Our biological systems need a few days to engender an immune response as described above. And once an infection is defeated, that response remains vigilant for a period of time before beginning to fade. Just how long we are protected from being reinfected is still not a certainty.
A recent BBC article cites a Public Health England study that shows an active immune response remains with us for at least five months. In some cases, previously infected COVID-19 patients got reinfected within a year. A King’s College London study indicated a drop in antibody levels only three months after infection. But it also noted that B-cells retained a longer-term memory and could begin manufacturing antibodies if a second infection occurs.
As a side note of interest, the article mentions that B-cells for the Spanish Flu could still be detected in people 90 years after that early 20th-century pandemic. Also, the article described how T-cells against SARS, the coronavirus pandemic that struck in 2003, were still detectable in people 17 years after being infected. It further stated that T-cells that target the common cold (another coronavirus) could be helpful in fighting COVID-19.
Reinfections do occur. The likely explanation is the new infection is not from the same virus, but from a variant. An example of note, a recent Hong Kong patient had experienced reinfection four months after first contracting COVID-19. DNA analysis showed the second infection was a variant. That’s why the body’s immune system didn’t respond immediately.
Unlike our natural immune response, a vaccine is designed to give our body systems targeted instructions to fight one or more virus strains (vaccines that can handle two or more variants are referred to as multivalent).
The current COVID-19 vaccines, whether mRNA or adenovirus, are specifically looking for a spike protein found on the virus’s outer coat. That triggers what B-cells normally do, the production of antibodies which then tag all infected cells and viruses. A multivalent booster vaccine is less specific because it can look for a range of viral characteristics to target.
The current vaccines also contain ingredients designed to induce more potent immune responses. These are called adjuvants, which consist of ingredients developed in past vaccines that are known kickstarters for our immune system. Both the Pfizer and Moderna mRNA vaccines include nanoparticles that target the immune response. So do adenovirus vaccines like AstraZeneca and Johnson&Johnson.
What are the ingredients in adjuvants? They don’t roll trippingly off the tongue and include molecules of alum (a combination of aluminum and potassium) and toll-like receptor (TLR) agonists that go by such names as AS03 (an oil-in-water emulsion composed of squalene, polysorbate 80 and vitamin E), MF59 (a derivative of shark liver oil), and CpG 1018 (a modified phosphorothioate found in Hepatitis B vaccines).
The adjuvants act like an irritant to promote B, T, and CD8 cell production shortly after entering the body. I am convinced based on my personal level of “irritation” after getting my second dose of the Pfizer vaccine that the adjuvants knocked me for a loop for more than half a day. And now that I know what they are all about, I suspect that’s why my joints ached, I developed a headache, bone-weary tiredness, and hot flashes, all of it happening less than 24-hours after getting the shot. But the outcome was fine because the next day I felt great.
Vaccine studies show stronger immune cell responses than ones looking at natural infection responses. That’s why vaccines are so important in tackling a pandemic. That’s also why 320 different COVID-19 vaccines are under development or already being produced, distributed, and administered. With them, the chances are much better for those who are vaccinated to develop immune responses that last well beyond two years.
A final note, if the SARS 2003 coronavirus pandemic response is any indicator, when that virus vanished before a vaccine could be delivered, with or without one, our body’s T-cells should demonstrate long-term memories of COVID-19. With, however, our body’s memory will be that much stronger.
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The compound is called (+)-SJ733. It is a molecule that kick starts the immune system to eliminate malaria-infected cells. A single dose administered in a mouse study killed 80% of infected cells in 24 hours aind in 48 hours test mice were disease free. Next step is safety trials in healthy adults to ensure no untoward side effects.
How does it work? The molecule-based compound inhibits the ATP4 protein in the malaria parasite. ATP4 is critical to maintaining the sodium levels in plasmodium, the parasite responsible for the disease. By inhibiting ATP4 a malaria-infected red blood cell begins to shrink in size and eventually becomes rigid, a normal characteristic of an aging red blood cell. And it is that aging which induces the immune system to do what it does normally, clean up and get rid of old blood cells. The infographic below clearly illustrates the impact of the compound on malaria-infected blood cells.
Today 3.4 billion, almost half the world’s population is at risk of malaria. And malaria is moving poleward as climate change affects the breeding range of the mosquitoes that carry the plasmodium parasite. In 2012 the world saw 207 million malaria cases and an estimated 627,000 deaths. The most vulnerable today are those living in the Developing World and in particular in Sub-Saharan Africa.
Our Biological Limits
In the latter part of the 18th century the average human lived 24 years. By the end of the 19th the average lifespan had doubled. In the second decade of the 21st century we are approaching a doubling again. Is there a biological limit?
We are the sum of our genetics. How long your parents lived may indicate how long you will live. But then again it may not. We know that altering genes can alter the lifespan of animals and plants we study in laboratories. We have doubled the lifespan of mice by splicing genetic material into their chromosomes.
In an earlier blog we described the structure of DNA, genes, base pairs and chromosomes. It may be helpful to click on the link provided as a quick refresher before reading further.
We have two DNA repositories in every cell in our body (blood cells not included). That DNA is found in the nucleus and mitochondria within the cell. The DNA organizes itself as chromosomes. When cells replicate the chromosomes divide and copy themselves. This is called mitosis.
