Scanning electron micrograph of a human T lymphocyte (T cell) from a healthy donor’s immune system.
Winter break had arrived in Stockholm in late February, and Soo Aleman watched as her fellow Swedes departed the capital city for ski vacations across Europe. Aleman’s colleagues at the Karolinska University Hospital, where she works as a researcher and physician, returned relaxed and invigorated, with stories to tell about their days on the slopes. But a few of the city’s residents also brought back a most unwelcome souvenir: the SARS-CoV-2 coronavirus.
Like much of the rest of the world, Sweden soon found itself in the grips of an outbreak. As Aleman pivoted from her work on the hepatitis B and C viruses to study COVID-19, she began screening patients for the novel infection and for signs of the body’s immune response. And that’s when things got weird.
The body should produce both protective antibodies, which keep the virus from invading, and killer T cells, which tell virus-infected human cells to destroy themselves to keep the virus from spreading. Normally, these immune responses appear in tandem. But in a subset of those who tested positive for COVID-19, Aleman found T...