Clinicians and scientists are still scrambling to understand SARS-CoV-2, the virus that causes COVID-19, as it sweeps the globe. When China first reported mysterious cases of severe pneumonia, it became clear that the world had a new respiratory illness on its hands. In response, governments, doctors, and public health experts urged people to stay home or take precautions only if they were experiencing fever, cough, or shortness of breath.
However, as more people became infected, this small cluster of symptoms expanded. Soon, people were testing positive for the novel coronavirus without respiratory symptoms. Instead, some experienced gastrointestinal distress, suffered strokes, or lost their sense of taste and smell. Many months into the pandemic, the experts have identified more than a dozen signs and symptoms that could indicate COVID-19.
A key factor that researchers agree is probably behind SARS-CoV-2’s multi-pronged attack on the body is its affinity for the ACE2 receptor, a protein found on the surface of cells throughout the body. SARS-CoV-2 targets cells with these receptors then attaches, replicates, and kills the cell. And because ACE2 receptors are on myriad cell types throughout the body, the virus has a doorway to damaging a variety of organs and tissues, including the lungs, kidneys, gut, brain, heart, and blood vessels.
While SARS-CoV-2’s ability to cause such a constellation of symptoms is unusual, it is not unprecedented, says Rachel Roper, an associate professor in the department of microbiology and immunology at East Carolina University Brody School of Medicine. While influenza viruses tend to stay in the respiratory system, she says, coronaviruses often do not.
“[With SARS-CoV-2], people are getting different diseases from the same virus,” she explains. “Diagnostically, it has been hard to understand. We’ve had patients come in with symptoms, and they didn’t realize until later that it was COVID-19. But this also happened with SARS1.”
An additional hypothesis that has gained traction is the “cytokine storm” explanation, which implies that a hyperactive immune response is causing as much destruction as the virus in some patients. This theory has led some researchers and clinicians to try therapies intended to suppress inflammation and temper the immune response.
Roper agrees that the so-called cytokine storm may play a role in some severe illness, especially where extreme lung damage results and patients can no longer get sufficient oxygen into their bloodstreams or to other organs.
However, she says, the virus itself is the likeliest culprit for most people.
“Generally, the early symptoms are directly from the virus, then some people have an overreaction of the immune response and that creates more problems,” she explains.
While the cytokine storm explanation is still being examined, some experts worry that indiscriminate use of the consequent immune suppressing approach could hinder the body’s ability to clear SARS-CoV-2 and increase patients’ vulnerability to secondary infections.
There is still much to learn, and many symptoms are not yet fully understood. The fact that SARS-CoV-2 infects and affects so many cells throughout the body, Roper says, does increase the complexity of studying it.
Fortunately, however, unprecedented collaboration means that the scientists working to develop therapeutics and vaccines have mass amounts of prior knowledge and diverse expertise upon which to build.