Telomeres are repeating DNA base pair sequences that sit at the end of each chromosome. They act as buffers to ensure that DNA replication during mitosis remains accurate. A ribonucleic protein enzyme, telomerase, maintains the telomeres. As cells divide some telomere information does not replicate, usually between 25 and 200 base pairs. The average telomere can be as long as 15,000 base pairs so what is lost is not significant until the cells divide many times. The accumulation of lost base pairs starts adding up.
Why do we lose telomeres? This may be a reflection of our natural aging process, the unwinding of our biological clock so to speak. Or telomeres may shorten because of external forces such as exposure to toxins, disease or injury. Ultimately when chromosomes no longer have a telomere buffer cells they no longer can divide and we call this cellular state senescence. The Hayflick limit, named after the scientist (see the image below) who, in 1961, first discovered this phenomenon, is the natural limit of a cell’s life after multiple replication.
Do all cells have a Hayflick limit? Apparently not as scientists have observed in studying cancer. Tumor cells do not suffer from DNA strand shortening. They can infinitely replicate because in cancer cells telomerase remains active restoring telomere length. Other cells that don’t exhibit the shortening of telomeres include sperm and egg cells. Hormones may impact telomerase activity and telomere lengths. It is believed that estrogen plays a role and may explain why women live on average longer than men.
If we were to alter the behaviour of our normal cells by stimulating telomerase could we reverse the aging process, ending senescence? This is possible. Use of telomerase in laboratory settings has shown that it can confer “immortality” on several types of human cells. That same capability makes telomerase one of the key factors in cancerous tumor cell growth and is leading to research into telomerase inhibitors that would transform cancer cells by starving them of the protein and putting them into senescence.
Telomeres alone do not extend life. If they were the sole means by which we could stop aging we have the technology to produce on mass altered cells containing high levels of telomerase and bank these for use to cure incalculable diseases. Right now scientists believe that stopping telomere shortening may add 10 to 30 years to the average life span. That would mean a child born today could expect to easily achieve an average lifespan of a century.
Other Factors to Consider that Impact Aging
If you are over 60, which I am, your risk dying doubles every 8 years. Research shows that shortening of telomeres only accounts for 4% of the difference. Chronological age and gender account for an additional 33%. The remaining 63% can be attributed to:
Oxidation sounds like a strange contributor to aging. After all, we need oxygen to breathe and a byproduct of this basic life function is oxidants. Oxidants result from oxygen combining with sugar to produce energy and byproducts called free radicals. Not all free radicals are internally produced. They can also come from infections, inflammation, alcohol, smoking, excessive sun exposure, radiation from x-rays and environmental toxins. Free radicals can have a negative impact on individual cells, proteins and fatty tissue. Free radicals over time can build up in the body and are associated with aging. In a recent study the lifespan of worms was increased by 44% by neutralizing oxidants.
Glycation involves excess glucose binding with our DNA, proteins and fats. Excess glucose begins to interfere with normal body tissue functions. The older we get the more the glucose creates health problems contributing to aging let alone body mass. Research shows that restricting calorie intake and selecting foods low in sugar leads to reduced age-related disease and extended lifespans in mice to monkeys.
Inflammation is the body’s natural response against infections and injuries. It also contributes to tissue injury and ultimately to aging. Chronic or persistent inflammation without significant infection is evidence of an immune system that no longer recognizes host body tissue as its own. As we age autoimmune conditions including chronic inflammation become more prevalent. Chronic inflammation destroys normal cells and contributes to the aging of the cardiovascular and nervous system. Inflammation contributes to age-related neurodegenerative diseases, such as Alzheimer’s and Parkinson’s.
Stress harms DNA and speeds the aging process. A study in 2004 showed that psychological stress shortens telomeres in immune cells. Evidence shows that stress, the endocrine system response and the occurrence of disease define age more than chronological aging. Certain diseases occur when anabolic hormone levels start to decline and catabolic hormones start to increase. The latter, such as Cortisol, can contribute to the breakdown of body tissue. As proof of just how much stress contributes to aging and premature death, interviewers who spoke with centenarians found that they exhibited healthy coping strategies in dealing with illness describing their behaviours as accepting, non worrying and taking life one day at a time.
Immune Response refers to the specialized cells generated by our bodies to fight off disease. Researchers in Israel at the Technion studied the natural decline in the immune system as we age. This inability to fight off diseases when we are older is one of the reasons for the statistics about the risks to humans when they reach 60 and over. By suppressing B-lymphocyte immune cells in aging mice and using a drug commonly used to treat rheumatoid arthritis, the mice were able to manufacture healthy replacements using bone marrow. Clinical trials have begun in human populations suffering from B-cell lymphoma.
What are the prospects for human immortality?
The SENS Foundation is dedicated to re-engineering our bodies to end aging through rejuvenation biotechnology. These biotechnologies cover major research areas including cell loss, tissue atrophy, nuclear and mitochondrial mutations, immunotherapy, and targeted ablation. The goals are:
If we eliminate all of these physical processes inherent in aging and develop appropriate delivery systems for restoration and repair some scientists project that we can live 1,000 years. Will someone born in the 21st century be the first millenarian?
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