Mary Petrone is a Ph.D. student and Nathan Grubaugh is an assistant professor in the Department of Epidemiology of Microbial Diseases at the Yale School of Public Health. Their lab specializes in using genomic epidemiology to track the emergence, spread and evolution of viruses. Read more about their research at grubaughlab.com. The views expressed in this commentary are solely those of the authors.

(CNN) A recent scientific article suggested that the novel coronavirus responsible for the Covid-19 epidemic has mutated into a more "aggressive" form. Is this something we need to worry about? No, and here's why.

The first claim that the coronavirus is mutating is actually true, and it's perfectly fine! Before you rage-close your browser, hear us out. We get that the word "mutation" is bandied about in popular culture to denote a dramatic and fundamental change in a living being. After all, mutation-inducing toxic waste in the sewers of New York City transformed benign adolescent reptiles into crime-fighting teenage turtles . However, fictional portrayals of mutation are simply that: fictional. The effects of mutation in real life are nuanced and generally innocuous. Using the idea of mutation to incite fear is harmful, especially in the midst of an epidemic like Covid-19.

A particularly fraught question during epidemics is whether the causative pathogen will mutate to become more dangerous. This is the wrong question. Mutation is a mundane aspect of existence for many viruses, and the novel coronavirus is no exception. The genetic material of the virus is RNA, not DNA like in humans. Unlike with human DNA, when viruses copy their genetic material, it does not proofread its work.

Because RNA viruses essentially operate without a spell-check, they often make mistakes. These "mistakes" are mutations, and viruses mutate rapidly compared to other organisms. While this might sound frightening, mistakes during replication usually produce changes that are neutral or even harmful to the newly generated virus. Neutral mutations, which neither improve nor hinder viruses' survival, may continue to circulate without any noticeable change in the people they infect. Mutations that are harmful to the viruses are less likely to survive and are eliminated through natural selection.

Fortunately, when mutations occur that help a virus spread or survive better, they are unlikely to make a difference in the course of an outbreak. Viral traits such as infectiousness and disease severity are controlled by multiple genes, and each of those genes may affect the virus' ability to spread in multiple ways. For example, a virus that causes severe symptoms may be less likely to be transmitted if infected people are sick enough to stay in bed. As such, these traits are like blocks in a Rubik's cube; a change in one characteristic will change another. The chances of a virus navigating these complex series of trade-offs to become more severe during the short timescale of an outbreak are extremely low.