An evolutionary perspective of the COVID19 pandemic
Is COVID-19 just one on the list of viral outbreaks that have come and gone? Or is there something at the genetic level of this virus, making this battle more difficult than the others. This article looks at the constant struggle between species, forcing them to evolve, adapt and overcome, and how it played out last year between Homo sapiens and SARS-CoV-2.
‘Stay Home, Stay Safe’- across the globe, people have become used to this phrase, in light of the Covid-19 Pandemic. Home quarantine, lockdown, masks, sanitizers and social distancing have become the norm.
The severity of the COVID19 (Coronavirus Disease 2019) spread is evident from the escalation of a few reports in Wuhan, China to a WHO Phase-6 Pandemic within months.1 Coronavirus is a big family of pathogens. Covid-19 is caused by the Coronavirus strain, SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2).2
Humans have battled SARS-CoV and MERS CoV (Middle East Respiratory Syndrome Coronavirus) earlier. SARS had previously spread across continents to 27 countries3 before being contained whereas MERS was relatively more concentrated in the Middle East and Africa, with only a few cases in the West. Both SARS and MERS spread through human contact. However, the spread never escalated to the level of COVID-19. Why? Does the answer lie in the genetic material?
Scientists of the Scripps Research Institute, have conducted extensive analyses of the genetic template for the protein coat armatures (protein shell of a virus which encloses its genetic material) that the SARS-CoV-2 uses to attach itself to cells and infect them. They have found that the Receptor-Binding Domain (a short fragment from a virus that binds to a specific receptor sequence to gain entry into host cells) was better equipped to effectively target a receptor involved in blood pressure regulation in human cells.4
Coronaviruses mutate faster than most other viruses, due to their genetic make-up (RNA particles which are less stable and thus change fast). Evolution and natural selection provide a suitable explanation as to why Covid-19 has spread faster and wider than SARS and MERS. The evidence of adaptations in the Receptor-Binding Domain that help SARS-CoV-2 bind efficiently to human cells explain the stronger binding and easier human-to-human transmission and thus, farther reach.
While the spread is much wider, the mortality rate due to COVID-19 is much lower compared to that of SARS and MERS. People with lower immunity are at greater risk and the young, healthy population seems to be able to stay alive for a long time, even after infection. SARS-CoV-2 also spreads asymptomatically. In the case of SARS and MERS however, infection led to comparatively quicker and visible symptoms, suffering, and almost sure death.5
Though counter-intuitive, this makes SARS-CoV-2 scarier. Why?
Consider the virus. It depends on the host to proliferate. The lesser the virus affects the host, the greater the chances of its replication and proliferation, and greater the spread across populations. Further, the delay of visible symptoms also delays identification and isolation, providing greater scope for human-to-human transmission. Evolution is thus once again to blame, for it seems to have provided the virus, not only better attachability to human cells, but also greater scope for survival and proliferation across populations. This also explains why SARS and MERS were more easily contained. Their human-to-human transmission was much less potent. The hosts showed symptoms comparatively quickly. Some even died before they could have contact with others to pass on the virus. All these factors reduced the scope for spread, allowing both SARS and MERS to be controlled and contained effectively.6
At a first glance it would seem that in the evolutionary race amongst the strains, SARS-CoV-2 is winning. Within a month of the first confirmed case of the Covid-19, the global total number of cases surpassed that of SARS and MERS put together. However, all was not lost because the human race also evolved simultaneously.
Evolution in the genetic sense is impossible in humans in such a short period, given the long life span and the genetic make-up (DNA particles which are more stable and change slowly). However, evolution must also include behavioural aspects. This includes the capacity of each individual’s immune response7 as well as the accumulation of knowledge within the system. Lockdown measures, quarantine, social distancing and isolation are all learned behaviours after all, based on past experience and aspects of evolution from a behavioural perspective. A ray of hope is in the fact that, given its success in proliferation and survival across populations, the SARS-CoV-2 virus seems to mutate slower, allowing us time to develop a vaccine and put a stop to it. This is an evolutionary arms race between humans and the virus in its own right.
The focus so far has been on the relationship between SARS-CoV-2 and humans. However, coronaviruses are mostly animal viruses. What about the manner in which the virus jumped from its animal hosts to man?
When viruses, in general, enter a non-compatible host, the immune system of the host successfully destroys the virus. However, when by some chance, the virus escapes said destruction, it tries its best to adapt to the new environment of this new ‘host’. Now and then, animal viruses manage to survive the human immune response and replicate within the human body. At this point, the virus can mutate and evolve under the human body constraints and improve itself for replication and proliferation in this species which is new to them.
Bats harbour several coronaviruses and still manage to live unaffected by them. Their unique immune capabilities enable them to carry a heavy viral load, without affecting their physiology. The SARS-CoV-2, like SARS-CoV and MERS-CoV, seems to have originated in bats and then jumped on to humans. However, the mode of infection, intermediate host and other details are still under study. As it stands, the human immune response to SARS-CoV-2 causes severe inflammation leading to the symptoms, which the bats have somehow evolved to cope with.
Even then, there surely must have been an evolutionary arms race between the viruses and the bats’ immune response.8 Researchers from the University of California Berkeley, USA have found evidence of the evolution of the coronaviruses towards greater cell-cell transmission capabilities, as a counter to the bats’ antiviral responses. This might have very well assisted the jump of SARS-CoV-2 from bats to humans, mostly through an intermediate host such as a Pangolin.9
The question that begs to be asked here is that, in the event that the virus does mutate and evolve further, wouldn't natural selection direct it to a form where it manages to survive and proliferate without causing severe impairments or death to the human hosts, like in bats? Wouldn't it be in the best interests of both the human population and the virus, given the virus gets a host to live in, and the human population is unaffected? In the words of Christopher Coleman, University of Nottingham, “This is by no means [always] true, but a virus that adapts to humans might be less dangerous in the long term because the ‘evolutionary arms race’ between virus and host has reached a sort of stalemate where neither is perfectly happy, but neither is killed off.”
Neither humans nor the virus, or any other organism for that matter, seem to be outside the grasp of an evolutionary arms race, trying to catch up with each others’ evolution-derived superpowers, to ensure survival. The result? Only time can tell.
Dakshesh Vasan is a 3rd Year student at the Department of Mathematics, IISER Kolkata. While he is fond of tinkering Mathematics into anything, wherever compatible, he has always been in love with the very concept of evolution. When he’s not in his room, he’s probably out discussing the latest campus happenings, while simultaneously campaigning for Inquivesta, and recently - Revival: The all IISER online cultural fest!.
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