Scientists might be closer to understanding one of the most common symptoms of even mild covid-19: the loss of smell and taste. A new study suggests that infection by the novel coronavirus can damage important cells that support the nerve cells responsible for relaying scent to the brain.
The partial or full loss of smell, also known as anosmia, is occasionally caused by many respiratory infections, including covid-19. There’s even some evidence that anosmia is a more accurate predictor of having covid-19 than other well-known symptoms, like fever or dry cough.
One mystery that has endured, though, is exactly how covid-19 leads to anosmia. This new study, published in Science Advances over the weekend, is one of the first attempts to figure that out.
The researchers looked at the cells that line our nasal cavity, including those in the upper region of the nose that houses the olfactory nerve. The olfactory nerve is the bundle of nerve fibers that are the first to receive information about odors from the outside world, via receptors that react to the various chemical compounds we know as scents. These fibers then send that information to the brain, where it’s processed into our perception of smell.
In the area of tissue where the olfactory nerve is located, the researchers found that cells expressed two proteins key to the coronavirus, ACE2 and TMPRSS2. The virus hijacks the receptors for these proteins as a way to enter and infect new cells. But other experiments showed that, surprisingly, it wasn’t the nerve cells that were expressing ACE2; it was their supporting cast. Specifically, it was two types of non-nerve cells: the sustentacular cells, which physically support and provide energy to the olfactory nerve, and basal cells, the stem cells that replace damaged cells in that area.
“Our findings indicate that the novel coronavirus changes the sense of smell in patients not by directly infecting neurons but by affecting the function of supporting cells,” said senior study author Sandeep Robert Datta, a neurobiologist at Harvard Medical School, in a statement released by the university.
That’s something of a surprise, since other viruses that cause anosmia, including other coronaviruses, tend to directly infect olfactory nerve cells. Ideally, that could also be good news for covid-19 survivors, since indirect damage to our sniffing process should be less likely to result in a long-term loss of smell, the authors said. It also supports other evidence suggesting that the brain is rarely attacked directly by the coronavirus. But it’s still too early to rule out that our olfactory nerve can’t be permanently harmed by covid-19 (one of several theories by the authors is that damage to these supporting cells is still enough to kill off olfactory nerve cells). And there have been reports of people being unable to smell long after their initial infection has subsided.
Even if only some people who get covid-19 suffer anosmia for the long haul, that still leaves a lot of survivors potentially at risk of a truly tragic deficit, the authors noted. By some estimates, anywhere from a third to two-thirds of people with covid-19 symptoms experience anosmia.
“Anosmia seems like a curious phenomenon, but it can be devastating for the small fraction of people in whom it’s persistent,” Datta said. “It can have serious psychological consequences and could be a major public health problem if we have a growing population with permanent loss of smell.”