Common cold season is back, which has people wondering why we catch the same virus, year after year. Why don't we ever develop immunity against the common cold? Professor Pierre Talbot at INRS has known about the incredible variability of coronaviruses for some time. They're responsible for the common cold as well as many other infections, including neurological diseases. Along with his research associate Marc Desforges, Professor Talbot worked on a study recently published in Nature Communications about the ways in which coronaviruses adapt and evolve, becoming ever more effective at infecting hosts without being defeated by the immune system. The small, spiky spheres, the coronaviruses are closely monitored by public health agencies, since they're able to be transmitted between species and some have a high potential mortality rate. Both SARS and MERS are caused by coronaviruses. Their ability to adapt to new environments seems due in part to the spikes on the surface of the virus--more specifically, a small, strategic part of the proteins that form those spikes. The spikes are made up of S proteins (S for spike). A specific part of the spike seems to allow the virus to attach itself to host cells. The spike's RBD (receptor binding domain), which initiates the interaction between cell and virus, is essential for infection. But RBDs are targeted by antibodies that neutralize the virus and allow the immune system to flush it out of the host's system. Coronaviruses are thus faced with an evolutionary problem. They can't infect cells without an RBD, which needs to be exposed so that it can latch onto cells. But the RBD needs to be masked to avoid being targeted by antibodies. In response, the coronavirus has developed a mechanism that helps it survive, and thrive. The RBD is made up of three parts that vary widely between strains. Thanks to this variation, antibodies are unable to detect new strains, whereas RBDs retain--and even improve--their affinity for the target cell. Plus, RBDs alternate between visible and masked states. https://www.technologynetworks.com/immunology/news/why-dont-we-ever-develop-immunity-against-the-common-cold-294551 But it gets worse. One of the four "common cold" coronaviruses, HCoV-NL63, binds to human ACE2 receptors (as does the Wuhan Enigma virus that causes COVID-19). Coronaviruses use S homotrimers to promote cell attachment and fusion of the viral and host membranes. Because it is virtually the only antigen present at the virus surface, S is the main target of neutralizing antibodies during infection and a focus of vaccine design... Our results suggest that HCoV-NL63 and other coronaviruses use molecular trickery, based on epitope masking with glycans and activating conformational changes, to evade the immune system of infected hosts, in a manner similar that described for HIV-1. https://www.nature.com/articles/nsmb.3293 Good luck with that vaccine. I'm kinda with dregalicous on this one. Best case it burns out and disappears after a couple of years. If SARS-CoV-2 evolves like the four "common cold" coronaviruses, it's going to be with us for a long time.
Why don't we ever develop immunity against the common cold?
I always assumed that we do acquire immunity. Working in a public setting, if I catch a cold early on in it's run, when others catch it later, I believe that I have been correct in assuming I won't catch it again. This seems to hold true. A lot of people get it, but you don't get it twice.
But that immunity is possibly short lived, or no longer good against the mutated version that appears the next year.
Shaman posted this yesterday, which indicates the common cold coronaviruses may stimulate the immune system and help fight off the Wuhan Enigma Virus. Importantly, we detected SARS-CoV-2−reactive CD4+ T cells in ∼40-60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS-CoV-2.
The small, spiky spheres, the coronaviruses are closely monitored by public health agencies, since they're able to be transmitted between species and some have a high potential mortality rate. Both SARS and MERS are caused by coronaviruses. Their ability to adapt to new environments seems due in part to the spikes on the surface of the virus--more specifically, a small, strategic part of the proteins that form those spikes.
The spikes are made up of S proteins (S for spike). A specific part of the spike seems to allow the virus to attach itself to host cells. The spike's RBD (receptor binding domain), which initiates the interaction between cell and virus, is essential for infection. But RBDs are targeted by antibodies that neutralize the virus and allow the immune system to flush it out of the host's system.
Coronaviruses are thus faced with an evolutionary problem. They can't infect cells without an RBD, which needs to be exposed so that it can latch onto cells. But the RBD needs to be masked to avoid being targeted by antibodies.
In response, the coronavirus has developed a mechanism that helps it survive, and thrive. The RBD is made up of three parts that vary widely between strains. Thanks to this variation, antibodies are unable to detect new strains, whereas RBDs retain--and even improve--their affinity for the target cell. Plus, RBDs alternate between visible and masked states.
https://www.technologynetworks.com/immunology/news/why-dont-we-ever-develop-immunity-against-the-common-cold-294551
But it gets worse. One of the four "common cold" coronaviruses, HCoV-NL63, binds to human ACE2 receptors (as does the Wuhan Enigma virus that causes COVID-19).
Coronaviruses use S homotrimers to promote cell attachment and fusion of the viral and host membranes. Because it is virtually the only antigen present at the virus surface, S is the main target of neutralizing antibodies during infection and a focus of vaccine design... Our results suggest that HCoV-NL63 and other coronaviruses use molecular trickery, based on epitope masking with glycans and activating conformational changes, to evade the immune system of infected hosts, in a manner similar that described for HIV-1.
https://www.nature.com/articles/nsmb.3293
Good luck with that vaccine. I'm kinda with dregalicous on this one. Best case it burns out and disappears after a couple of years. If SARS-CoV-2 evolves like the four "common cold" coronaviruses, it's going to be with us for a long time.