Four evolutionary scenarios of coronavirus causing Covid-19

MeIn the ongoing struggle between the SARS-CoV-2 gene and our wisdom, the virus that causes Covid-19 constantly investigates human defense with the new gene Gambit. New variants of this highly contagious coronavirus are emerging every few months, and this scenario may continue.

Some experts believe that pandemics appear to be on an evolutionary slide to becoming a “new normal” endemic disease in which humans and viruses coexist, as is currently done with influenza. .. But the coronavirus is smart. Although a unique solution may be visible, SARS-CoV-2 can shock humanity with a catastrophic evolutionary leap.

Here are four possible scenarios: Each is taken directly from a known scenario. Evolutionary playbook Of the coronavirus.

advertisement

Slide to fashion

Epidemic means “to people” (epi + demo). Endemic means “in people” (en + demo). I hope that Covid-19 will change from the former to the latter.

Humans are currently co-existing with four known endemic coronaviruses. Their scientific designations sound like technical codes: 229E, OC43, NL63, and HKU1. Almost everyone on earth It infects all four viruses in childhood. These infections tend to be mild and cause only transient upper respiratory tract infections, so they are a convenient abbreviation for the common cold coronavirus (CCC) of these four gangsters. Immunity to these coronaviruses declines over time, so infections can recur throughout human life.

advertisement

Where CCCs are hazy when they emerge, but genetic analysis probably suggests them Derived from various animal species Before interacting with humans hundreds of years ago. The origin of OC43’s ancestors may be bovine coronavirus. The nearest neighbor of the 229E is the Lama coronavirus.And others probably happened like this Interspecies jump From the vast global reservoir of bat coronavirus.

If the common cold coronavirus first appeared in humans from the cross-species jump of animal viruses before the pathogen theory and modern science of microbiology, they were probably mistaken for influenza and were not recognized as new diseases. Probably. The coronaviruses that make these species jump have adapted to humans, so there would have been selective pressure for more efficient transmission. When a virus adapts to a new host, there is no survival benefit by debilitating or killing that host. The exact opposite. Respiratory viruses are more easily transmitted by mobile, socially interacting hosts.

Just as the four common cold coronaviruses began as new epidemic viruses that evolved towards the epidemic, SARS-CoV-2 could follow the same path and become the fifth CCC.

Changes in illness and symptoms

In this scenario, SARS-CoV-2 evolves to infect and affect new cell types in the human body, from those that primarily infect and affect the respiratory system to those that infect and affect other organ systems. It will change. This scenario can lead to better or worse results, depending on the damaged organ and its extent.

Most animal coronaviruses, including SARS-CoV-2, Line the gastrointestinal tract Similar to what is in the airways. Mutations can switch the ability of a virus to multiply in cells of one organ system to cells of another organ system. In the pig A big shift has occurred When the transmissible gastroenteritis virus mutated into the porcine respiratory virus in 1984.In chickens, all strains of infectious bronchitis virus affect the trachea, but some mutant strains have emerged. Damage the kidneys..

In humans, SARS-CoV-2 Intestines, kidneys, central nervous system.. The new SARS-CoV-2 variant, redirected to prioritize new organs (organ tropism), can cause signs and symptoms of new Covid-19.

The emergence of a new recombinant coronavirus

Viruses such as influenza, HIV and coronavirus are routine Exchange genetic material Between strains. Combining the genetic material of human SARS-CoV-2 with the genetic material of existing animal coronaviruses (such as poultry, pigs, rodents, and even viruses endemic to dogs and cats) could create hybrids. there is. It causes a new pandemic, as it is known that occasional hybridization of the human and bird influenza virus causes a human influenza pandemic. When an animal cell happens to be co-infected with two different coronaviruses, recombination between the two parent chains can occur, resulting in a new hybrid genome that may have better replication than the parent.

There is Evidence already The SARS-CoV-2 strain is recombinated with another SARS-CoV-2 strain. Poultry coronavirus When Pig coronavirus It is a common problem in commercial livestock and Murine hepatitis virus A nasty infection commonly found in laboratory mouse colonies. Individuals infected with SARS-CoV-2, which are in close contact with animals infected with coronavirus, may easily serve as a host for the production of recombinant virus.

Considering a huge number of humans infected with SARS-CoV-2, someone on the planet is infected with SARS-CoV-2 and animal coronavirus at the same time, and some of its cells are infected with both, which is novel. It is likely to produce sex. Hybrid virus recombinant.

