Of course, you know alpha, beta and delta (Prince style, the virus formerly known as B.1.617.2).
But do you know the delta AY? And what about epsilon, gamma, iota, lambda, mu and theta? All of these variants of SARS-CoV-2 have been registered in Southern California, and dozens more versions of the virus are circulating around the world, vying for world domination, like tiny Doctor Evil in the Austin Powers film.
So what happened to the “original” virus? The very first to jump out of bats or laboratories – or elsewhere – into humans who were immunologically powerless against it, ultimately leading to nearly 5 million deaths and virtually halting the global economy?
Gone are “on the path of dinosaurs, at least humans,” said Dr. George Rutherford, professor of epidemiology and biostatistics at the University of California, San Francisco.
“It has been moved. “Out of the way of newer, more competitive strains,” said Andrew Neumer, an epidemiologist and demographer at the University of California, Irvine, who studies infectious diseases.
However, according to Neumer, no one can say with 100% certainty that he disappeared. And Rutherford adds this caveat:
“God knows what happens to bats.”
Welcome to this friendly tutorial on viral mutation and why your life can depend on it.
The researchers say SARS-CoV-2, discovered in Wuhan, China, in 2019 most likely was not original. And the version that swept across the US in the fall of 2020 was already a mutation of the Wuhan version. And the one that swept the United States this summer was different.
Scientists have documented many versions of the virus that causes COVID-19 around the world, and through genetic sequencing, they can pinpoint which ones are circulating. Sometimes these genetic changes don’t matter much. They sometimes make the virus much better at infecting people or avoiding treatment, and therefore more dangerous.
The US Centers for Disease Control and Prevention lists only the highly infectious delta lines B.1.617.2 and AY as “options of concern” here in the US, while the World Health Organization also includes alpha, beta, and gamma in their “options of concern” “.
Watching the coming mutants? WHO monitors lambda and mu.
Once in viral time
Scientists foresaw this.
Michael Buchmeier, an infectious disease researcher at the UCI who has been studying coronaviruses for decades, takes us roughly 20 years back to the original strain that caused the SARS-1 outbreak in 2002-2003.
At that time, only 12 other animal or human coronaviruses were known.
SARS-1 likely originated when two or more strains of bat coronaviruses combined and switched to palm civets, a masked animal that resembles a raccoon and is widely sold in live animal markets across Asia, he said. There, the virus was amplified and adapted and eventually infected people. It has spread widely in China, Hong Kong, Taiwan and Canada due to travel.
The mortality rate was 10%; for people over 50 years old – about 50%.
However, there is a key difference between SARS-1 and SARS-2: SARS-1 infections have, in fact, always been symptomatic, making it much easier to identify and contain outbreaks. SARS-2 can be transmitted by people without symptoms, so it is much more difficult to stop it.
So where is this virus now?
“SARS-1 as a unique pathogen appears to be ‘extinct’ in nature, but the conditions that gave rise to it still exist,” Buchmeier said.
“That is, the presence of coronaviruses, which are present in wild bats, especially the horseshoe bats common in South Asia and China, and the maintenance of suitable amplifying hosts such as the civet, the raccoon dog, and now the pangolin and possibly others are able to adapt a virus to infect people more easily. “
Hundreds of viruses have been isolated from bats in Asia and around the world, he said, many of them coronaviruses that can recombine into dangerous pathogens.
An article in Clinical Microbiology Reviews published in 2007 warned: “It is well known that coronaviruses undergo genetic recombination, which can lead to new genotypes and outbreaks. The large reservoir of SARS-CoV viruses in horseshoe bats, along with the culture of eating exotic mammals in southern China, is a ticking time bomb. The possibility of SARS and other new viruses re-emerging in animals or in laboratories, and therefore the need for preparedness, cannot be ignored. ”
In 2015, another article published in the journal Nature warned of “the potential risk of SARS-CoV re-emergence due to viruses that are currently circulating in bat populations.”
So here we are. The exact origin of the virus that triggered the COVID-19 pandemic is still an official mystery and can always be so. In addition to the widespread theory of the bat market and wet market, there are suspicions that the virus may have leaked from a laboratory in Wuhan. WHO has appointed a new 25-member scientific advisory group on the origin of new pathogens with scientists from around the world to try to figure out this part.
Genetic flexibility is the superpower of the RNA virus.
“This flexibility leads to the creation of a swarm of related viral ‘offspring’ at each stage of replication, allowing the virus to select the genetic pattern most suitable for a given host, in the form of the variant viruses that we now face,” Buchmeier said in a recent explanation.
“Mutations are always present in the offspring of viruses and can be selected if there is an advantage offered to replicate in a new host species.”
The alpha variant, which was discovered in the UK last year, was far more contagious than earlier versions. And alpha spawned beta, gamma and delta variants. Delta, as we know from summer tides, is about twice as contagious as alpha.
How did Delta do it? It is adapted to produce 1,000 times more virus in the nasal passages and upper respiratory tract in the early stages of infection, when people may not show symptoms.
This has two obvious advantages from the point of view of the virus: droplets from a person’s upper respiratory tract — say, when sneezing — will spew much more virus into the air to find new hosts; According to Buchmeier, the human immune response in the upper respiratory tract is not as robust as in the lower respiratory tract.
This combination results in many asymptomatic carriers who then transmit the infection to others.
So far, the options don’t appear to have diminished the effectiveness of the vaccines, but they have reduced the effectiveness of the treatment.
According to the California Department of Health, gamma, beta, kappa, mu, and zeta variants may be moderately less susceptible to some antibody treatments, while iota is significantly less sensitive to some antibody treatments.
Meanwhile, epsilon appears to result in a 20% increase in transmission with a significant decrease in the effectiveness of some antibody treatments.
Mutation of the nation
Each new infection is a new opportunity for the virus to mutate into something else. Maybe something less troublesome. Maybe something more troublesome.
“In the coming winter wave, my concern is not so much the options, but rather that we need more vaccinated people,” said Neumer of the UCI. “Seventy-five percent is not enough to protect certain age groups.”
Vaccination does not prevent infection, but it is very protective against serious illness, hospitalization and death, even in the highly contagious delta variant.
“It is clear that as long as the vaccination of the population remains incomplete and there is no clearly effective social distancing and camouflage, we are likely to see more waves,” Buchmeier said.
Does SARS-CoV-2 mutate into something more deadly? Crystal balls are cloudy, but many experts don’t expect this. However, they expect it to remain in circulation as part of the “human virome” – the cumulative collection of viruses within and on the human body – for a very, very long time.
Viral variants will continue to appear, and some of them may be more capable of spreading.
But even if we eventually come to terms with this virus – as we did with the flu – threats loom. Buchmeier said the predecessors of SARS-CoV-1 and SARS-CoV-2 remain in bats and could serve as a reservoir for future cycles of human infection.