Some have begun to talk about the end of COVID-19 with new reductions in infection rates and vaccine deployments. But in my opinion, the rhetoric is not well thought out and premature. Based on what we currently know about SARS-CoV-2, it is no longer a problem months before the end of the pandemic, but a problem of years, if not decades. We need to plan it.
The virus exists to thrive. People who infect humans face an impressive set of defensive weapons, including not only our natural adaptive immunity, but also intelligently designed defenses such as vaccines, drugs and social control. In order for the virus to survive, it must be able to adapt to the ecological niche of choice (in this case, we) and allow more complex adaptations to overcome the best efforts in prevention and treatment.
Initially, many thought that coronaviruses in general, especially SARS-CoV-2, were more stable and difficult to adapt than other RNA viruses due to their error-prevention mechanism. But since then we have proven to be wrong.Last summer, Texas researchers found a mutant SARS-CoV-2 virus with a peaplomer-replaced virus. Overtaken the previous form To become the dominant stock. Since then, several new mutants have emerged with mutations that can make the virus more contagious. More deadly And can do more Avoid our immune defenses..
These varieties seem to have been forged in the fire we made ourselves. In Boston Middle-aged man I had been suffering from COVID-19 infection for 5 months before giving in to my illness. He was treated with immunosuppressive drugs when he became ill, and during his illness he received multiple additional treatments with remdesivir non-immunogamma globulin and monoclonal antibodies. Under this strong immune pressure, significant mutations in the virus emerged. Doctors and scientists who witnessed their birth called it “accelerated viral evolution.”
Other viruses, such as influenza, show that rapid evolution is possible as well when faced with our best defenses. In fact, based on what we have seen about SARS-CoV-2 and its mutagenic potential, I think this virus is much more like influenza than any other virus known so far.
In short, the evolutionary pathway of influenza may have important clues as to the path that COVID-19 follows.
As we know, influenza travels in seasonal waves in the northern and southern hemispheres. In the tropics, it occurs all year round and has only shallow peaks.This pattern mimics what we know Coronavirus that causes colds, Since its discovery in the 1960s, it has returned to infect us every year. In the case of influenza, antigenic drift (accumulation of small genetic changes in the virus) is the main explanation for recurrent seasonal epidemics. The predominant influenza strain is evolving year by year, and the immunity we develop in response to the old strain has only a modest effect on the new strain.We learned more these days Your immune system to the flu is also weakened and often disappears within a year, making you more susceptible to reinfection.
I used to believe that the coronavirus that causes the common cold is stable, that is, there is no antigenic drift, but it returns every year due to weakened immune protection.However, over the past year, a better understanding of the coronavirus has led to at least one of the cold-causing coronaviruses called the 229E. Receive continuous antigenic variation Similar to influenza.
SARS-CoV-2, like the 229E, has already shown that it can drift. However, it also shows that, like the flu, it can make far more rapid and substantial changes in itself. One way these major changes occur is when the virus jumps into a new population, for example from an animal to a human, or back again. When the virus makes this jump, the big things, and often the bad things, materialize. Both influenza and SARS-CoV-2 have huge animal reservoirs. Coronavirus infects all types of vertebrates, from whales and bats to salamanders and snakes.Influenza Similarly.. This means that both can evolve and cause even greater damage to our population. The outbreaks of the two previous coronaviruses began when the coronavirus surged from animals to humans, from civets in SARS in 2003, and from camels in MERS in 2012. 1918 influenza pandemic Probably started with a jump from an animal..
If you are lucky, SARS-CoV-2 will evolve like a 1918 virus called the “Spanish flu” and become less lethal. The 1918 flu virus receded after infecting an estimated 500 million people worldwide and killing at least 50 million. However, expecting this coronavirus to decay over time does not guarantee that it will decay. We already know that the coronavirus can be much more deadly. There is no need to look at anything other than SARS-CoV-1, which killed 50% of people over the age of 65, and MERS, which killed one in three infected people.
So where does it leave us?
First, we must accept the harsh truths of this virus and its variants. It may recur, but it may recur in the next few years. If it recurs, you need to be prepared for the possibility of being more deadly and contagious than the currently existing variants. Vaccine development pipelines and public health interventions need to be coordinated for urgent and future changes.COVID needs to be developed, similar to the one proposed for influenza Risk assessment tool This allows you to identify the viral properties of the dominant strain (infectivity and resistance to current drugs and vaccines) and align your public health response to the level of risk. Otherwise, we will be prepared for failure again.
I often liken SARS-CoV-2 to the mythical Proteus of the Homers Odyssey. Like Proteus, SARS-CoV-2 is a typical shape shifter that can change its shape at any time when grasped. The great hero Menelaus can only wrestle with Proteus with complete tenacity. If you claim victory too soon, you run the risk of losing the fight against this transforming virus. This tragedy is not a word, it kills millions more.
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