COVID-19 is an emerging highly transmissible coronavirus that causes high mortality among those individuals of advanced age.

While it is widely reported the COVID-19 coronavirus infection strikes older individuals who are most vulnerable to it and subsequent hospitalization and death, it is also widely known that senior adults experience more severe bouts of infectious disease and do not respond well to vaccination.  Efforts to prevent or slow aging should follow.

A report published in AGING & DISEASE states:

“Now we see in front of our own eyes the disastrous consequences of the deficit in such preventive measures, and the portent this gap in our approach represents for the future.  We are witnessing how this new infectious disease is wreaking havoc among individuals, the healthcare system and the entire social fabric around the world, while the rapid aging of the population represents the main risk factor and aggravating condition.  Therefore, arguably, one of the most important lessons to be learned from this pandemic, is the need to therapeutically address degenerative aging processes to prevent aging-related ill health as a whole.”

Of interest to longevity seekers, an anti-aging pill (everolimus-Rapamycin autoimmune drug ) is now reported to reduce immune-senescence (aging) in healthy elderly volunteers and enhances response to the flu vaccine by around 20%.

COVID-19 and aging

The lung infection coined as COVID-19 coronavirus, that can sometimes result in severe lung damage and lead to one’s demise, is now recognized as a disease of aging.  It strikes 80+ year-olds far more than any other age group.  Growing youngsters are at almost zero risk for a mortal outcome.  School children represented just 1/10th of one-percent of deaths.

The most recently published report (Oct 23, 2020) from the Centers For Disease Control as of the writing of this report reveals 216,000 reported COVID-19 related deaths (data provided on 114,411 of those deaths) in the U.S., with 78.2% of decedents age 65-years and older.

U.S. adults age 18-49 represented only 5.4% of COVID-19 related deaths. (Note: only 6% or just 12,960 of these 216,000 deaths are attributed to COVID-19 coronavirus infection alone; 94% involved co-morbid factors such as diabetes, hypertension, obesity and autoimmunity.)

An estimated 42% of COVID-19 related deaths occurred among nursing home patients.  If COVID-19 is man-made, it certainly performs a sinister social function.  It wipes out elderly nursing home patients and other frail older individuals who cost government the most money.

Dying of COVID-19 or weakened immunity?

People are not dying of COVID-19 per se.  They are succumbing to a weakened immune system which almost invariably accompanies aging.

T-cells, produced in the thymus gland, “are the ultimate agent of protection” in most viral diseases.  T-cells seem to be most severely affected by aging.

Immunosenescence is a decline in the immune system with advancing age characterized by decline in zinc dependent naïve T-cells that produce memory antibodies against infectious bacteria, viruses and fungi, as well as diminished B-cell and natural killer cell activity resulting in a pronounced inability to produce antibodies upon vaccination.

Only 17-53% of elderly adults can produce specific antibodies in response to vaccination, in contrast to 70-90% of young adults.  Outbreaks of infectious disease can occur in nursing homes even when vaccination rates reach 80-98%.

The public hears of antibodies that are produced by vaccines and by natural infection.  However, it is now reported that immunity facilitated by antibodies against COVID-19 may be fleeting.  Real long-lasting immunity is now known to come from T-cells produced in the thymus gland. The thymus requires zinc to make T-cells and selenium is needed to free zinc from its binding protein (metallothionein) so it can be utilized.

The human immune response is divided into first-responding white blood cells (innate immunity), largely neutrophils (white blood cells that seek and destroy pathogens) and macrophages, white blood cells that literally digest or engulf infectious microbes (adaptive immunity) characterized by late-arriving T (thymus gland) and B (bone marrow)-cells 7-10 days following initial infection.

While the number of T-cells remains relatively constant throughout life, a striking change occurs in the number of new naïve T-cells as a result of involution (shrinkage) of the thymus gland with advancing age.

T-Cells predominate

T-cells are subject to aging changes.  These aging changes include involution (atrophy or shrinkage) of the thymus gland in which they are converted from B to T cells and decreased production of naïve T-cells (T-cells that have not produced antibodies as yet).

A striking finding during this COVID-10 pandemic is that T-cells and not antibodies are the active viral killers in the human body.  In fact, “everyone who gets COVID-19, even people with mild or asymptomatic cases, develop zinc-dependent T-cells that can hunt down the coronavirus if they get exposed again years later.”

In healthy individuals T-cells, in particular so-called naïve T-cells that have not produced antibodies yet, are at the ready to attach to incoming pathogens.

