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Coronavirus Immunity: How Does Your Age Play a Factor?

COVID-19 shows how important it is to keep your immune system strong

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On April 3, the Washington Post reported some good news about COVID-19. A man named William “Bill” Lapschies celebrated his birthday — and his full recovery from the novel coronavirus. He took ill in early March and was one of the first confirmed cases in Oregon. On April 1, not a fools’ day joke in sight, his doctors declared him clear of the virus.

Bill Lapschies is — and will continue to be — 104 years old.

Meanwhile, also on April 1, news broke that Adam Schlesinger, songwriter for the rock group Fountains of Wayne, died of COVID-19 complications. He was 52 — exactly half Bill Lapschies’ age.

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Every large statistical group has outliers, but in a pandemic that overwhelmingly targets older people, these two stories beg some oft-begged questions: How did Bill survive? Why did Adam die? What factors make some of us more fit, immunity-wise, than others — regardless of age? What does it mean if, for example, your partner or child gets sick and you don't — or vice versa?

We know that our immune system function declines with age. Doctors call it immunosenescence. It's slow and insidious; think of a photo of yourself 10 years ago versus one taken this afternoon.

"You see changes in your face, skin and hair color,” says Insoo Kang, M.D., associate professor of medicine and director of allergy, immunology and internal medicine at the Yale School of Medicine. “It takes time. Same process with your immune system."

Kang has been studying human aging for 20 years. “Immune cells, especially CD8+ T cells [a type of white blood cell], change with aging. We see fewer naive CD8+ T cells, which are needed to recognize newly emerging microorganisms like the COVID-19 virus. It happens to everyone on some level, just not at the same rate."

The difference in rate of decline between individuals is one of science's big mysteries. The immune system is complex, but most of us understand the basics: Our body detects an intruder — a virus, bacterium, parasite or foreign object — and produces white blood cells to combat the problem. How many of these cells you produce when you're, say, 73 versus when you were 45 is the million-dollar question — and it's at the heart of the COVID-19 pandemic as well: How does a 104-year-old man survive when people half his age, or younger, do not?

Fortunately, we won't always be in a pandemic. But we can use this one to gain an understanding of how our immune system changes with age — and how it might be possible to slow the decline and raise our immune reserves for the next time we get sick.

Terms to Know

  • Immunosenescence: Natural tendency toward diminished immunity as we age
  • Inflammaging: Natural tendency toward more inflammation as we age
  • T cells: White blood cells that attack viruses
  • B cells: White blood cells that make antibodies to fight infection
  • Memory cells: T cells that “remember” past viruses and give us immunity to them
  • Naive cells: T cells that “teach” themselves to fight new viruses, such as COVID-19
  • Cytokines: Small protein molecules released by a variety of cells in the body that help regulate immune response and inflammation. When the immune system is dysregulated, the body can overproduce cytokines, causing inflammation and disease.
  • Myokines: Immune-boosting, anti-inflammatory compounds released by muscle that bolster the immune system

Aging Effect No. 1: Fewer immune cells

Our body simply doesn't produce as many immune cells as we get older, says Atul Butte, M.D., distinguished professor of epidemiology, biostatistics and pediatrics at the University of California, San Francisco. “And no one really knows why."

Butte worked with a research team on an extensive review of 242 immunity studies that revealed patterns in how our immune systems change as we get older. Certain key immune cells — B cells and T cells, which are the virus fighters — become fewer in number with age. For example, we possess two different types of T cells: “memory” cells that have encountered a certain pathogen and “remember” how to fight it, and “naive” cells that have yet to fight anything. “We've seen especially that the number of naive T cells seem to be lower as we age,” Butte says.

So let's say COVID-19 shows up. Nothing we've seen before as humans matches this one, so we have no memory T cells to mobilize. The naive cells have to take on the fight, and older folks have fewer of those to fight with. That makes us more vulnerable.

Or rather, that makes most of us more vulnerable. The mystery of immunity decline is complicated by the fact that not everyone's immune system declines in the same way. For example, another factor Butte observed in his study review: Some healthy older people had little or no decline in T cells. Some had as many as younger people, and women seemed to have higher amounts in general as they aged.

Part of the reason B and T cells are so enigmatic is that no one really knows just what a healthy amount of B and T cells is. Says Butte: “If you want to have a test for your hemoglobin, they know what a normal range is. If you want your iron levels tested, they know what the normal range is. We have no idea what the normal level is for these cells. We don't even measure them in a regular blood test."

