One of the more concerning events during the COVID-19 pandemic has been the detection and emergence of virus variants.
These variant strains have mutations that slightly alter their genetic code such that they are more readily transmissible, a worrying feature given the issues with control already occurring.
Even more frightening, there is growing evidence that the new variants are more deadly. So far, these variant strains are reported to have originated in South Africa, the United Kingdom and Brazil. Without a doubt, there are many other mutated versions of this coronavirus out there that have yet to be detected.
This was predictable — coronaviruses are notoriously lax with their reproduction. Because they are made of RNA, versus the more stable DNA, they are prone to copying mistakes. RNA copying is a bit like ancient monk scribes diligently hand-writing manuscripts; they invariably introduce mistakes compared to the exacting copy-and-paste functions of modern computers, which are more similar to DNA replication.
Lucky mistakes become mutations that offer the virus a better chance at survival through such factors as increased ability to cause infection or easier transmission.
Some scientists have described RNA viruses as quasi-species, where there are so many copy mistakes and resultant mutations that a wide diversity of the virus is biologically capable of survival.
Another familiar example of RNA viruses are influenza viruses. With their vast genetic diversity, influenza viruses can infect birds, pigs and people, with occasional jumps between these host species.
Pathogens are wily foes. The viruses, bacteria and parasite pathogens that infect people and animals continually evolve. If we were to personify them, their mission is to infect the most individuals possible. The more individuals a pathogen infects, the greater chance there is for the pathogen to be selected for better characteristics.
Some scientists have likened the relationship between pathogens and animals to that of a battle. There is a continuous arms race between pathogens and the individual’s immune system, each trying to outgun the other.
Most pathogens strike a balance between killing their hosts and making them sick. Pathogens that are too deadly are unlikely to be passed to many other individuals and it is thought that these types gradually lose their pathogenicity in favour of a more mundane existence of causing illness.
The bacteria that causes anthrax is an interesting exception — it is highly lethal to cattle but does not spread directly between animals. Instead, it develops exceptionally hardy spores that survive in the soil, lying in wait for its next victim to come along, even if it takes decades.
Some pathogens adapt to their main host so well that they cause little or no clinical disease. But these pathogens can wreak havoc when spread to other susceptible species. An example of this is ovine herpesvirus 2, a virus that causes no disease when it infects sheep hosts. But when it jumps into bison, it can cause the deadly disease malignant catarrhal fever.
The increasing problem of antimicrobial resistance is another excellent example of how pathogens can evolve. In this case, the selection pressure of antibiotic medications has favoured those bacterial strains that have mechanisms to inactivate or otherwise make the medications ineffective. With time, these resistant strains become the predominant pathogen in our animals. The challenges we face with growing antimicrobial resistance are directly linked to the ability of pathogens to evolve.
With the COVID-19 pandemic, we are seeing virus evolution play out in real time. But the evolution of pathogens has always been with us. The lessons of disease control apply to animal infectious diseases as well and should inspire us to manage animal infections in a serious fashion.
Dr. Jamie Rothenburger, DVM, MVetSc,PhD, DACVP, is a veterinarian who practices pathology and is an assistant professor at the University of Calgary’s Faculty of Veterinary Medicine. Twitter: @JRothenburger