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Coronavirus Disease 2019
The Novel Coronavirus Has Its Own Evolutionary Strategy
SARS-CoV-2 spreads by using evolutionary deception.
Posted April 30, 2020 Reviewed by Matt Huston
Set a thief to catch a thief. The best deer hunters are those who can think like a deer. To understand—and ultimately get the better of—the novel coronavirus, it would help to walk a mile in its evolutionary shoes. So let’s try.
Confronted with a pathogen, medicine nearly always focuses on how the human body responds to the invader: with inflammation, fever, malaise, coughing, sneezing, perhaps internal hemorrhaging, organ failure and any number of other symptoms, some minor and some life-threatening.
The view from evolutionary biology, however, is that pathogens—be they bacteria, fungi, protozoa or viruses—warrant being considered entities with their own agendas, unlike a nail we might step on or a hot stove we might accidentally touch. Inorganic structures aren’t the products of evolution; hence, neither nail nor stove has agency, unlike your body, which responds to their assaults in various adaptive ways. Fortunately for us, neither the nail nor the stove fights back.
But viruses have evolved and accordingly, they have their own agendas. Just as the goal of a bacterium is to become bacteria, the goal of a coronavirus is to become many coronaviruses. Except that within this seeming simplicity resides a great deal of complexity, largely because your body—no less than the virus—has its own evolutionary project, and in large part, host and pathogen are in conflict.
From the virus’s perspective, there is a lot of work to do. First, it must penetrate your body’s outer defenses, such as skin, hair, mucous and the like. Then it has to evade or overwhelm the body’s next line of defense, the immune system, before getting inside its target cells and hijacking their chemicals to make more virus particles. After this, the new replicants need to escape from the husk of their victimized cell and proceed to penetrate other cells. Rinse and repeat.
That’s not all. Unless a virus is content for its descendants to remain indefinitely inside the body of its host, they need somehow to get into a new body and then continue the process. The received wisdom among parasitologists, microbiologists, and evolutionary biologists has long been that to escape from an infected body into a new one, well-adapted pathogens actually evolve toward benignity; they do not routinely kill their hosts, because selection would rule out an organism that consistently consigns itself to a literal dead end.
This view has recently been challenged, however, bearing in mind that natural selection, acting on pathogens, simply favors making as many successful copies as possible, which involves not only replication within a host but also the capacity to jump between hosts. On the one hand, the longer you keep your victim alive the greater the opportunity to get yourself transferred to a new victim. But natural selection doesn’t care how this bottom line—maximum reproductive success—is achieved, and we know that in some cases, acute infection leading to prompt mortality can provide an alternative route.
Take Ebola, for example. This virus doesn’t scruple to kill its hosts much more quickly than would be predicted by the theory that a well-adapted pathogen is necessarily a benevolent one, predisposed to live and let live. By causing severe hemorrhaging and leakage of other body fluids swarming with Ebola viruses, the pathogen has hit upon an effective way of enhancing its evolutionary success, since exposure to such fluids spreads it to new victims, even if the previous host is killed in the process.
The novel coronavirus (officially known as SARS-CoV-2) appears to employ an alternative strategy, one that is elegantly nasty. Although the symptoms of the disease it produces, COVID-19, can be severe and ultimately deadly, infected individuals are capable of spreading the virus for up to two weeks before showing any symptoms, and it appears that in many cases, such individuals may remain asymptomatic carriers. They can have a virulent infection but be no worse off as a result, while potentially endangering the rest of us.
Virulence is a complex and sometimes contradictory phenomenon. It can mean the rate at which the pathogen reproduces within a host, and also the degree to which the disease is hurtful to the body in question. Virulence thus can be an evolutionary paradox insofar as natural selection favors rapid replication, but if this leads to the early death of the host, it could reduce evolutionary success. Rapid replication by a virus and severe symptoms for the host are usually correlated, but not necessarily, and it doesn’t matter to the pathogenic perpetrator so long as it satisfies its evolutionary mandate to reproduce itself. Either technique—Ebola’s fulminant lethality or SARS-CoV-2’s frequent asymptomatic masquerade—will do.
Asymptomatic carriers, especially when a novel virus is involved, therefore probably do not indicate peaceful coexistence between pathogen and host/victim. Nor are they simply the result of mutations that fortuitously benefit the host. Rather, the likelihood is that they reflect an evolutionary strategy by the virus to maximize its spread. At our expense.
Until recently, the application of evolutionary thinking to disease dynamics has been limited to the problem of pathogens evolving resistance to antibiotics. Extending that perspective to the strategies of both pathogen and host sets the stage for additional, unexpected insights.
When disease symptoms occur, we might ask whether they are defenses by the victim or a manipulation by the pathogen. If the former, then treating such symptoms by damping them down may well prolong the disease while also possibly making it more severe. If the latter, then supportive treatment that attacks these symptoms would likely reduce the spread of the disease while also aiding the victim.
For example, although in some cases fever can be highly detrimental to the host (in which case good clinical practice involves reducing the patient’s temperature), in others it turns out that increased body temperature reduces a pathogen’s virulence, in which case good practice is to respect the wisdom of the body and allow the fever to run its course.
By dislodging disease-causing organisms, coughing and sneezing can be beneficial to the disease sufferer, in which case suppressants are ill-advised. But these symptoms can also result from pathogens manipulating the host so as to get themselves dispersed, in which case the less coughing and sneezing, the better. Some diseases such as tuberculosis and many cancers result in diminished appetite. Is this a strategy by tuberculosis bacteria or cancer cells to weaken their hosts, or by the body to reduce the nutrients available for those invading bacteria or tumors? The answers have important implications, not discernible unless we carefully examine pathogen-host interactions as the evolutionary arms races that they are.
The SARS-CoV-2 technique of generating asymptomatic hosts appears to be another front in such competition, whereby the invader seeks to take advantage of a species with a high pre-existing level of social preference. And within such a species, it can act with particular vigor against individuals who because of economic necessity or personality traits (and political ideology?) are unable or unwilling to engage in social isolation, and who are therefore more liable to encounter carriers and therefore to become infected.
Maybe part of COVID-19’s symptom profile is that it works as a viral ecstasy drug, or perhaps via a small tweak of the dopamine system, making its hosts just a bit more extroverted. More likely, its effectiveness is simply attributable to having latched onto a highly social victim species (us), which also has a hard time perceiving someone else as dangerous to their own health so long as these others lack obvious illness.
Despite its fiendish strategy, the Ebola virus was ultimately contained because it couldn’t cope with intense medical intervention that reduced its ability to infect new victims. So it eventually burned itself out. By the same token, in addition to developing effective clinical treatment of victims and ultimately a vaccine, we can overcome the current coronavirus pandemic by an intervention comparable to what has worked against Ebola, namely stymying its clever adaptive strategy by identifying who is carrying the virus, thereby parrying its evolution-generated attempts at spreading.
Ebola is not subtle; it comes at us with guns blazing, leaving no doubt as to who is a victim. COVID-19 is sneakier. To overcome its unique undercover maneuver, the mandate of public health plus the insights of evolutionary biology both tell us to be cleverer yet and unmask its deception by our own uniquely human technological counter-maneuver: vigorous, accurate, and widespread testing.
David P. Barash is professor of psychology emeritus at the University of Washington. Among his recent books is Through a Glass Brightly: using science to see ourselves as we really are (2018, Oxford University Press).