And considering the large number of SARS-CoV-2 genomes Human sewage systemCoronavirus-infected rodents or birds can encounter human SARS-CoV-2 through contact with human waste.

Regardless of where and how new recombinant progeny of SARS-CoV-2 develop, the new virus circumvents SARS-CoV-2 immunity and causes symptoms of disease different from those seen in Covid-19. It may even show.

Use of antibody

In this nasty scenario, SARS-CoV-2 evolves to not only avoid the immune response of the human host, but also actively utilize it. To date, a series of major variants of SARS-CoV-2 (alpha to omicron) have shown that continuous evolution of the virus helps evade the immune system. But some coronaviruses, Feline infectious peritonitis virusTake evasion to the next level: exploitation.

When a person (in this case a cat) encounters a virus or is vaccinated, immune cells begin to make antibodies. These proteins bind to the virus and nullify it.Paradoxically, antibodies against feline infectious peritonitis virus infused into non-immunized cats render animals. more More susceptible to peritonitis and serious illness than cats that have not been injected with anti-feline infectious peritonitis virus antibodies.

Similar terrible exploitation of the immune system is carried out by humans Infected with dengue virus, Not a coronavirus. The first infection with the dengue virus usually causes a self-limited week-long illness with high fever, myalgia, and joint pain. The antibody immune response to that initial infection immunizes a person against future exposure to the same type of dengue virus. However, if an individual is later exposed to another type of dengue virus, the initial infection increases the risk of serious illness rather than providing protection against it. How? In the human body, some cells have dengue virus receptors on their surface, while others have antibody receptors. Antibodies that bind to the virus usually prevent the virus from adhering to cells that have dengue receptors. However, viruses coated with these antibodies can instead bind to, invade, and multiply inside cells that have antibody receptors on their surface.This process is called Enhanced antibody dependence Of virus growth.

Other coronaviruses that infect humans, SARS-CoV-1 When MERS-CoVHas been shown in laboratory studies to utilize bound antibodies as a way to attach to cells and initiate intracellular replication. SARS-CoV-2 virus Also uses antibody-dependent enhancement effect It has been shown that it binds to cells at antibody receptors and the virus enters the cells and initiates replication. However, in previous experiments, the complete viral replication cycle was not completed in the test cells.

The concern here is that if SARS-CoV-2 evolves to increase viral growth and infection using antibody-dependent enhancement, new mutants will explode the spread throughout the immune population. Is possible.

Which scenario is it?

I’m not sure how the end of the pandemic will progress. I think the most likely future scenario for SARS-CoV-2 is that it will be endemic, but the other more annoying scenarios described here are within the scope of the possibilities. Or a variant that utilizes immunity. And these scenarios are not mutually exclusive. A new SARS-CoV-2 recombinant virus containing the animal coronavirus gene can cause disease changes.

It’s also worth considering some other scenarios that I haven’t discussed. For example, it can spread from human to animal and then to humans many times, and it can become more contagious from people who are chronically infected with “long Covid”.

None of these epidemic scenarios are illusions. These are all known evolutionary variations of the real-world coronavirus. New viral variants, such as SAR-CoV-2, can appear anywhere on Earth and cover the Earth in a matter of weeks. Indeed, somewhere on Earth, the SARS-CoV-2 strain may have already evolved in one or more of the directions I describe here, but it has not yet been detected.

The world cannot afford to be blind again. Pandemic planners in the United States, the World Health Organization, and other countries and organizations need to develop formal risk assessments and emergency response plans for the various potential pandemic futures.

Virus evolution requires continuous virus transmission and replication. The more new virus particles produced, the more likely it is that new virus variants and recombinants will emerge. Of course, preventing illness and death is a major goal around the world. However, countering the evolution of new subspecies viruses is another important mission. To do this, it is necessary to control SARS-CoV-2 replication by controlling human-to-human viral transmission.And this should happen everywhere on earth, not just in the United States

Technical and financial support to bring Infection prevention vaccine Donations to low- and middle-income countries are more than just charity.It’s an expression Enlightened public self-interest.. National security in the United States and all other nations depends on winning this global viral war.

Donald S. Burke is a professor of infectious disease epidemiology at the University of Pittsburgh Graduate School of Public Health and was previously the Dean of the Department.