In 2020, the COVID-19 pandemic swept across the world with a voracity we haven’t seen from a virus in decades. We didn’t know much about this novel virus when this all began. Now, a year later and with significant global effort, we have learned a lot about this viral threat.
We know more about how SARS-CoV-2 is, and isn’t, transmitted. We’ve learned enough about its genetic makeup that we came up with several effective vaccines against it. Now that we’re armed with better tools, let's have a look at the future of our fight against COVID-19 and what that might entail.
COVID-19: invaders from a viral dimension
SARS-CoV-2 is a specific virus that belongs to a large family of viruses known as coronaviruses. Coronaviruses get their name from the crown-like spikes that cover the virus. There are seven human coronaviruses; the commonly transmitted 229E, NL63, OC43, and HKU1; the less common MERS-CoV and SARS-CoV; and the infamous SARS-CoV-2, the virus responsible for the COVID-19 pandemic. The four common coronaviruses continually circulate through the global population and cause flu-like or cold-like symptoms, accounting for around 10 to 30 percent of common colds. Some scientists are worried that COVID-19 is going to join the list as one of the permanently-circulating common human coronaviruses.
Our future living with SARS-CoV-2 remains unclear; a lot of this future depends on how COVID-19 evolves and mutates. It’s possible the virus will evolve in a way that will make it a mild nuisance, like the common cold. It could also evolve to be a more serious and lethal threat, like MERS-CoV and SARS-CoV. It could pop up every year or every couple of years like the seasonal flu does, either in a weaker or stronger form than we see today. A lot depends on whether humans who achieve immunity, from vaccines or having had an infection, keep this immunity for a long time, and if the virus mutates in a way to make existing immunity less effective. The main thing we’re fighting against is the possibility of dangerous future mutations.
The more people COVID-19 is able to infect, the more chances it has to mutate into a new variant. COVID-19’s ubiquitous spread throughout the world has already given rise to several new variants of the disease. The SARS-CoV-2 variants we’ve discovered aren’t significantly more dangerous than the original disease, but some are considerably more communicative, and they are worth paying attention too. Some of them, like the B.1.351 variant, might make our vaccines less effective. This type of mutation is one of the most concerning for scientists and is among the reasons it’s so important to reach a high level of immunity.
Herd immunity: We’re stronger together
Ultimately, to fully defeat SARS-CoV-2, it would be necessary for populations to achieve herd immunity. Herd immunity is obtained when most of a population has immunity to an infectious disease. It works by making it much harder for the disease to spread through a population because there are fewer people who are susceptible.
Herd immunity can be achieved either through surviving an infection and developing antibodies or through an effective vaccination drive with high participation; both can immunize a population. We can eradicate a disease if we completely stop its transmission before it mutates, and if the disease does not have an animal reservoir to retreat to (as was the case with smallpox, for example).
Generally speaking, a population needs between 60 and 90 percent immunity to achieve herd immunity, depending on how contagious the virus is. If a population has an immunity rate of 75 percent, then three in every four people who interact with a sick person are immune. Because this is just a matter of probability, the higher the level of immunity in a population, the greater the benefit. In addition to protecting individuals in a population at large, herd immunity also has the important goal to protect the more vulnerable members of our community, because those with immunity act as a “shield,” preventing the spread of a disease.
We’ve been able to achieve herd immunity in the past with diseases like chickenpox, measles, and polio, but what about SARS-CoV-2? Health experts aren’t so sure. Many scientists estimate we need at least a 60 to 70 percent immunity rate to reach herd immunity against SARS-CoV-2. The best hope we have to reach a herd immunity threshold high enough to eliminate COVID-19 is to vaccinate people as quickly as possible while maintaining public health standards like social distancing and masking. Issues with vaccine hesitancy and vaccine availability are negatively affecting the global vaccination drive causing experts to believe reaching herd immunity is unlikely.
Breaking the shield: How does a virus defeat immunity
Viruses evolve and change very rapidly. Most of the time, these mutations are minor and don’t really affect the way humans interact with them. Sometimes, a mutation can completely alter our relationship with a virus. Most of our knowledge of viral mutations as it relates to vaccination efforts comes from studying influenza viruses, which could offer some insight into our efforts to develop a coronavirus vaccine. Generally, viruses mutate in one of two ways; through antigenic drift or antigenic shift.
Two ways viruses mutate
Antigenic drift is the most common type of mutation. Sometimes, when a virus replicates, it will have a random replication error, so that the replicated virus is a little different from the original. Over time, as a viral line accumulates more and more genetic mutations, it can lead to a change in antigens or surface proteins of the virus. Antibodies are created as an immune response to specific antigens, so when a virus’s antigen fingerprint changes, it makes it harder for our immune system to identify it. When a virus drifts sufficiently, we become susceptible to it again, which requires us to update our vaccine.
Antigenic shift is a more rare but much more transformative mutation. This happens when a host cell becomes infected by two or more different variants of the same virus. Influenza viruses are made from eight segments of RNA and will sometimes go through a process called “reassortment” where the viruses combine their genomes and create a new subtype of the virus. When a shift happens, most people have little or no immunity against the resulting new virus.
Coronaviruses cannot go through this same reassortment process because they have one long strand of RNA, rather than segments, but they can do something similar. When two or more coronaviruses infect a host cell, they can recombine to create a new RNA genome from pieces of the parental genomes. This can lead to the creation of novel coronaviruses that may have very different properties from the original.
Looking to the future: What to do now
As always, look to local health organizations for guidelines and ordinances in effect in your local area. Wearing masks and social distancing whenever interacting with other people, especially indoors, has consistently been one of the best things we can do to keep COVID-19 under control. Get vaccinated if you’re eligible and lobby governments to make the vaccine available across the world. If you are vaccinated, still be vigilant in public spaces when interacting with or around people. The goal is to limit the number of opportunities SARS-CoV-2 has to mutate and spread. Hopefully, we’re in the last months and days of this pandemic.