Here’s one reason young people may not get so sick – Times-Herald
Previous infection with less harmful cousins of the COVID-19 virus could reduce the severity of the disease, according to new research from Stanford University.
People who carry immune cells created after exposure to common seasonal coronaviruses may be less sick with infection with the more dangerous COVID-19 virus, called SARS CoV-2, reports Mark Davis, director of the Institute for the Stanford immunity, transplantation and infection.
“A lot of people have pre-existing immunity,” Davis said. “And that can mean the difference between never noticing you’re infected – or dying from an infection.”
The new findings, published in The Thursday issue of the journal Science Immunology, could explain why young people are less vulnerable to COVID-19.
That’s because several milder coronavirus species are rampant in daycares and schools, causing routine respiratory tract infections. About 80% of children in the United States are exposed to these viruses in the first few years of life.
But as we age, our immunological memory of this experience weakens. And when we can’t recognize the viral invader, we fail to launch a quick and accurate defense.
Since the start of the pandemic, scientists have wondered about the broad spectrum of the COVID-19 disease.
“A lot of people get very sick or die from COVID-19, while others are walking around not knowing they have it. Why? ”Davis mused, professor of microbiology and immunology.
He wondered: are people exposed before the coronavirus pandemic less susceptible?
His team focused on immune cells, called killer T cells. Unlike antibody tests, T cell tests are laborious and expensive, so they have been more difficult to study.
T cells do not prevent infection. Rather, their job is to patrol the body for infected cells and then kill them, reducing the severity of the disease.
They also generate ‘memory T cells’, which can persist for a long time, ready to kick in if needed.
In this project, the Stanford team first took a close look at the genetic structure of different viruses. The extents of the SARS CoV-2 virus and other coronaviruses are almost identical, they saw.
Then they studied the patients’ blood to see how their T cells targeted the virus.
Patients with milder symptoms had lots of T cells that targeted the part of the SARS-CoV-2 virus that is common to all strains of coronavirus. This indicated that they had already encountered one of the related coronavirus strains – and that those cells had proliferated.
“T cells have recognized parts of the viral genomes that are similar between coronaviruses,” Davis said.
Additionally, many of their killer T cells were in “memory” mode, they noted.
Because they have already encountered a milder cousin, these cells are better equipped to mobilize quickly against SARS-CoV-2, the team concluded.
“They might respond more quickly to the infection,” Davis said. This response “can be the difference between never noticing you have an illness and dying from it.”
“Memory cells are an essential thing in immunology because they allow you to avoid infection if it recurs,” he said.
In contrast, the T cells of the sickest patients targeted the part of the virus that is unique to SARS-CoV-2. Without any memory of previous exposure, the immune system of these patients did not recognize the virus.
“If you have to start from scratch, it takes more time and more difficulty to get ahead of the virus,” he said.
This is the second recent finding to suggest a benefit from a previous coronavirus infection.
In April, a team from the University of Pennsylvania reported in the journal Science that people with high concentrations of antibodies that had been triggered by infection with beta-coronaviruses – a category that includes SARS-CoV-2 – recovered faster from COVID-19.
The Stanford discovery suggests that future vaccines could be designed to boost T cell immunity, not just antibody production, according to the report.
It is not yet known how long our immune system will retain a memory of the COVID-19 virus.
This has implications for how long our vaccines will remain effective. Protection against tetanus, for example, lasts only 10 years. But a yellow fever vaccine is good for life.
“The whole area of immune memory durability,” Davis said, “it’s not something that we really have a very good understanding of.”