Matthew tweeted his new theory, which is his, about why Covid-19 patients very often experience “smell blindness”, technically known as anosmia—the loss of one’s sense of smell (which of course also reduces one’s ability to taste). I asked him if he wanted to post it here, and he’s rewritten it so it’s understandable by the science-friendly layperson. And so, without further ado:
A hypothesis to explain why the Covid-19 virus affects the sense of smell in some people
By Matthew Cobb
In a recent study by King’s College, London of 579 people who reported having a positive Covid-19 test, 59% said they had reported a loss of smell or taste. This is not unique to Covid-19 – many other viruses can cause the same effect. It has never been quite clear how this occurs. The great amount of attention being paid to Covid-19 has helped reveal one possible mechanism.
We smell volatile molecules, but we don’t directly detect them in the air – our smell neurons would shrivel up and die. Our neurons are protected by a layer of mucus, and the smell molecules have to get through that.
The chemical structure of most smells means they are what is known as hydrophobic – they won’t dissolve easily in water, such as that found in the mucus. It is widely thought that the smells are transported by rather mysterious chaperones called olfactory binding proteins (OBPs).
These molecules are secreted into the mucus by cells called Bowman’s cells in the olfactory epithelium – the layer of skin, high up in the roof of your nasal cavity, which is where you smell things. Many scientists think that OBPs deliver the odour to the receptor on the neuron, and then appear to be taken up by cells called sustentacular cells which lie next door.
A paper that appeared a few days ago suggests that our olfactory neurons don’t express the ACE proteins that are the virus target, and that disruption to our neurons is therefore not the cause of anosmia. However, other cells in the olfactory epithelium, the sustentacular cells and the Bowman’s cells that produce OBPs, do express the ACE protein. Both these cell types are involved in the way that OBPs work.
If the virus is attacking these cells, then the metabolism of OBPs, and thereby the balance of detection of molecules will be altered. This may explain the widespread reports of anosmia following covid-19 infection, and, in some cases like that of the science journalist Adam Rutherford, who had symptoms of covid-19, hyperosmia (increased sensitivity). Sustentacular cells are also electrically active in newborn mice, perhaps indicating a more complex function for these cell types.
All this suggests that the return of normal olfactory functioning in patients with covid-19, or other coronaviruses, which may also cause these effects, probably depends on the time it takes for the Bowman’s cells and the sustentacular cells to recover.
A simpler explanation – advanced by @stevenmunger on Twitter in response to this – is that infection of these specific cell types merely causes inflammation, which alters tissue function. There may be other hypotheses, too. And some scientists don’t agree that OBPs play much of a role at all in olfaction. “For example, although humans have a number of genes that encode for OBPs, only one kind has so far been identified in the human olfactory epithelium. We clearly need to understand more about this aspect of how we smell.”
Whatever the exact mechanism involved, as Prof Tim Spector of King’s College said: “When combined with other symptoms, people with loss of smell and taste appear to be three times more likely to have contracted Covid-19 according to our data, and should therefore self-isolate for seven days to reduce the spread of the disease.”
For advice on living with anosmia:
BBC report of the King’s College study:
Brann et al (2020) – Gene expression in olfactory epithelium, on covid-19 and entry:
Strotmann & Breer (2011) – OBPs and sustentacular cells
Vogalis et al (2005) – Electrical activity in sustentacular cells
Badonnel et al (2009) – OBPs secreted by Bowman’s cells