God has a way of prepping the human body for potentially deadly viruses to somewhat mitigate the amount of death we'd otherwise suffer every year from all sorts of microbiological threats. COVID-19 is not different.
The latest research on T cells, white blood cells produced by the immune system to ward off infections through memory of past pathogens, show that even those patients who never develop antibodies or have lost them over time will retain T cell immunity that remembers to fight off coronaviruses in the future. Moreover, the study provides new evidence for the theory that herd immunity could be achieved at an approximately 20% infection rate for most cities, thanks to T cell cross-immunity from other coronaviruses.
The latest version of panic porn being propagated by the media is that many people don't produce antibodies and that even more of those infected will lose them over time, potentially opening them up to reinfection.
Why we automatically assume the worst of this virus and base our response on the idea of this virus defying all known patterns remains a mystery, but this study from Singapore should place the onus on naysayers to show why this form of coronavirus would be different from others.
Researchers in Singapore conducted a study, first out in preprint in May and now peer-reviewed and published at Nature, of 23 patients who recovered from SARS in 2003 and found that all 23 retained memory T cells induced by that original pathogen still in their systems. That in itself is terrific news to find this immunity after 17 years. Then they studied 36 convalescent SARS-CoV-2 patients and found that they had also produced similar T cells. While SARS-CoV-2 is a new virus and distinct from SARS-CoV-1, there is strong reason to believe that T cell memory produced by the body to protect from future relapses of this virus would not be weaker or more short-lived than T cell memory from SARS-1.
If the implications of this research turn out to be true, it would mean that all those infected with SARS-Cov-2 will retain at least partial immunity to the virus. This doesn't necessarily mean they will be fully immune. This would likely mean, for many previously infected patients, that they could theoretically test positive again with a PCR test, but the T cells would ward off the symptoms and reduce their infective capabilities to transmit to others.
But there's more good news, not just for those who have already gotten the virus but for many who may get it. Very few people in America have been exposed to SARS and would therefore not have that immunity. However, researchers have long suspected that there is cross-immunity from other coronaviruses – four of which are forms of the common cold that could account for anywhere between 15% and 30% of colds on a given year. The cross-immunity theory has been proven across other pathogens and was established during the H1N1 outbreak in 2009 when many people appeared to be immune, presumably, to similar prior outbreaks of seasonal H1N1 flues.
Cross-immunity with other coronaviruses was at least partially confirmed when the researchers in the Singapore study found the samples of T cells from convalescent SARS-1 patients to have cross-reactive potential against SARS-CoV-2 during lab simulations. To test this out further on more common forms of coronavirus – OC43, HKU1, NL63, and 229E – they took samples from 37 random blood donors who had no history of SARS, COVID-19, or contact with SARS/COVID-19 patients. They found that 19 of the 37 had T cells that were reactive to SARS-CoV-2, even though they had no known exposure to this virus.
How can that be? A large portion of the population likely has at least partial cross-immunity through T cell memory cells induced by contracting one of those four common cold coronaviruses. This would explain why so many places seem to experience a burnout of the virus after it reaches only 15%-20% prevalence, according to serology tests. Yes, only 15%-20% have antibodies, but many more likely have cross-immunity through T cells, as Nobel laureate Michael Levitt, Oxford epidemiologist Sunetra Gupta, and Stanford Professor John Ioannidis predicted.
This harmonizes with a previous study from the La Joya Institute of Immunology in California that showed such cross-reactive responses in 40%-60% of random blood donors
This might also explain why so many people are found to be asymptomatic and possibly many more have had the virus asymptomatically but never tested positive for antibodies. Studies have found as many as 40% of asymptomatic patients lose antibodies after the early convalescent period. Thus, just because you find an antibody serology test implying only 5%-15% of the population has antibodies doesn't mean that an even greater portion has not already been exposed to the virus but only produced T cells to ward it off, and a certain greater percentage never even became infected with the virus because they had full immunity. A study of 200 blood donors in Sweden found twice as many samples with T cells as samples with antibodies.
Also, the same reason why someone initially got the virus asymptomatically, likely because of T cell memory produced by cross-immunity, is the same reason they will continue to be free of symptoms in the future, even if they don't possesses antibodies.
The number of people who have this cross-immunity is likely different throughout the world. One recent preprint study analyzing T cell immunity in blood donors in Germany detected "Cross-reactive SARS-CoV-2 T-cell epitopes revealed preexisting T-cell responses in 81% of unexposed individuals." Accordingly, many people might stop making the antibodies after a few months or years, especially following a mild infection, but their immune system produces the cells that remember the recipe for defeating the virus if it returns.
While we are still learning more about this virus and the human immune system response to it every day, these findings should make us optimistic in the long run, unless the media has made us immune to any good news.