As we enter the colder months in the Northern hemisphere, we’re beginning to see an influx of people sniffling, coughing, and sneezing all around us. The common cold usually makes its first appearance around this time, spreading like wildfire through offices, schools, and homes. But why is it that we seem to catch this same virus every single year? Why hasn’t our body developed an immunity to it yet?
These are questions that new research published in Nature Communications might just answer. Professor Pierre Talbot from Institut National de la Recherche Scientifique (INRS) in Canada has been studying coronaviruses – which include the common cold – for many years. These viruses come in a wide variety, and include other infections such as neurological diseases. In this study, Talbot and his colleagues attempted to find out why coronaviruses are able to adapt and evolve so effectively while evading a host’s immune system.
In appearance, coronaviruses look like tiny, spiky spheres. Now, the researchers believe that these spikes play a role in the virus’s ability to adapt to new environments. The spikes are made up of S proteins (the S stands for spike, of course), which allow the virus to attach itself to host cells. Specifically, the spike’s receptor binding domain (RBD) initiates the interaction between a cell and the virus. However, these RBDs are also targets for antibodies in the host’s immune system that are seeking to neutralize the virus.
So for coronaviruses to infect a host cell, it needs an exposed RBD. But that same RBD is a target for antibodies, so in order for the virus to be effective, the RBD needs to be masked. Talbot and his colleagues figured out that the coronavirus does this by having an RBD that is made up of three parts that vary significantly between strains. Due to this variation, antibodies are unable to detect a new strain, but the RBD still retains – and in some cases improves – its affinity for the target cell. Furthermore, the RBDs can alternate between visible and masked states.
The research team analyzed the RBD’s structure up close, finding three long loops that attach to the host cell protein. Previous analyses of these viruses dating back roughly a half-century have found that these loops are essentially the only thing that varies from one coronavirus strain to the next.
Through this research, we now have a better understanding of why the common cold is so persistent. Although there is a lot more work to be done, it’s possible that research such as this could lead to a welcome reduction in wintertime sniffling, coughing, and sneezing.