Beyond antibodies, the immune response to coronavirus is complicated

Red/Blue/Green fluorescent image of cells.

Enlarge / T-cells attacking
a cell recognized as foreign. (credit: NIH)

Ultimately, the only way for societies to return to some
semblance of normal in the wake of the current pandemic is to reach
a state called herd immunity. This is where a large-enough
percentage of the population has acquired immunity to
SARS-CoV-2—either through infection or a vaccine—that most
people exposed to the virus are already immune to it. This will
mean that the infection rate will slow and eventually fizzle out,
protecting society as a whole.

Given that this is our ultimate goal, we need to understand how
the immune system responds to this virus. Most of what we know is
based on a combination of what we know about other coronavirus that
infect humans and the antibody response to SARS-CoV-2. But now,
data is coming in on the response of T-cells, and it indicates that
their response is more complex: longer-lasting, broadly based, and
including an overlap with the response to prior coronavirus
infections. What this means for the prospect of long-lasting
protection remains unclear.

What we know now

SARS-CoV-2 is one of seven coronaviruses known to infect humans.
Some of these, like SARS and MERS, have only made the jump to
humans recently. While more lethal than SARS-CoV-2, we are
fortunate that they spread among humans less efficiently. These
viruses seem to provoke a long-lasting immune response following
infections. That’s a sharp contrast to the four coronaviruses that
circulate widely with humans, causing cold-like symptoms. These
viruses induce an immunity that seems to last less than a year.

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Beyond antibodies, the immune response to coronavirus is