It's been three years into the pandemic, and the medical community has yet to fully solve the mystery of long COVID. But this week, an expert shared what could be responsible for this mind-boggling phenomenon.

According to Brent Palmer, Ph.D., an associate professor of allergy and clinical immunology at the University of Colorado School of Medicine, viral reservoirs that linger in the body could be causing the immune system to remain overactive for long periods, leading to persistent symptoms.

“We think it’s an overexaggerated immune response that’s causing the problem. What we hypothesize is that there’s residual virus somewhere in the body, but it’s not detected by a nasal swab. It has been shown that individuals who died of severe acute COVID had virus all over their body. When they do autopsies on these individuals, they can find virus in the brain, the kidney, the lung, and the gut,” Palmer explained in a news release.

Last June, David R. Walt and his colleagues at Harvard Medical School also proposed a similar idea after detecting SARS-CoV-2 proteins in the blood of 65% of long COVID patients up to 12 months after their acute infection.

“The half-life of spike protein in the body is pretty short, so its presence indicates that there must be some kind of active viral reservoir,” Walt explained at the time, noting that spike protein was not detected in the blood of COVID-19 patients without long-term symptoms.

For Palmer, vaccines and antiviral medication such as Paxlovid can help relieve symptoms of long COVID. The two help the immune system yield a better antibody response against the virus, reducing the chances of developing long-term symptoms.

“There have been studies in individuals with long COVID that have shown that vaccination causes a modest decrease in symptoms. If you vaccinate them, you bump up their immune response even more, maybe you get a better antibody response, you root out these viral reservoirs, and that leads to reduced symptoms. Other studies have shown that giving patients Paxlovid can suppress viral replication, and once the viral application is suppressed, the virus-specific immune response will drop off," he said.