Complex condition
A key barrier to developing long-COVID treatments has been uncertainty about the condition’s root cause. Over the past two years, a number of hypotheses have emerged as frontrunners, and researchers hope that insight into which ones are correct could help them to develop therapies. Evidence is mounting that lingering SARS-CoV-2 — or fragments of it —
continues to cause trouble by stimulating the immune system. There are also signs that the infection
generates antibodies that mistakenly attack the body’s own proteins, causing damage long after the initial illness. Researchers have found hints that
COVID-19 could cause microscopic blood clots that block oxygen flow to tissues. It is also possible that a SARS-CoV-2 infection can wreak long-term havoc on gut microorganisms.
These hypotheses are not mutually exclusive: many researchers think that long COVID can have multiple causes. Each idea suggests a route to relief. Antiviral drugs
might vanquish persistent reservoirs of SARS-CoV-2. Drugs that suppress the immune system could quench a misguided immune response. Powerful anti-coagulants could dissolve micro-clots.
Although evidence is gradually accumulating in support of each of these possibilities, their links to long COVID are still tenuous enough to give some investigators pause before launching clinical trials. “The hypotheses are getting a bit stronger,” says Altmann. “But they’re not cast iron.”