonal imbalance, elevated glucose and lipids, obesity, and the male gender. Preventive methods designed to empower immunity are explored. 

Section Overview

The COVID-19 classification and evolution through its multiple mutations have increased its transmissibility rate up to 70% or more globally, threatening to undermine the promise of a number of emerging medications and vaccines that primarily focus on the immune detection of the Spike trimer.         

Mutations have been long considered as random events, or mistakes during the viral RNA replication. Usually, what can go wrong will go wrong; therefore, repeated transformations lead to the extinction of a virus.  On the contrary, the aggregate result of over 300,000 COVID-19 variants have expanded its transmissibility and infectiousness.  COVID-19 mutations do not degrade the virus; they empower and facilitate its disguise to evade detection. Unlike other coronaviruses, COVID-19 amino acid switches do not reflect the random unfolding of errors that eventually eradicate the disease.  COVID-19 appears to use mutations adaptively in the service of its survival and expansion.             

One of the COVID-19 primary strategies is to inhibit the production of interferon type (INF) that is involved in recognizing the virus.  The deleterious consequences of the cytokine storm where the CD8+ killer cells injure the vital organs of the host may well be collateral damage, as the blind immune system struggles to annihilate the unidentified COVID-19.  It is probable that evolution has programmed COVID-19 with an adeptness designed to debilitate key systemic defences to secure its subsistence.  To date the infectiousness of the COVID-19 pandemic is exponentially increasing, denoting the possibility of an even more dangerously elusive, inconspicuous, and sophisticated version of the disease.

 

COVID-19 Affinity for ACE2 receptors in Adipose Tissue and Testes. 

 

Summary:
The imminent danger of the COVID-19 pandemic has accelerated research in pharmaceuticals that either target the fusion of the Spike protein with ACE2 receptors, or the infectious RNA replication that often overwhelms immune defences.  The scope of this review was to elucidate the main human vulnerabilities to COVID-19, including the accumulation of ACE2 receptors in testes, adipose tissue, thyroid, heart and kidneys that escalate viral affinity in males, the aged, and certain medical conditions, including diabetes, CVD, and pulmonary diseases. Pre-existing inflammation inherent in obesity may exacerbate the “cytokine storm,” a rampaging immune reaction during the course of COVID-19 that is deleterious to the host. A number of new therapeutics have emerged in the pharmaceutical market along with alternative techniques that include hormone replacement procedures and mesenchymal stem cells. None of them appear to offer a conclusive solution which leaves only preventive and protective interventions designed to enhance immunity. The current perspective explores the primary components of dysregulated health predisposing individuals to COVID-19, including hormonal imbalance, increased lipids and lipoproteins, thyroid dysfunction, degraded fitness, age-related testosterone decline and cortisol increase that provokes stress eating behaviours and weight accumulation. Obesity facilitates COVID-19 proliferation in human cells  due to the abundance of ACE2 receptors in adipose tissue. ACE2 receptors are sparce in muscle cells, therefore, physical activity, regular exercise or any alternative to exercise may restrict COVID-19 escalation, by exchanging fat with muscle mass.

 

Conclusion
         
COVID-19 is a global lethal pandemic that has stirred an enormous body of clinical trials including both therapeutic methods and protective / preventive interventions. Research primarily targets the COVID-19 point of entry via the fusion of the S glycoprotein with ACE2 receptors, or the involvement of the N protein in the RNA viral replication. The abundance of ACE2 receptors in adipose tissue and the testes renders obese males highly susceptible to the decease. The heart, liver, and thyroid are also enriched with ACE2 expression, precipitating increased mortality rates among CVD and diabetic patients, as well as overweight individuals with excess visceral fat that often results in non-alcoholic hepatic steatosis. The diminished incidence of ACE2 receptors in muscle tissue spotlights physical activity or its effortless exercise alternative as a protective shield against the virus, due to the body’s propensity to utilize fat as an energy source to build muscle. However, strenuous activity can be detrimental by increasing inflammation and escalating the stress hormone, cortisol, while decreasing testosterone and the anorexic hormone leptin leading to increased food consumption, and eventual fat accumulation. This process is exacerbated by age-related testosterone decline. The anti-inflammatory properties of oestradiol are highlighted within the moderation of hormonal balance. Overall, adiposity is featured as the epicentre of inflammation, which increases the probability of the cytokine storm rampaging the body, following COVID-19 infection. This lethal process is facilitated and accelerated by the plenitude of ACE2 receptors in adipose tissue.

 

There are several weight management techniques, including different versions of lasers and RF, some of which may exacerbate inflammatory conditions, and none of which contributes to decreased visceral fat or increased fitness. A metanalysis of recently published clinical trials that used a novel London University effortless exercise invention, demonstrated a statistically significant decrease of adiposity that was validated by the absence of fatty liver post treatment, increase muscle mass and overall hormonal balance. None of these clinical trials involved COVID-19 patients or claimed to address a COVID-19 therapeutic intervention. The purpose was defined as investigating effective methods to reinforce health and fitness which could enhance immunity and protect against the detrimental consequences of COVID-19 .