The reasons these key cells decline over time could be manifold: Our bone marrow produces white blood cells. Is that where the problem lies? Is it genetic? Lifestyle? An apple a day? All of the above? All immunologists can do is keep looking. “We know genetics plays a part,” Butte says. “But it's debatable how big of a part compared with environment and lifestyle."

Aging Effect No. 2: Rising inflammation

The term immunosenescence has a partner term that's relatively new: “inflammaging.” It refers to chronic low-grade inflammation that develops with advanced age.

Inflammation — when the immune system causes a part of your body to become reddened, swollen, hot and sometimes painful — is how the body fights disease, fixes injuries and rids you of inappropriate germs or invaders. It's meant to be short term. But chronic inflammaging tends to occur with age for a variety of reasons: Weight gain, poor diet, lousy sleep and chronic stress are among the big lifestyle causes. But other systemic issues can also contribute, such as persistent viral infections, decreased liver or kidney function, increased gut permeability (leaky gut) and autoimmune diseases.

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All of this degrades the immune system; when our bodies are in a state of chronic, low-grade inflammation, our immune system is constantly firing and operating abnormally. That accelerates the aging process on a cellular level. It can lead to heart disease, type 2 diabetes, Alzheimer's disease and more.

"Most systems in our body are tightly regulated,” says Sean Xiao Leng, M.D., professor of medicine, molecular microbiology and immunology at the Johns Hopkins University School of Medicine and Bloomberg School of Public Health. “The immune system is no exception, which is why this dysregulation is so dangerous."

If it gets bad enough (a twofold to fourfold increase in blood levels of inflammatory cytokines, according to one 2019 study), a person can officially become a “chronic low-level inflammatory phenotype.” You don't want to be that person.

The insidious nature of chronic inflammation is its relationship to so many organs and processes in the body. For example, unregulated stress (inflammatory) can motivate you to stress-eat highly processed sugary/fatty/salty foods (inflammatory), and they can also pack a calorie punch for weight gain (inflammatory), promote a poor bacterial balance in your gut microbiome (inflammatory), and over time push you into metabolic syndrome or type 2 diabetes (inflammatory).

What's more, chronic inflammation is silent and produces no symptoms. Your immune system may be compromised and you don't even know it.

How to save your immune system

You can't do anything about your genetic makeup, but, luckily, many factors that positively affect your immune system are within your control. Take them seriously, Leng urges. While you may not be able to stop immunosenescence, any slowdown you can produce means a higher immune reserve at any given time. That's critical when it comes to infections.

"If you talk about vulnerability in older adults, it's definitely two important parts,” he says. “One is incidence — whether you get the infection or not. But the other part is severity. Even if you don't have the incidence outcome you want, having a stronger immune function may determine how badly you'll be infected.” In other words, every bit of the following helps.


Regular workouts boost immune function and lower inflammation. A 2019 study in Nature Reviews: Immunology noted that skeletal muscle is a “major immune regulatory organ” that generates anti-inflammatory and immunoprotective proteins called myokines. A 2018 study found that higher-intensity workouts may blunt immunosenescence in older adults. “Exercise strengthens the body and may be the most important lifestyle intervention you can add,” Kang says.

Weight management

Obesity is deadly when it comes to inflammation. Belly fat is metabolically active tissue; it releases inflammatory cytokines into your body, which then trigger more weight gain — and more inflammation. Kang states it simply: “Getting to a healthy weight could be a major factor in decreasing inflammation levels."


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Butte suggests that people gain a better understanding of where their health is right now. For example, those with asthma may want to start measuring their peak airflow to know what their normal lung function is. “The more we can use digital devices and tools, the more we'll understand,” he says. “If something changes, you're not just going to the doctor and saying, ‘I'm having trouble breathing.’ You can say, ‘My airflow has dropped 8 percent.’ “ Staying on top of whatever chronic conditions you have will allow you to spot declines quickly, so you and your doctor can decide on a better course of therapy.


Eating right should be common sense, but research reveals specific nutritional effects on immune function in older adults. A 2018 study reviewed in the journal Nutrients showed that basic nutrients like vitamins A, C, D, E and the B vitamins, along with folic acid, iron, selenium and zinc, are essential for “immunocompetence,” with deficiencies causing lower T cell production and an inability to resolve inflammation.

Strive for balance, Kang says: “Eat not just vegetables but also good proteins and fiber.” The latter is important because it feeds the good bacteria in your gut and can help lower inflammation. “We have a lot of immune cells in the gut that help regulate health. Dietary fiber may have more than the single effect of making the bowel move."


