Why Viruses Mutate Fast?
The only function of viruses is to multiply, and they excel at it.
Viruses can mutate fast because they invest zero energy in their progeny.
Viruses are parasites: they do not produce any energy, they steal it from their host. Because viruses do not invest any energy, their progeny is expendable. Viruses make massive amounts of copies of themselves. For example, one influenza virus infecting one cell can produce thousands of new viruses. One influenza-infected person can shed billions (10⁹) of viruses in one day. Due to mutations, most of the copies of fast mutating viruses are worse in infecting than the original virus, some are the same, and a few are better. But for a virus, one in a million chance is great odds.
Mutations arise when a polymerase enzyme replicates genomes.
Genomes are made of repeating units of four nucleotides. The polymerase joins the nucleotides into a correct order using the original genome as a model. Yet, polymerases are not perfect, and sometimes they make mistakes: they use a wrong nucleotide, miss a nucleotide, or add an extra one.
Whenever a cell divides, it replicates its genome. Therefore, all genomes accumulate mutations in time, and that is why cancer incidence increases as we age. However, unlike viruses, cells have to care about their progeny. A single mutated cell might evolve into cancer or other disease and damage the whole system. Or even worse, a damaging mutation might pass to the next generation and hurt the population.
Viruses do not have a system or a population that a substandard progeny could harm.
We mutate slowly because we are complicated and most of the genetic changes are deleterious to us. Cells use much energy to keep their genomes pristine by numerous mechanisms that surveil and correct mutations. For example, our polymerases are 100 000 times more accurate than some virus polymerases.
Without mutations, evolution would stop.
Although viruses depend on their host for resources, virus genes determine their ability to multiply. Viruses must evolve to improve. For example, the so-called UK variant (B.1.1.7 or VOC-202012/01) of SARS-CoV-2 has 17 mutations. Most of the changes affect the spike protein that is on the virus’s surface. The virus uses the protein to get inside the host cell. The spike protein is also the most likely target for immune defence. Mutations in the spike protein may increase the virus’s efficiency to enter the host cells and evade the host immune system. Thus, the UK variant may spread faster because it infects more cells and produces more virus copies. SARS-CoV-2 is still adapting to humans.
The more viruses multiply, the more they mutate, and the more opportunity they have to improve. But where does it lead?
If viruses evolve to multiply more efficiently, they have many successful lifestyle options. For example, all humans carry hundreds of retroviruses inherited from our monkey ancestors millions of years ago. Adeno-associated viruses infect over half of the human population without causing any diseases. Epstein-Barr virus infects 90 % of humans, with minimal consequences to most of us. Common cold viruses, which include several virus species, travel worldwide each year and infect and reinfect many of us. The influenza virus that killed 50 million people during 1918 pandemia has since then jumped to pigs, disappeared, reappeared, and evolved a much lower mortality rate.
Disease and death are sometimes side effects of virus evolution, but not the objective.
References
virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations/563
bionumbers.hms.harvard.edu/search.aspx
