Dr. Jack Kruse

The current state of what we know about C-19 on 8/11/20

Added 2020-08-11 14:16:15 +0000 UTC

Present knowledge: London, UK, hospital staff COVID19 antibody #seroprevalence is very high, with 34.7% for those with direct patient contact, and 22.6% for those with no patient contact. London’s general population is at 17.5%.

This is how Herd Immunity is achieved...

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/1F3C3898F2D770164E356D8EA3418D6B/S0899823X2000402Xa.pdf/seroprevalence_of_sarscov2_antibodies_in_healthcare_workers_at_a_london_nhs_trust.pdf

The higher percentages are likely due to density with high-touch high viral load, which is expected in hospitals. This is similar to what was seen in Mumbai’s slums, Australian cruises and prisons across the globe.

There is growing evidence that T-cell immunity allows populations to reach herd immunity once only 10-20% are infected with SARS-CoV-2.

This would explain why a highly transmissible virus in densely populated areas peaked at 10-20% infected regardless of lockdowns or masks.

The pervasive misconception is that we have zero immunity against COVID-19. Based on this flawed understanding, epidemiologists projected that herd immunity is not reached until 60-70% are infected.

This is almost certainly wrong.

Of course, the media ignores this research. While antibodies against COVID-19 may only last months, T cell immunity can remain protective for years.

CONSIDER THE LINK OF THE SUN TO T-CELL FUNCTIONING:

Role of vitamin D in immunity during C19 is critical to get right. Going outside in the sun is more wise than taking a Vitamin D pill.

A. Vitamin D is a major precursor for activation of T-cell (for any disease)

B. Vitamin D controls cytokines storm in COVID that causes blood clot & vascular damage of the organs like kidneys, heart, brain, and ultimately death.

STUDIES:

1. Review @SpringerOpen provides detailed insight on the role of Vitamin D in building immunity by modulating monocytes, dendritic cells, T and B cells. https://link.springer.com/chapter/10.1007/5584_2018_246

2. Scientists @uni_copenhagen have discovered that Vitamin D is crucial to activating our immune defenses & w/out sufficient intake of the vitamin, T cells will not be able to react to and fight off serious infections in the body. LINK: https://www.sciencedaily.com/releases/2010/03/100307215534.htm

3. In this ancillary study of a randomized controlled trial, authors found that short term HIGH-dose vitamin D3 significantly reduced CD4 T-cell activation compared to low-dose vitamin D3, providing human evidence that vitamin D can influence cell-mediated immunity. LINK: https://academic.oup.com/jcem/article/101/2/533/2810779

In a study of 23 people who survived SARS in 2003, every single one had memory T cells that recognized the SARS virus 17 years later. (Nature) https://www.nature.com/articles/s41586-020-2550-z

BACK TO THE PRESENT

Moreover, blood samples from all 23 individuals showed “robust cross-reactivity” against SARS-CoV-2.

This can be called crossover immunity.

Crossover immunity is not limited to just people who were infected with SARS years ago though. In the same study, in 37 persons with no history of SARS or COVID-19 (negative serology and/or samples taken before COVID-19), over 50% had SARS-CoV-2 specific T cells.

This is not surprising because there are at least 4 strains of coronaviruses that cause the "common cold". The above study is not the only one to show this level of cross-reactivity.

In a study from April 2020, in 68 healthy donors never exposed to COVID-19, 34% had T cells that reacted to SARS-CoV-2. https://www.medrxiv.org/content/10.1101/2020.04.17.20061440v1

This finding was confirmed in yet another study published in Cell in June 2020 showing that 40-60% of unexposed individuals had T cell recognition of SARS-CoV-2.

The authors hypothesized that crossover immunity came from “common cold” coronaviruses. https://www.sciencedirect.com/science/article/pii/S0092867420306103?via%3Dihub

Crossover immunity may explain why so many young and middle-aged individuals are asymptomatic even when testing positive for coronavirus. This is why a positive test should not be alarmist with this RNA virus.

It is likely that their T cells recognized the virus and mounted an immune response before even mild symptoms surfaced. What does this mean? This is how natural herd immunity without a vaccine occurs in Nature. This is not a narrative that is being pushed in the media or medical circles right now. You need to understand why.