Research has shown that unregulated stress can accelerate immunosenescence. It comes down to a chronic immune response to whatever's stressing you, with the resulting rise in inflammation. Self-care in this area becomes critical — from anti-stress activities (meditation, mindfulness, exercise) to asking for help in unresolved stressful situations (work, money, caregiving). People don't talk enough about the effect of stress on immunity because it's not as tangible as other factors such as hours of exercise or how many packs per day you smoke, Leng notes.


Age takes its toll on vaccine effectiveness as well as immunity. Vaccines are designed to provoke the production of antigens — the influenza vaccine is made of influenza cells — but our aging immune reserve doesn't respond as robustly as it did in our earlier years. None of that should make you lazy about vaccines. “It's true they become less effective as people get older. But even if you do get infected, the disease will be less severe. People should get whatever vaccines their doctors recommend based on age and underlying medical conditions,” Kang says.


Certain prescription medications may inhibit your immune system. For example, oral and inhaled corticosteroids (common for arthritis, allergies, asthma and inflammatory bowel disease) may raise your risk of fungal infections. The same is true for TNF inhibitors that treat autoimmune conditions like rheumatoid arthritis and psoriasis. “Even antibiotics could kill gut bacteria and trigger some kinds of infection,” Kang says. If you're on any ongoing medications, talk to your doctor about possible immune system side effects and how to address them.

COVID-19 lessons

Aside from a deeply ingrained knowledge of handwashing and just how far away 6 feet is, the COVID-19 pandemic will, in the end, teach us more about our health vulnerabilities — individually and as an aging population.

Butte believes it will usher in a new era in immunity research. “We're going to learn a lot in a hurry. We have the genomics of this virus and can get the genomic sequence down in hours. We can see how it's changing from this point in Seattle to that point in San Francisco.”

Leng foresees a large push into learning more about aging and immunity by studying the older adult population and unlocking the unknown mechanisms in the immune response. He's already part of a massive National Institutes of Health initiative into geriatric science involving hundreds of researchers.

"The traditional medical model focuses on individual disease,” he says. “With something like COVID-19, you're chasing one thing. But we'll try to see if we can find an underlying mechanism in immunity, something upstream in the process. Then we can do a wider search rather than chase after individual diseases. If we can do that, the older population will handle all immune challenges better.”

Mike Zimmerman is the author of The 14-Day Anti-Inflammation Diet

Your Preexisting Condition Guide

Certain health conditions can cause people to be immunocompromised, meaning their immune systems are less able to fight off a viral infection. Much of this can be traced to age-related immunosenescence and inflammation, but some illnesses bring their own complications. If you have been diagnosed with any of these conditions, take every precaution to protect yourself, and talk with your doctor about adjusting your treatments, if necessary.


What makes you vulnerable: Adipose tissue (fat) is now recognized as an active endocrine and immune organ that can directly inhibit metabolic immune function, according to emerging research. A 2018 study of influenza patients over three flu seasons found that obese adults took 42 percent longer to fight off the virus than did nonobese people.


What makes you vulnerable: High blood sugar (hyperglycemia) is an inflammatory condition that tends to inhibit the immune response and raise your risk of infection. People with uncontrolled high blood sugar are particularly vulnerable.


What makes you vulnerable: Both cancer and its treatments can reduce white blood cell counts and make patients more open to infection, while also making it harder to fight any infection they do get. If you're a cancer patient or survivor, the American Cancer Society recommends discussing your situation with a doctor who is familiar with your medical history.

Heart disease

What makes you vulnerable: Age, hypertension and underlying cardiac issues all raise your infection risk, according to the American Heart Association. Based on early reports, as many as 40 percent of COVID-19 patients who required hospitalization had existing cardiovascular disease, the American College of Cardiology reports.

Asthma, COPD and other respiratory diseases

What makes you vulnerable: Viruses love to attack the lungs, so people with existing lung conditions are at risk of more severe symptoms when they get sick. COPD patients are particularly vulnerable to lung infections, which can further damage already compromised air sacs.

Autoimmune diseases

What makes you vulnerable: Not only can an infection trigger a flare-up of autoimmune diseases such as rheumatoid arthritis, multiple sclerosis or psoriasis, the treatment of those conditions often involves immunosuppressive drugs that can raise your infection risk. Also, autoimmune conditions can cause interstitial lung disease, a dangerous condition that can cause lung scarring.

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