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Wheezing after sitting on a treadmill. Swallowing air while doing housework. Shortness of breath is one of the many frightening and frustrating symptoms that can linger in COVID patients months after the initial infection. But while these symptoms were a mystery at the start of the pandemic, scientists are slowly discovering what causes them — bringing us closer to finding a cure.
In a paper recently published in European Respiratory JournalNow, researchers at the University of Manchester in the UK have identified a possible culprit – immune cells known as monocytes. These squishy, blue-gray cells float in the bloodstream, looking for signs of disorder. When they encounter an invading pathogen, such as a bacteria or virus, they generate other important immune cells and alert the immune system to activate additional defenses. Monocytes are particularly important during lung injury. At the first sign of trouble, they travel to the lungs, producing many specialized macrophages—immune cells that eat pathogens—which become the first line of immune defense against invading germs.
But it appears that Covid infection can really mess with how these immune cells function – meaning they “can respond abnormally to subsequent events”, says Lawrence Bermin, clinical lecturer at the University of Manchester and co-author of the paper. In Covid patients with persistent shortness of breath after infection, the researchers found that monocytes were dysregulated. Compared to healthy subjects, these patients had monocytes with different levels of associated proteins that are essential for directing the cells toward the lungs. Scientists say these findings link the abnormal monocytes to the long-running Covid virus and lung infection – paving the way for potential treatments to correct abnormalities or relieve symptoms.
Pearmain and the team had good reason to suspect these cells. Other researchers have already found that SARS-CoV-2 affects monocytes. According to Judy Lieberman, a biologist at Harvard Medical School, in severe cases of COVID-19, monocytes infected with the virus often die in a way that releases too many alarm molecules into the body, leading to large amounts of additional inflammation. “It’s like a feed-forward loop,” she says. “Once this starts, it’s very difficult to control.” These results indicated the potential role of dysfunctional monocytes in prolonged COVID, as inflammation is known to contribute to some of the persistent symptoms.
Pearmain and the team decide to investigate. To find out exactly what these cells were doing during Covid and long Covid, scientists resorted to taking blood samples. Starting in the summer of 2020, across several hospitals in the UK, Pearmain and the team took blood from 71 patients during their hospital stays for Covid. Over the next few months, they also collected blood from 142 separate patients who had previously been hospitalized for Covid, and collected samples during follow-up visits.
The patients followed had contracted Covid about six months ago, and by that point after infection, Bermin says, any disruption to the immune system caused by the virus is expected to have stabilized. However, this was not what the team was seeing. “It was clear that a lot of people were still really short of breath, tired, and a lot of other prolonged Covid symptoms,” he says. Specifically, 48 percent of patients followed reported shortness of breath, and 44 percent reported fatigue. The team has found a long Covid population to study – so it’s time to take a closer look at their immune cells.