The Spanish flu pandemic kicked off in late spring of 1918 as a moderately severe influenza outbreak at first. Only after the virus mutated during summer and returned much more virulent in the fall of the same year did a large number of people die.
Since the start of the current pandemic researchers and policymakers have worried about possible mutations of SARS-CoV-2. A recent paper based on over 18 500 virus genome samples collected thus far concludes that these worries are unfounded.
Viral mutations occur when errors are made in the replication of viral RNA during the infection. The process can be compared to making photocopies of building instructions for a chair. Sometimes the instructions get crumpled up, sometimes the photocopy machine is dirty or does not work properly so that in the end the copied building instructions are slightly different.
If the number of chair legs to be attached changes in the manual this could make the chair either more or less stable. Likewise, additions and deletions in the viral RNA can make the resulting virus more or less virulent.
At least 6 different strains of SARS-CoV-2
While researchers have identified at least 6 different strains of SARS-CoV-2, these strains do not show a large genetic variance. Unlike other pathogens like HIV or the influenza virus, the SARS-CoV-2 genome is rather simple, due to it being a single strand of RNA.
Sticking with the analogy above, its building instruction is contained in one big book and copying it therefore less prone to error compared to other pathogens where the building instructions are shorter but spread out across multiple books written in foreign languages. Furthermore, just like its predecessor SARS-CoV, the novel coronavirus appears to revert back to its original form as mutations appear to be less efficient at reproduction.
Furthermore, vaccines that were developed using the genetic information obtained in January 2020 will probably still be effective for the currently dominant variants of the virus. Most vaccines target the spike proteins on the virus’ hull that act like as key to the human cells it tries to infect.
There were only two observed mutations related to the make-up of these spike proteins and they had no effect on the ability of antibodies to bind to that area and render the virus ineffective.
Image: genetic family tree where branch length accounts for genetic divergence
Prognoses are no reliable indicator for future performance.