Scientists have found out why the risk of contracting COVID-19 again is extremely low

Antibodies have become a familiar concept in the pandemic era, suggesting that they are the best way to tame the deadly coronavirus. But when major data on COVID-19 vaccines was released recently, an unsung immune player took center stage: T cells. Talks about this Bloomberg.

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AstraZeneca Plc, Pfizer Inc. and BioNTech SE, as well as China's CanSino Biologics Inc. welcomed the presence of these cells in vaccine recipients as a sign that their experimental trials are working.

T cells, or T lymphocytes, are a reminder that the body's defenses rely on more than one weapon, and that much of the immune response to COVID-19 still remains a mystery—especially after researchers discovered that the much-vaunted Antibodies lack endurance.

“Antibodies are only a small part of the picture,” said Paul Griffin, an associate professor of medicine at the University of Queensland in Brisbane, who is leading clinical trials in Australia on two potential COVID-19 vaccines. “But we really haven’t reached the goal of fully understanding people’s immunity to the new coronavirus.”

At first, scientists focused on antibodies (proteins that adhere to and block foreign organisms), because their detection is the basis for most successful vaccines. Immune proteins are also easier to measure than T cells and can be used to assess past infection.

Research showing that antibodies are rapidly decreasing in patients with mild disease has dashed hopes that antibodies would provide some lasting form of immunity.

On the subject: 'Fragile and short-lived': experts doubt the reliability of immunity to coronavirus

Unsung Warriors

T cells, on the contrary, are able to kill virus-infected cells, “remember” past illnesses for decades, and awaken new antibodies to fight viruses long after the first antibodies have already left the “battlefield.” For example, people infected with the same coronavirus that caused the SARS epidemic in 2003 still have a T-cell response to the disease - 17 years later.

This suggests that T cells, at least hypothetically, may be ready to protect SARS survivors nearly two decades later - both from the same infection and to enhance their protection from COVID-19, Griffin noted.

“They may have a slightly milder form or a shorter duration of illness, but I certainly don’t think that’s going to be completely protective,” he said.

One study found that some patients without COVID-19 symptoms had T cells that recognized the virus—even when they had no detectable antibodies. Another indicated a certain level of immunity in people who had never been exposed to the current strain of coronavirus: perhaps due to exposure to one or more long-known coronaviruses that cause the common cold.

Required balance

More research is needed to determine if the T-cell response to the virus can explain why some COVID-19 patients experience little to no symptoms, while others get very sick and even die. It is clear that a balance of both antibodies and T cells is required for optimal protection, Griffin says.

Corey Smith, head of immunology at the QIMR Berghofer Medical Research Institute in Brisbane, says the findings about the short lifespan of antibodies do not mean that immunity completely disappears, precisely because of the presence of T cells.

So-called helper T cells and memory T and B cells are able to induce the primary production of antibodies to respond to an infection before it causes severe symptoms, said Smith, who is studying the immune response to the SARS-CoV-2 virus.

The current virus, like other common cold-causing coronaviruses, can evade antibodies, Smith said, leading to reinfection.

“But cellular immunity is enough to suppress any serious symptoms,” the expert says.

On the subject: 'Safe and causes an immune response': already the second vaccine has been shown to be effective against COVID-19

Perhaps it is T cells that ultimately suppress and dull the pandemic virus that killed more than 600 people in less than seven months.

“If we can't eradicate it, will it become something like a circulating virus, another cold virus? - says Smith. “I’m not sure, but it’s interesting.”

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