All those runny noses from the common cold prepared our T cells to fight COVID-19.

Although it has been ominously called the “novel-coronavirus”, SARS-CoV-2 is yet another coronavirus with many similarities in structure to the common cold coronaviruses. Why are the elderly hit so hard by COVID-19 though?

Indeed the strain of coronavirus that we faced in 2020 is more lethal than those in the past, specifically in the elderly and immunocompromised...With an understanding of T cell immunity, it makes sense that the elderly are more affected by COVID-19.

It is well known that persons in advanced age and/or who are immunocompromised lose T cells. https://medicalxpress.com/news/2020-06-cell-immunity-elderly.html

Let’s get back to herd immunity via T cells.

If ~50% of people had T cell immunity prior to SARS-CoV-2, then that leaves 50% of the population susceptible.

In the regions hit hardest by COVID-19, serology studies show new cases and deaths peaked at around 10-20% infected. Adding the 50% who already had T cell immunity from common cold viruses to the newly infected 10-20% equals about 60-70% immunity.

Not coincidentally, 60-70% is the percentage epidemiologists project is necessary for herd immunity with a respiratory virus. It is likely that many of the hardest hit regions of the world (e.g. Lombardy, NYC, Madrid, London, Stockholm) are now at herd immunity.

Lockdowns & mask ordinances (mostly coming after the peak) likely had little effect, with the exception of perhaps prolonging the spread. Sweden is an example of what herd immunity looks like without lockdowns or masks.

Based on serology testing, ~20% of Stockholm was infected by April.

Deaths peaked in Sweden in April.

Today, the pandemic is over in Sweden with zero deaths per day and subsiding new infections. Lockdown advocates will challenge this thesis and point to Indian slums and areas in Peru that reached much higher infection prevalence.

However, malnourishment is rampant in these very poor regions…And it is well known that T cell function is reduced in the malnourished. This research on T cell immunity is largely being ignored by the mainstream media, possibly due to political and pharmaceutical interests.

Hint: Assuming $35 per vaccine dose (Moderna’s price), vaccinating just the USA alone will result in a revenue of ~$10 billion annually. Considering that the coronavirus vaccine industry has the potential to be the biggest profit maker big pharma has ever seen, it is not surprising that we are seeing an overly aggressive push for lockdowns and masks until there is a vaccine—no matter the cost to the public or governments.

A recent paper out in Cell needs to be highlighted.

COVID-19, hijacks proteins in host cells that serve as master regulators of key cellular processes. These regulators are called kinases. Sunlight has a massive effect on kinases involved with C-19 and this is why the class of viruses are considered seasonal RNA viruses. By doing so, the virus is able to rewire the cell’s internal circuitry to promote its own spread and survival when the solar redox is poor to activate the kinase pathways in the body. But the reliance of the virus on host-cell proteins may also prove to be its Achilles’ heel, as these same proteins can be easily targeted with existing drugs that are cheap and off patent. These are drugs that Big Pharma does not want anyone to know about because they want everyone believing the narrative the vaccine is the ONLY acceptable way out of this pandemic.

THIS IS FALSE

In a study published June 28, 2020, in Cell, the researchers found that when SARS-CoV-2 infects cells, it assumes control over a family of enzymes known as kinases. Under normal circumstances, kinases serve as master regulators of metabolism, growth, movement, repair and other important cellular functions. Kinases work by attaching tiny chemical tags to proteins through a process known as phosphorylation. This is how sunlight sculpts matter in your cells to alter your immunity and keep you safe. Once attached, these tags act as switches that turn proteins on or off, which keeps the complex machinery of the cell running smoothly.

When a cell is commandeered by SARS-CoV-2, however, these same kinases behave in ways that disrupt normal cell function and transform the host cell into a virus factory. Cell division comes to a halt, inflammation pathways are activated, and the cell even begins to produce tentacle-like structures known as filopodia, which protrude from the cell’s surface and may serve as molecular highways that help the virus spread rapidly to neighboring cells.

