Natural selection and evolution of the SARS-CoV-2 virus
Nature is analog. It is not a binary system. In the living world, there are no explicit switches that quietly turn systems on or off. Rather, nature adjusts systems using analog dials, like an old radio – gradually changing variables to achieve balance and equilibrium to ensure that life is sustainable and continues.
Evolution happens this way, with new life forms appearing and some disappearing over millennia – or, in the case of microbial pathogens (viruses, bacteria and parasites) over days or weeks.
Evolutionary change results from two opposing forces: positive selection breeds beneficial genetic variations that allow the virus to survive, while negative selection pressure hampers the virus’ survival and ability to reproduce.
Evolution can be studied at the molecular level. For many years my research focused on the African trypanosome, the parasite responsible for African sleeping sickness.
Trypanosomes live in the bloodstream of their mammalian hosts (including humans) and early observations of their numbers showed a steady pattern of wave-like increase followed by decreasing numbers, then, after about a week, of a further increase in numbers.
Trypanosomes are vulnerable to antibodies produced by their host’s immune system, which bind to the parasite and eliminate it. This immune response causes the number of trypanosomes to drop, as illustrated by the low points in the wave pattern. But before the trypanosomes disappear completely, their numbers increase again and the wave repeats itself.
This intriguing growth pattern sparked a lot of interest and research in my lab, and ultimately we learned that the parasite can alter its molecular identity to evade host antibodies before it is completely eliminated. This means that the population of trypanosomes responsible for each of the wave peaks is a distinct variant from all the others. Antibodies against one variant have no effect on subsequent variants, so the wave pattern continues.
The trypanosome’s highly successful strategy evolved to help it survive in the face of constant negative selection pressure from antibodies. This mechanism that helps a parasite or pathogen evade the host’s immune system is called antigenic variation.
Waves of COVID-19 look like sleeping sickness
I remember the trypanosome growth curve when I look at the trend in the number of Canadian cases from the COVID-19[female[feminine pandemic.
The case spikes reflect the arrival of new variants, the most recent of which is omicron, the variant now circulating most widely in the world.
The strategy used by SARS-CoV-2, the virus that causes COVID-19, is similar to that of the trypanosome, although the mechanism for generating new variants is quite different. For the virus, new variants arise through mutations in genes that code for the so-called “spike protein”, the part of the virus that allows it to enter cells and infect people.
Mutations arise due to ‘errors’ that occur when the virus replicates in cells of the host’s respiratory system. Because the virus has a mechanism that can attempt to fix “mistakes”, SARS-CoV-2 evolves more slowly than the trypanosome. It evolves more slowly because the virus has a mechanism that can attempt to fix “mistakes”. However, this repair process is not perfect and some mutations are retained.
If mutations result in a spike protein that is distinct from any other variant that precedes it, we will see a new variant emerge. The omicron variant is of particular interest (and somewhat concerning) due to its high number of mutations, not only in the spike protein but also in other viral genes.
By employing this strategy of antigenic variation, the survival of the SARS-CoV-2 virus is ensured. Thus, the appearance of new variants is due to mutations that represent the force of positive selection: genetic variations that help the organism to reproduce.
The decline in the number of cases during a pandemic is due to negative selection forces. These include effective public health interventions that limit person-to-person spread (such as masks), as well as the host immune response (antibodies) resulting either from infection or vaccination or both.
An infected person will, over time, generate antibodies against the virus and begin to eliminate this variant, as in the case of the trypanosome. But because SARS-CoV-2 mutations happen slowly, the virus has to find a new, non-immune person to keep going. In order to find new non-immune hosts, the virus induces symptoms that help it spread: coughs and sneezes that allow it to jump from person to person via droplets.
Antibodies and disease
Given the ability of SARS-CoV-2 to mutate, new variants are certainly emerging all the time. However, if medical and public health interventions are successful in reducing transmission between infected and uninfected/unvaccinated people, it is entirely possible that the virus could evolve into a less virulent variant that could become established as an infection. endemic producing mild symptoms.
When people infected with a pathogenic microbe show symptoms of disease, those symptoms often have a purpose: they can help either the survival of the microbe or the survival of the infected host. A classic case is diarrhea resulting from cholera infection or amoebic dysentery. Both infections produce life-threatening diarrhea, but the symptom has different purposes in each disease.
In the case of cholera, this symptom serves the microbe as it allows the bacterium to exit the body of the host and, in places with poor sanitation, to contaminate the water supply and spread to many. new hosts. In the case of amoebic dysentery, the symptom is the result of the host body’s attempt to rid itself of the infection.
Clinicians must be able to distinguish between these two scenarios in the management of infectious diseases to avoid compounding the problem rather than solving it. In the case of COVID-19, clinical symptoms like sneezing and coughing that allow the virus to spread through the air positively select variants that help the virus spread to new susceptible individuals (such as unvaccinated people ).
This means that measures such as masking, social distancing and vaccination can prevent the spread by helping to prevent aerosol transmission.
Continued efforts to achieve a fully immunized population are crucial. The unvaccinated and uninfected are ideal hosts for SARS-CoV-2, and ideal for generating new variants due to the lack of negative selection by antibodies, which facilitates virus replication and production of new mutations.
While nature may move slowly analogically, humans can flip binary switches, and we can act now to ensure global vaccine equity. Ensuring global vaccination coverage is not only evolutionarily imperative, it is also clearly an ethical option.
Written by Michael Clarke, Adjunct Professor, Interfaculty Program in Public Health, Schulich School of Medicine and Dentistry, Western University.
This article first appeared in The Conversation.