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.
Still, a common perception is that the continuous acquisition of mutations will cause our future coronavirus vaccines to be ineffective. While virus evolution may confer vaccine resistance, this process often takes many years for the right mutations to accumulate. Many vaccines to RNA viruses, such as yellow fever, measles, and mumps, were developed throughout the 1930s-70s and are all still highly effective. And those viruses mutate at rates as fast or faster than coronaviruses. In fact, the two proposed “S” and “L” coronavirus strains only differ by two mutations and are 99.993% identical. It’s extremely likely that any vaccine designed for one coronavirus will be protective against the other. The reason we need an annual influenza vaccine has more to do with how that virus reshuffles its genome than how it mutates.