This dependence of SARS-CoV-2 on kinases was revealed in experiments in which the researchers counted and catalogued all the proteins found in both infected and uninfected cells. Though they observed no significant differences in the total amount of protein found in each group, the scientists noticed huge disparities in phosphorylation levels – a clear sign that SARS-CoV-2 was changing kinase behavior in infected cells.

This work is being coordinated at UCSF in California. It is being done at UCSF’s Quantitative Biosciences Institute (QBI). Soon after COVID-19 emerged as a threat to global health, QBI Director Nevan Krogan, PhD, assembled a crew comprised of dozens of UCSF scientists representing a broad range of scientific disciplines in an effort to address the pandemic from as many perspectives as possible. The QBI Coronavirus Research Group (QCRG), as the cross-disciplinary team is now known, includes a number of scientists with expertise in kinases, as well as the drugs that can be used to disable them. These drugs work against cancers. You might be shocked to learn that hydroxychloroquine is one of these drugs. You might begin to understand why the media and Big Pharma want to limit its use. The media number one advertiser is Big Pharma.

For example, Dr Fauci's NIH branch has placed a blockade in effect on Chlorquine in this cancer paper. Ask yourself why he would do this? Check the status on this article....EMBARGO....to be released at a later date...once you find a copy and read it....you understand why it's been delayed....crooks against any good science that will limit the patent power for a new vaccine that Dr. Fauci and his Gates cabal will benefit from for sure. It is a good paper to review for a Black Swan. Chloroquine (CQ) a drug closely related to hydroxychloroquine (HCQ) interfers with phosphorylation of extracellular signal-regulated kinases (ERK)1/2 and the ERK-activating kinases mitogen-activating protein/ERK kinase (MEK)1/2. This decreases TNF which controls all the inflammatory pathways in the body that control mitochondrial autophagy.

At pharmacological concentrations, CQ and HCQ have significant effects on tissue homeostasis, targeting diverse signaling pathways in mammalian cells. A key target pathway is autophagy, which regulates macromolecule turnover in the cell. It also recycles defective mitochondrial from direct C19 attack. In addition to affecting cellular metabolism and bioenergetic flow equilibrium as I laid out in my July 2020 lecture here on Patreon, autophagy plays a pivotal role at the interface between inflammation and cancer progression. Chloroquines consequently have critical effects in tissue metabolic activity and importantly, in key functions of the immune system. This is the major reason why these antibotic drugs work in viral diseases. Dr. Fauci knew this information in 2005 as seen above. Do you still trust the CV task force leader?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7011648/

SUMMARY

Innate cellular immunity involves nonspecific cells like Natural Killer T cells. They are activated anytime we get exposed to a viral pathogen, known to us or not. They are like a sniper that is told to kill anyone that looks like they don’t belong, as in virally infected cells. They are not specific to any virus or family of viruses.

Adaptive cellular immunity mainly involves the TNF pathways that deal with CD4 and CD8 T cells. These are produced anytime you have a particular virus. They are like a Mafia hit man who is contracted to kill someone and everyone related to that person, so a Coronavirus or any of its cousins. More specific than the NK T cells but nonspecific enough to take out infected cells of a family of viruses if the individual has good cellular immune function. They also provide longer lasting immunity than antibodies for most respiratory viruses.

The humoral immune response involves the production of antibodies (Immunoglobulins IgM, IgG) by B cells that are activated by the cellular immune response if the threat is bad enough. Think about these antibodies like an assassin with an individual target, like Jason Bourne getting a photo of his target and going after that specific person. Antibodies are like a lock and key in their response, very specific to that particular virus and even that particular strain of virus. They do not often offer cross reactive defense to other mutations or related viruses in the family.
THIS is why I have been focused on helping myself, my family, and my friends improve the innate and adaptive cellular immune response, antibodies are fine but less predictable and don’t always last for this type of virus. Also the T Cell immunity offers defense against the future viral threats that we may face, I suspect there will be more.

That is a basic immune system lesson to use when you get confused! And remember Sunlight properly shapes life and health, how’s it shaping yours? Artificial light improperly shapes your immune system and sets your up for mitochondrial damage making a C19 infection more likely. Is that what you want now?