The thymus gland, located underneath the breast bone, shrinks (atrophies) to the size of a pea in the latter years of life.  This is due to a shortage of zinc. Fewer T-cells are then made.  There is no corrective effort for this aging change by modern medicine, leaving older populations at increased risk for infectious disease.

A report published in Mechanisms of Ageing & Development states:

“It is incontrovertible that the human immune system… appears to be different in younger and older adults both in its architecture, composition and function.   We would predict that immunosenescence (senescence = to grow old) in older humans would include low amounts of naïve T and B cells and potentially over-active innate immune cells.  The expectation is that the whole-body number of naïve CD-8 T-cells is indeed low due to markedly reduced thymic output.  T- Cell mortality declines owing to a lifetime’s exposure to pathogens.  CD-8 T-cells are required for clearing virally-infected cells.”  But no mention is made of zinc.

There is no single food outside of oysters that can provide a sufficient amount of zinc.  Maybe 20% of dietary zinc is absorbed.  Typical dietary consumption of zinc is ~10 milligrams.

Be aware when selecting zinc supplements: zinc oxide is poorly absorbedAntacids reduce zinc absorption.

Be mindful, the symptoms of COVID-19 coronavirus infection match symptoms zinc deficiency.

Infectious link with premature aging

Most older people possess a greatly reduced pool of naïve T cells.  Failure to produce T-cells is associated with a herpes-class infection called cytomegalovirus (CMV).

Cytomegalovirus, a herpes-family virus, commonly infects 60-90% of older adults, with persistent CMV infection being associated with increased infections and health risks.  In emerging countries CMV infection it is almost 100%.  An estimated 4+ billion people are infected with CMV.  It is usually asymptomatic.

One of the hallmarks of immunosenescence is the loss of naïve T cells, especially CD8 cells.  Infection with cytomegalovirus has been proposed as the key pathogenic driver of this senescent CD8 cell subset.  CD8 T-cell senescence is an overall impairment of the adaptive immune response with reduction in the ability to fight novel infections and impairment in response to vaccination in the elderly.

Cytomegalovirus infection has been shown to enhance immunity in young adults but has a negative impact on older adults.  CMV infection is a driver of cardiovascular disease and diabetes.  That makes a vaccine against CMV of immense importance globally.  No CMV vaccine has been licensed as yet.  Cytomegalovirus should be re-named the Accelerated Aging Virus.

Therefore, senescence of the immune system may be largely associated with a CMV trigger.

It is not surprising to learn as many as 50% of CD8 T-cells and 30% of DC4 T-cells may be programmed to provide immunity against CMV.

More worrisome, CMV infection may act to worsen COVID-19 lung infections.  Circuitously, COVID-19 infection also may reactivate dormant cytomegalovirus.  Therefore, combined COVID-19/cytomegalovirus infection may be particularly harmful.  It is not uncommon for COVID-19 infected patients to appear much older after recovery.

Parkinson’s disease may be an exception

As published in the Journal of Neuroinflammation in 2018, for the first time it was discovered that samples of blood from peripheral tissues unexpectedly exhibit a lack of CD8 T-cell replicative senescence among patients with Parkinson’s disease.  The anticipated aging shift produced by CMV infection is not observed.

While CMV infection is generally regarded as having a negative impact on the health of senior adults, there is a faction within the ranks of geriatric immunologists who support the idea that CMV infection “stimulates a sustained immunological alertness that savors a better immune response.”  One wonders if this occurs in cases of Parkinson’s disease.

Natural remedies for COVID-19, aging and cytomegalovirus infection

Fortunately, mankind does not need to wait for a coronavirus or a cytomegalovirus vaccine.  Natural remedies are posed against COVID-19 coronavirus and cytomegalovirus.

Resveratrol and cytomegalovirus

Resveratrol is the most widely studied anti-aging molecule.

Resveratrol exhibits anti-coronavirus activity in the laboratory.

Resveratrol also blocks synthesis of cytomegalovirus proteins and decreases replication of the virus.  Resveratrol is in a class of natural molecules called polyphenols.  Quercetin, another polyphenol that also inhibits cytomegalovirus.

Vitamin D and cytomegalovirus

Furthermore, low vitamin D levels are a risk factor for cytomegalovirus infectionsCytomegalovirus infection inhibits the vitamin D systemLow vitamin D levels foster congenital (from birth) cytomegalovirus infections, which suggests early-in-life CMV infection may hasten aging and explain differences in the aging changes among genetically-similar individuals (twins).

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