Could nearly half the population not already infected with SARS-CoV-2 be immune to it from having already contracted other forms of coronavirus in recent years?

That is one implication of a major study conducted by over a dozen researchers from several microbiology and immunology institutions in the U.S.

The purveyors of panic are warning of a second wave of the virus and that even if we are correct in asserting that the general fatality rate is extremely low for most people, it will still result in millions of deaths worldwide if we need 70 percent of the population to get the virus in order to achieve herd immunity. Putting aside the fact that their strategy of lockdown doesn’t provide a solution to this hypothetical problem either, even as it kills more people from the collateral damage, there is now promising evidence that more people might already be immune to the virus.

The study is built upon the principle that T cells play a central role in destroying viruses and providing immunity. Not only were these cells discovered in all the blood samples of confirmed recovered COVID-19 patients, but they were also found in 6 of the 11 blood samples from 2015-2018, before those individual donors could possibly have contracted the virus.

Until now, the assumption was that only those with IgG or IgM antibodies can be immune because they are the ones who have already contracted the disease. However, this study examined the cellular defenses that are created in the body and have been proven to serve as a defense against SARS-CoV-2, then discovered them among 40%-60% of their samples not infected with SARS-CoV-2.

In order to prove the efficacy of these T cells developed in the recovered population, the researchers exposed immune cells from 10 recovered patients to the virus. They found those cells effectively fight the virus. 100% of the samples of 20 donors contained “helper” T cells, known as CD4+, and 70 percent contained killer T cells, known as CD8+, which directly kill the viral cells. Then they discovered “SARS-CoV-2−reactive CD4+ T cells in ∼40-60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS-CoV-2."

The hypothesis is that numerous common colds are forms of coronavirus and that a significant percentage of the population that has already contracted those forms of coronavirus have cross-immunity to COVID-19. It’s unclear to what degree these people are immune, but it might help explain why some people in certain areas react so violently to COVID-19, whereas so many others are asymptomatic. In other words, it's possible that people with cross-immunity could still catch the virus, but their reaction to it will either never present symptoms or present very mildly due to the pre-existing T cells working for them.

The authors note that more time and cell numbers are needed to study identification of the cross-reactive chains of cells.

A similar T cell study published April 22 by German immunologist Andreas Thiel found that 34% of 68 blood samples from people not infected with SARS-CoV-2 hosted helper T cells that nevertheless recognized the novel coronavirus.

The authors of the newer study posit that the concept of “crossreactive memory T cell responses might have been one factor contributing to the lesser severity of the H1N1 flu pandemic.” There is still no way of proving whether those T cells discovered in non-infected individuals are definitively effective in warding off the virus or blunting its symptoms, but the theory might explain some enigmatic behaviors of this virus.

On the one hand, this virus seems to be extremely contagious and transmissible. On the other hand, it appears to have been around for a while, possibly in December, and didn’t kill too many people until super-spreading events in March.

On the one hand, the virus seems to kill a lot of vulnerable people for several weeks. But then it peaks after six weeks or so and nearly disappears a month or so later. We’ve seen the same curve in every country, almost as if it hits a brick wall and then runs out of steam.

But why is that the case? Most antibody tests show no more than 10%-15% of the population contain antibodies in a given area – 25% in the most extreme case of New York City. Why would the virus not continue cutting through the population like butter, as it did the first number of people who contracted the virus? The theory of a more ubiquitous cross-immunity from other coronaviruses would answer those questions and explain that invisible brick wall.

A theory of partial immunity, at least from helper T cells (if not killer T cells) could also explain why, on the one hand, once the virus gets into prisons, most test positive for it, but on the other hand, nearly all of them seem asymptomatic. The outcome of prisons as a fully confined and defined population could be a harbinger of what would theoretically happen if the entire world were exposed to the virus after it had already targeted the most vulnerable population. It’s possible that upwards of 95% would be asymptomatic, just like we are seeing in prisons.

Perhaps, it could also explain why there appears to be a massive gap in severity of the virus in Asia vs. Western countries. Asian countries are regularly exposed to coronaviruses.

Professor Karol Sikora, founder of University of Buckingham Medical Schools, has a short video explaining in layman’s terms the significance of this T cell study and cross-immunity.

Sunetra Gupta, professor of theoretical epidemiology at the University of Oxford, is also a strong believer in the likelihood of cross-immunity. “We may also be able to fend off the virus with pre-existing responses against other coronaviruses, which I think is very likely to play a role in protection, specifically against severity of the disease,” said Professor Gupta in a recent interview with a British media outlet.

