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Previous Exposure to the Common Cold May Protect Some People from COVID-19

woman on couch in mask with cold

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Key Takeaways

  • Memory T cells have been identified in some individuals who have not been exposed to SARS-CoV-2.
  • T cells may recognize SARS-CoV-2 because of its molecular resemblance to other coronaviruses, like the common cold.
  • Past exposure to other, more harmless coronaviruses may provide people with trained immunity against COVID-19.

Memory cells from the common cold may provide some people with the immune response necessary to fight COVID-19, even if they've never been exposed to it. 

A recent research article published in Science shows that 20 to 50% of people with no exposure to SARS-CoV-2, a type of coronavirus that causes COVID-19, had T cells that reacted to the virus. These T cells, previously developed in response to coronaviruses that cause the common cold, seem to be able to recognize SARS-CoV-2.

According to the researchers, this preexisting T cell memory could be the reason some people exhibit only mild symptoms of COVID-19, or even no symptoms at all. And according to patients actually living with the disease, this makes sense.

Cinzia Carlo, a 50-year-old California resident, has been struggling with symptoms ranging from shortness of breath and nerve pain to cardiac and circulatory issues since she was diagnosed with COVID-19 in March. She believes one of the reasons she has such severe manifestations of COVID-19 is because she had no immunity from other coronaviruses in her system. 

"I haven’t had a cold or flu in 14 years. Nothing. Zero," Carlo tells Verywell. "If there’s a correlation between the common cold and this virus's immune response, that could explain why I got so sick. I had no immunity to this, and people that get sick more might have had more immunity.”

T Cells and Immunity

When a new virus enters your body, your immune system initially responds with its innate, natural defenses. Sometimes this is enough to stop an invader. Other times, your body needs to call on a second line of defense. This is an adaptive immune response—a response coordinated by different types of white blood cells. T cells are one of the types.

T cells directly destroy pathogens and aid in the creation of antibodies. After effectively fighting a virus, T cells retreat into your organs and remain there in the form of memory cells, leaving behind a blueprint for other cells to use in case that same virus—or a very similar virus—strikes again.

Antibody Tests Show Colds Can Be Protective

The Science study researchers aren't the only ones exploring the link between colds and COVID-19 immunity. Cary Gunn, PhD, founder and CEO of the COVID-19 antibody test company Genalyte, wanted to see how the more endemic coronaviruses—the ones that commonly circulate and cause colds—leave their mark in the body compared to SARS-CoV-2. He found it depends on the person.

“Our immune systems are as varied as the way we look,” Gunn tells Verywell. “Everyone’s going to respond to every pathogen differently.” 

With the Genalyte antibody test, Gunn and his team were able to measure the cross-reactivity of eight different viruses to detect whether the antibodies in someone’s system were from SARS-CoV-2 or other coronaviruses.

Cross-reactivity refers to an antibody's ability to react not only to the antigen—in this case, a virus—it's intended for, but also a structurally similar antigen.

“We took 300 patients who had been diagnosed with SARS-CoV-2 and looked at what their signature antibodies looked like, and then we went back to our lab and examined the blood of 1,000 patients whose blood we drew pre-COVID-19,” he says. “We then used a machine learning algorithm to identify if someone’s antibodies are from a recent SARS-CoV-2 infection or if their antibodies are from a prior benign coronavirus.”

Genalyte is able to detect both Immunoglobulin M (IgM) and Immunoglobulin G (IgG) antibodies—indicators of which stage of infection you’re currently in. IgM antibodies are produced early on in an infection. IgG antibodies take longer to produce, and remain on guard once the infection has passed.

Gunn and his team discovered that the immune response created in many of his SARS-CoV-2 patients skipped the innate immunity phase of IgM antibody production, and instead directly jumped into an adaptive immune response of IgG antibodies. 

“What we found is that a surprising number of people don’t develop IgM antibodies; they develop IgG antibodies, which looks like a secondary immune response,” Gunn says. “The first time you get exposed to a virus, your body makes IgM antibodies, then the second time you get exposed, your body just goes straight to the IgG in your memory B and T cells. We are seeing a lot of IgG antibodies as the primary immune response [to SARS-CoV-2], which supports the theory that infection from a prior coronavirus is involved here.” 

The Importance of Antibody Testing 

Gunn predicts SARS-CoV-2 will become an endemic virus—something that will circulate in the population alongside the seasonal flu and the common cold. Widespread use of antibody testing could be essential to virus-mapping in the future. But it could also help immediately.

"I think a broad, nationwide program that measures antibodies is going to help us identify when the vast majority of us have good protection so we can go back to school and work without fear," he says.

Makeda Robinson, MD, PhD, an infectious disease specialist at Stanford University, agrees—as long as antibody tests are accurate.

"Early on, the sensitivity and specificity of antibody tests were really hit or miss, so many cases were missed or misdiagnosed," she tells Verywell. "As they become more accurate, they will be able to help us understand more about our progress toward herd immunity by getting a better sense of the rate of viral infection and immunity within our population."

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  1. Mateus J, Grifoni A, Tarke A, et al. Selective and cross-reactive SARS-CoV-2 T cell epitopes in unexposed humans. Science. 2020. doi:10.1126/science.abd3871

  2. Cano RLE, Lopera HDE. Introduction to T and B lymphocytes. In: Anaya JM, Shoenfeld Y, Rojas-Villarraga A, et al., editors. Autoimmunity: From Bench to Bedside [Internet]. Bogota (Colombia): El Rosario University Press; 2013 Jul 18. Chapter 5.