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Evolutionary biologists and research epidemiologists are studying older coronaviruses for clues about whether COVID-19 will transform into something mild (like a common cold), something more threatening (like a flu) or something much more contagious and deadly.
Scientists are mostly paying attention to two types of viral mutations in COVID, according to Nature.com.
The first mutation type makes COVID-19 more infectious or transmissible by allowing the virus to quickly replicate inside a person's body, increasing their contagious viral load and the likelihood of passing it onto others. This is the first kind of mutation that most viruses develop.
Delta and Omicron, for instance, multiply faster in infected peoples' airways than the original and Alpha stains. This helped the virus spread more quickly to people close to the infected.
But as more and more humans get vaccinated and develop antibodies through past infections, viruses start to develop the second type of mutation: one that enables a virus to overcome a person's immune response. This mutation concerns researchers the most because it allows the virus to bypass the immunity offered by vaccinations as well as the antibodies created during past infections.
Evolutionary biologist Jesse Bloom found this exact sort of mutation in one of four "seasonal" mild cold coronaviruses that have been circulating amongst humans for decades. By examining human blood samples from the 1980s to the current day, Bloom found clues about how such viruses developed over time.
One such coronavirus (called 229E) gradually evolved to evade the immunity granted by antibodies from previous infections. COVID-19's Delta and Omicron variants developed similarly.
Early into the pandemic, genome sequencing of COVID-19 showed the coronavirus developing "single-letter mutations" about once a month. Such mutations involve the changing of a single chemical letter in a virus' DNA.
While these tiny changes made the virus slightly more transmissible, it takes larger changes to mutate the virus into something much more capable of spreading.
The better-known and more widespread COVID-19 variants—such as Alpha, Delta, Gamma and Omicron—all became more contagious mostly due to changes in their spike proteins. Spike proteins determine a virus' ability to attach onto and replicate within human cells.
Researchers believe that the Omicron variant may have 32 mutations in its spike protein, more than double the number found in Delta. Omicron's quick rise in South Africa and, later in the U.S., suggests that the variant also developed other changes that allowed it to dodge human immunity.
Omicron is now the predominant strain in the U.S., in part because it can surpass immunity offered by vaccines and boosters.
The aforementioned variants also shared another trait: they made immunocompromised and unvaccinated people sicker—doctors said that patients' symptoms were worse and that they stayed hospitalized for longer.
The prolonged infections made researchers suspect that perhaps the virus had figured out a way to keep evolving. By increasing the symptomatic period, the virus could infect more people over a longer time span.
This raises concerns, especially as some countries lift their COVID-19 prevention measures and other parts of the developing world face difficulties vaccinating their populations.
Continued outbreaks with long symptomatic periods will allow the virus time to adapt and change in human bodies and among communities, increasing the likelihood that new variants of concern will evolve in significant ways.
To survive, however, COVID-19 will have to balance between both kinds of mutations: replicating in high enough levels to become more contagious, but also keeping people healthy enough to infect others, Trevor Bedford, an evolutionary biologist at the Fred Hutchinson research center, told Nature.com.
Bedford suspects that the virus may gradually make people less sick but contagious for a longer infection period, ideal for infecting others. However, other researchers say it's a mistake to think that future variants will have milder and milder symptoms.
"There's this assumption that something more transmissible becomes less virulent. I don't think that's the position we should take," Francois Balloux, a computational biologist at University College London, told the aforementioned website.
Bloom also said that COVID-19 just can't keep increasing its number or chemical makeup of spike proteins to become more contagious. If it did, the virus would run the risk of not properly binding to human cells. Also, if future variants keep returning with altered spikes, the human body could gradually develop a natural immunity to different spikes that COVID-19 could have difficulty overcoming.
It's unrealistic to think that COVID-19 will ever completely go away, according to Balloux. It's more likely that it will continue causing outbreaks of different sizes, just like the flu and other common respiratory illnesses.
As such, COVID-19 is likely to reach one of several possible conclusions.
If more people get vaccinated, it could become nearly eradicated. But, considering anti-vaccination sentiment and the challenges of vaccinating rural populations in poorer countries, this is highly unlikely.
The population could eventually become so immune to COVID-19, through vaccinations and antibodies caused by previous infections, that the virus will mostly affect the very young. Even adults that contract it could end up developing very mild symptoms, due to childhood exposure.
COVID-19 could also turn into a seasonal epidemic, like the flu, with newly developed vaccinations and boosters needed to stop new variants. Naturally, some new variants will still evolve faster than the vaccines created to stop them.
While researchers suspect the last scenario is most likely, they say that the virus' continued evolution, perhaps into something far more infectious and deadly, depends on whether the virus has the chance to infect large numbers of people, changing in the human body before infecting others.