“In almost every context we’ve seen the epidemic grow, turn around and die away — almost like clockwork. Different countries have had different lockdown policies, and yet what we’ve observed is almost a uniform pattern of behavior which is highly consistent with the SIR model. To me that suggests that much of the driving force here was due to the build-up of immunity.”

Stanford professor of epidemiology John P.A. Ioannidis has also posited the existence of cross-immunity and the idea that many people’s bodies are using innate cellular immunity to ward off the virus.

This theory might also explain why Sweden believes it reached herd immunity with just 20 percent infected and why some studies suggest a similar ratio could be achieved elsewhere.

To be clear, these are all unproven theories at this point. But if our government and media were willing to run with unproven theories of doom and gloom even as the facts on the ground refuted them, shouldn’t they at least examine some good news when the fact pattern of the virus itself seems to harmonize with the theory?

Why are American politicians immune to good news as if it were the plague?

Most people are more likely to wind up six feet under because of almost anything else under the sun other than COVID-19.

The CDC just came out with a report that should be earth-shattering to the narrative of the political class, yet it will go into the thick pile of vital data and information about the virus that is not getting out to the public. For the first time, the CDC has attempted to offer a real estimate of the overall death rate for COVID-19, and under its most likely scenario, the number is 0.26%. Officials estimate a 0.4% fatality rate among those who are symptomatic and project a 35% rate of asymptomatic cases among those infected, which drops the overall infection fatality rate (IFR) to just 0.26% — almost exactly where Stanford researchers pegged it a month ago.

Until now, we have been ridiculed for thinking the death rate was that low, as opposed to the 3.4% estimate of the World Health Organization, which helped drive the panic and the lockdowns. Now the CDC is agreeing to the lower rate in plain ink.

Plus, ultimately we might find out that the IFR is even lower because numerous studies and hard counts of confined populations have shown a much higher percentage of asymptomatic cases. Simply adjusting for a 50% asymptomatic rate would drop their fatality rate to 0.2% – exactly the rate of fatality Dr. John Ionnidis of Stanford University projected.

More importantly, as I mentioned before, the overall death rate is meaningless because the numbers are so lopsided. Given that at least half of the deaths were in nursing homes, a back-of-the-envelope estimate would show that the infection fatality rate for non-nursing home residents would only be 0.1% or 1 in 1,000. And that includes people of all ages and all health statuses outside of nursing homes. Since nearly all of the deaths are those with comorbidities.

The CDC estimates the death rate from COVID-19 for those under 50 is 1 in 5,000 for those with symptoms, which would be 1 in 6,725 overall, but again, almost all those who die have specific comorbidities or underlying conditions. Those without them are more likely to die in a car accident. And schoolchildren, whose lives, mental health, and education we are destroying, are more likely to get struck by lightning.

To put this in perspective, one Twitter commentator juxtaposed the age-separated infection fatality rates in Spain to the average yearly probability of dying of anything for the same age groups, based on data from the Social Security Administration. He used Spain because we don’t have a detailed infection fatality rate estimate for each age group from any survey in the U.S. However, we know that Spain fared worse than almost every other country. This data is actually working with a top-line IFR of 1%, roughly four times what the CDC estimates for the U.S., so if anything, the corresponding numbers for the U.S. will be lower.

As you can see, even in Spain, the death rates from COVID-19 for younger people are very low and are well below the annual death rate for any age group in a given year. For children, despite their young age, they are 10-30 times more likely to die from other causes in any given year.

While obviously yearly death rates factor in myriad of causes of death and COVID-19 is just one virus, it still provides much-needed perspective to a public policy response that is completely divorced from the risk for all but the oldest and sickest people in the country.

Also, keep in mind, these numbers represent your chance of dying once you have already contracted the virus, aka the infection fatality rate. Once you couple the chance of contracting the virus in the first place together with the chance of dying from it, many younger people have a higher chance of dying from a lightning strike.

Four infectious disease doctors in Canada estimate that the individual rate of death from COVID-19 for people under 65 years of age is six per million people, or 0.0006 per cent – 1 in 166,666, which is “roughly equivalent to the risk of dying from a motor vehicle accident during the same time period.” These numbers are for Canada, which did have fewer deaths per capita than the U.S.; however, if you take New York City and its surrounding counties out of the equation, the two countries are pretty much the same. Also, remember, so much of the death is associated with the suicidal political decisions of certain states and countries to place COVID-19 patients in nursing homes. An astounding 62 percent of all COVID-19 deaths were in the six states confirmed to have done this, even though they only compose 18 percent of the national population.

We destroyed our entire country and suspended democracy all for a lie, and these people perpetrated the unscientific degree of panic. Will they ever admit the grave consequences of their error?