As quarantine and social distancing pushes on and we all await each day’s news updates about coronavirus, the development of a vaccine, information on the dreaded second wave, and how long the pandemic will last, you’ve probably often heard one of the scariest words there is when it comes to virus discussion. Mutate. So why’s this so scary? To fully understand the importance and complications that arise with the verb, we must first understand viruses, and what it truly means for them to mutate.
Viruses themselves are rather strange in terms of their behavior and classification, and this complicated nature to our understanding of them definitely seems to add to their fear factor. Viruses themselves exist in a strange realm between being an organism and a particle, or between life and chemistry. Like bacteria, they are microscopic and contain nucleic acids (DNA or RNA), bound inside a protein membrane. They can take many different shapes, some looking like teenie nanobots that could be featured in spy movies while others look like an odd fruit or orb. In fact, many viruses are classified according to shape variation, just like COVID-19, which is actually part of a family of viruses known as coronaviruses due to their crown-like shape. Viruses also operate like a parasite, as they are unable to survive independently and must latch onto a host. Once there, their motives become pretty questionable (and this is where the scary part starts). Viruses work by latching onto and corrupting cells. Once attached, the virus sheds its protein barrier and begins to alter the genetic code being replicated in a host cell’s reproductive mechanisms, altering it to the point that the host begins to reproduce the virus’s own genetic material instead of the host’s. That’s right; viruses work by hijacking your cells and making them into little virus factories for itself. From there, these new viruses go out and attack and corrupt other cells, and then the infection spreads. Because of their weird nature that inhabits a space somewhere between chemistry and life, viruses have sometimes been called “a kind of borrowed life,” but have no real autonomy or capacity for independent replication, and therefore cannot be considered truly alive. However, their ability to adapt to situations definitely helps blur the living/not living distinction.
Because a host usually has defence mechanisms in store (for most animals, this is your immune system and white blood cells), a virus usually doesn’t get away with its hijacking of cells for very long. Eventually, your immune system becomes aware that your body is under attack and responds. Therefore, a virus must mutate, or change its tactics to become more resilient and effective. This can also happen when it becomes resistant to a certain kind of treatment, or evolves to be transmitted in new ways. It’s not all as Darwinian as it seems, though. The mutation of viruses is more accidental than adaptive. The mutations themselves occur when subtle differences happen to the genetic material inside viruses as they replicate and create new copies. Only a small portion of these mutations will end up being advantageous to the virus, leading to new “strains” of illness that use the advantage of unpredictability to become more and more infectious or resistant. Usually, though, they’re such tiny changes that there’s no noticeable difference to the virus’s behavior, or they weaken the virus.
Now, what does this mean for COVID-19? COVID-19, scientifically called SARS-CoV-2, is an enveloped RNA virus, which means it contains single-stranded RNA material that it uses host cells to replicate. It’s common for RNA viruses to mutate very quickly, even extraordinarily so, since the enzymes used in their replication are prone to making errors when pumping out new virus copies. Fortunately, though, SARS-CoV-2 has demonstrated rather low mutation rates, mutating significantly less than the common flu. Unfortunately, some of the mutations of the virus have already been shown to increase infection rates. The most significant of these is an alteration to the spike proteins that coat the virus, which are crucial for infection as they help the virus bind to the host cell. And right now, this more infectious strain seems to be the dominant one. Scientists are still struggling to understand the ramifications of the mutations, and as to whether the mutation causes a more severe illness or increases the risk of death. It also remains to be seen whether the illness itself and its associated symptoms have changed as the virus mutates. As for now, the illness and hospitalization rates seem to be similar between variations in the viral strains.
What mutations truly pose a challenge for, though, is the development of a vaccine and immunization against SARS-CoV-2. While the opinions and conclusions of much research on the mutations themselves and their ramifications seems to be divided, the hope for a vaccine is more so. Some say that accounting for the different strains of COVID-19 shouldn’t pose a difficulty for the development of an effective vaccine, while others are less optimistic. Largely, though, vaccines are developed based on early variations of viruses, and the slow mutation rate of SARS-CoV-2 means that aside from spikes in infectiousness of the virus itself, a vaccine should have no trouble targeting the virus, as newer strains have preserved enough features of the original to make a universal vaccine feasible. What remains to be seen are significant developments in the creation of such a vaccine, and we will wait with baited breath until we have one.Until then, stay safe and protect yourself with products like N95 respirators.