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Immune T Cells May Offer Lasting Protection Against COVID-19

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Healthy human T Cell
Caption: Scanning electron micrograph of a human T lymphocyte (T cell) from a healthy donor’s immune system. Credit: National Institute of Allergy and Infectious Diseases/NIH

Much of the study on the immune response to SARS-CoV-2, the novel coronavirus that causes COVID-19, has focused on the production of antibodies. But, in fact, immune cells known as memory T cells also play an important role in the ability of our immune systems to protect us against many viral infections, including—it now appears—COVID-19.

An intriguing new study of these memory T cells suggests they might protect some people newly infected with SARS-CoV-2 by remembering past encounters with other human coronaviruses. This might potentially explain why some people seem to fend off the virus and may be less susceptible to becoming severely ill with COVID-19.

The findings, reported in the journal Nature, come from the lab of Antonio Bertoletti at the Duke-NUS Medical School in Singapore [1]. Bertoletti is an expert in viral infections, particularly hepatitis B. But, like so many researchers around the world, his team has shifted their focus recently to help fight the COVID-19 pandemic.

Bertoletti’s team recognized that many factors could help to explain how a single virus can cause respiratory, circulatory, and other symptoms that vary widely in their nature and severity—as we’ve witnessed in this pandemic. One of those potential factors is prior immunity to other, closely related viruses.

SARS-CoV-2 belongs to a large family of coronaviruses, six of which were previously known to infect humans. Four of them are responsible for the common cold. The other two are more dangerous: SARS-CoV-1, the virus responsible for the outbreak of Severe Acute Respiratory Syndrome (SARS), which ended in 2004; and MERS-CoV, the virus that causes Middle East Respiratory Syndrome (MERS), first identified in Saudi Arabia in 2012.

All six previously known coronaviruses spark production of both antibodies and memory T cells. In addition, studies of immunity to SARS-CoV-1 have shown that T cells stick around for many years longer than acquired antibodies. So, Bertoletti’s team set out to gain a better understanding of T cell immunity against the novel coronavirus.

The researchers gathered blood samples from 36 people who’d recently recovered from mild to severe COVID-19. They focused their attention on T cells (including CD4 helper and CD8 cytotoxic, both of which can function as memory T cells). They identified T cells that respond to the SARS-CoV-2 nucleocapsid, which is a structural protein inside the virus. They also detected T cell responses to two non-structural proteins that SARS-CoV-2 needs to make additional copies of its genome and spread. The team found that all those recently recovered from COVID-19 produced T cells that recognize multiple parts of SARS-CoV-2.

Next, they looked at blood samples from 23 people who’d survived SARS. Their studies showed that those individuals still had lasting memory T cells today, 17 years after the outbreak. Those memory T cells, acquired in response to SARS-CoV-1, also recognized parts of SARS-CoV-2.

Finally, Bertoletti’s team looked for such T cells in blood samples from 37 healthy individuals with no history of either COVID-19 or SARS. To their surprise, more than half had T cells that recognize one or more of the SARS-CoV-2 proteins under study here. It’s still not clear if this acquired immunity stems from previous infection with coronaviruses that cause the common cold or perhaps from exposure to other as-yet unknown coronaviruses.

What’s clear from this study is our past experiences with coronavirus infections may have something important to tell us about COVID-19. Bertoletti’s team and others are pursuing this intriguing lead to see where it will lead—not only in explaining our varied responses to the virus, but also in designing new treatments and optimized vaccines.

Reference:

[1] SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls. Le Bert N, Tan AT, Kunasegaran K, et al. Nature. 2020 July 15. [published online ahead of print]

Links:

Coronavirus (COVID-19) (NIH)

Overview of the Immune System (National Institute of Allergy and Infectious Diseases/NIAID)

Bertoletti Lab (Duke-NUS Medical School, Singapore)

43 Comments

  • bggu says:

    This is a matter of primary concern right now. Here is encouraging data. The public is eagerly awaiting covid 19 vaccine. Many thanks for the article from you.

  • Kate W. says:

    If a person had Covid 19 and recovered due to her memory T cells, would she also produce detectable antibodies?

  • Anil K Chauhan says:

    The viral RNA by binding to immunoglobulins will form immune complexes (ICs). These ICs by engaging CD16a and CD32a will differentiate the naive CD4+ T cells to become effector T cells that secrete proinflammatory cytokines. During contraction phase, this will lead to the development of long lasting memory cells. Originally, it was reported that Th2 responses were involved in COVID-19 pathology, but recent reports have implicated Th1 and Th17. We have shown in several papers in JBC, the role of ICs in the development of Th1, Tj17 and Tfh cells. However, upon vaccination, the populations reported in NEZM are very low and does not look convincing due to lack of availability of gating data. Immunology community has been nicely fooled by a single group that claims that CD4 T cells do not express FcRs. Several groups in HIV-1 patients have now shown the expression of CD32a and explored this receptor as possible marker for viral latency.

  • bestf says:

    I hope this informative article will help me prepare for covid-19.

  • nguyên h. says:

    Thanks for this very helpful topic. I love it and will learn more about it. Thank you very much.

  • Neamhach says:

    Do I understand from this article that perhaps 50% of population (more tests/stats needed for better “confidence level”?) MAY already have immunity of be immune to the Covid-19?

    • John Hasty BS, MT(ASCP) Retired says:

      That’s why natural active viral infections are important in immunity. Would you believe IT if I told you that the live oral Poliomyelitis vaccine that I received as a child has given me T memory cells that still help protect me from Polio today. Would you believe IT if I told you that it has been proven that an active viral infection will help protect you from other entirely different viruses. You go first and tell me all of the ACTIVE natural viral infection you have had in your life. Now, I will tell you all the ACTIVE natural viral infection that I have had in my life of 75 years: Polio (live vaccine), influenza, Chicken Pox, Small Pox (live vaccine 2 or 3 times), measles, mumps and probably rubella we called them childhood diseases. There were probably a couple more I received before service in Vietnam. 75 strong healthy and active and confident in my immune system.

      • John Hasty says:

        In addition to being an active 75 year old I also participate in the Million Veteran Research Program where a pre Covid-19 blood specimen is on file. This program is conducted by the Veterans Administration. Also, I am enrolled in the All of Us Research Program where a pre Covid-19 DNA saliva specimen is on file. This program is one of the largest sponsored by the NIH.

        • John Hasty says:

          In the midst of this current pandemic I would like to participate (volunteer) in any clinical trials that uses the live-attenuated COVID-19 virus created by deoptimizing the codon pairs of the virus.

          I am afraid I will be overlooked for one reason or another. I believe this specific technology may also be receiving some support from NIH. Thanks

  • iplaytx says:

    Thank you John Hasty’s very good comment. No lessons have passed through practical experience lessons

  • Daria says:

    Your information is useful and necessary, Please continue this wonderful work. Thanks so much for sharing,

    • John Hasty BS, MT(ASCP) Retired says:

      In the midst of this current pandemic I would like to participate (volunteer) in any clinical trials that uses the live-attenuated COVID-19 virus created by deoptimizing the codon bias of the virus.

      I am afraid I will be overlooked for one reason or another. I believe this specific technology may also be receiving some support from NIH. Thanks

  • Lawrence A says:

    If we add t-cell immunity (greater than 50% ) to antibody immunity (around 20%) we have over 60% immunity in the general population which qualifies as population immunity (herd immunity). This is why we have not seen exponential growth of the disease anywhere in the world and why we will not see a second wave…

  • h. nguyen says:

    Thanks for the information.

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