“Conversations” Editor’s Note: Omicron Editions SARS-CoV-2virus that causes COVID-19, has led to a rapid increase in cases globally. We asked a team of virologists and immunologists from the University of Colorado Boulder to consider some of the most important questions people are asking about the new version.
How is Omicron different from the previous variants?
There are two major differences between Omicron and the previous variant of the SARS-CoV-2 virus that surfaced in late 2019. Preliminary data suggest that omicron cases are milder than infections caused by the delta variant. On the other hand, the Omicron is far more transmissible than the previous variant – which means it spreads easily. It can be confusing to think about the overall effects of a mild virus that is also far more contagious.
When the Delta version became the dominant and displaced Alpha in the summer of 2021, it managed to do so because it was 40% to 60% more permeable. Now, the Omicron version is even more permeable than Delta.
It is difficult to tell by numbers how one type is intrinsically more permeable than another, as human behavior and vaccination percentages are in constant flux. Those factors, along with transmission, affect how the virus fares in a population.
Compared to the original strain of SARS-CoV-2, Omicron has 72 mutations throughout its genome. Some of these mutations are responsible for the complex new characteristics that characterize this type. Half of those changes occur in the spike protein, the important surface protein that enables the virus to take hold of and infect cells. It is also the major virus trait that is recognized by the human immune system.
Why is Omicron spreading so fast?
Preliminary studies suggest that Omicron is more effective at reproducing in the upper airways, including the nose, throat, and mouth, than earlier types, which makes it more similar to a common cold virus. If the data from these initial studies hold true, it could help explain Omron’s higher transmittance: viruses that replicate in the upper airway can spread more easily, although the reasons for this are not fully understood.
In addition, the omicron is often able to evade existing immunity to initiate infection, cause symptoms, and pass on to the next person. This explains why re-infection and vaccine breakthrough infections with Omicron appear to be more common.
Those qualities, and the timing of such emergence during the holiday season, resulted in an extraordinary increase in COVID-19 infections in the US, add to the winter time – which brought people indoors – as well as the fatigue of the pandemic, And you have the perfect storm for fast transmission.
The good news is that vaccinations and vaccine boosters nevertheless provide good protection against serious illness and hospitalization. But given the current number of cases, that means a lot of illnesses, hospitalizations and deaths in the coming weeks.
Could Omicron move the population closer to herd immunity?
Herd immunity occurs when enough people have immunity to the virus that it no longer spreads well. This is possible only when two conditions are met. First, a large proportion of the population must be vaccinated or recover from a prior infection. Second, vaccination or prior infection should provide sufficient immunity to prevent or slow down future infections. Will vaccination campaigns, coupled with widespread Omicron infection, be enough to bring about herd immunity?
Three issues complicate the hope of achieving long-term herd immunity after Omicron. The first is that immunity naturally decreases over time, whether it comes from a vaccine or a prior infection. It is not yet clear how long immunity remains after infection or vaccination with the virus, as SARS-CoV-2 has been infecting humans for only two years. Eventually, controlled studies will be able to determine this.
Second, children under the age of 5 are not yet eligible for COVID-19 vaccines, and new susceptible children are born every day. Therefore, until people of all age groups become eligible for vaccination, transmission among children will continue.
And third, we cannot rule out that newer versions may evade existing immunity. As Omicron has shown, infection with one variant does not guarantee protection from infection by future variants.
Together, these three factors suggest that even if a large proportion of the population recovers from Omicron, long-term herd immunity is unlikely. This is why humans never acquire long-lasting herd immunity to influenza and have to get a new flu vaccine every year.
It is important to remember that, as with all types so far, the vast majority of people hospitalized for COVID-19 have not been vaccinated. This suggests that vaccines are an effective tool for reducing disease severity and may also be beneficial against new forms.
Where do new variants like Omicron come from?
When viruses make more copies of themselves inside human cells, they make mistakes in that process — mutations — that alter their genetic code. Most of these mutations would not be beneficial to the virus. However, in some instances, a virus hits the jackpot of one or more beneficial mutations that promote its spread through a population. The alpha version has certain mutations in the spike protein that make it easier for the virus to infect cells. The delta variant contained additional mutations that improved viral spread. Omicron, with its staggering number of mutations, is a true oddity. It is rare for a coronavirus to rapidly accumulate so many mutations in its genome.
The origins of Omicron are still poorly understood. A prevailing theory is that an immunocompromised person was infected with a coronavirus for an extended period, leading to accelerated viral development. Another theory speculates that Omicron may have evolved into another animal species and then reinfected humans. Alternatively, Omicron could have evolved more slowly at a site with poor sequencing monitoring. There is still much that needs to be understood about the factors that led to the emergence of this highly mutated variant.
Could Omicron mutate to become more lethal?
The variants that have increased in prominence have done so because they contain mutations beneficial to the coronavirus. We are essentially watching Darwinian evolution – survival of the fittest – in real time. Variants with beneficial mutations, such as those that survive antibodies or shorter incubation periods, are increasingly displacing their less fit predecessors.
The most important thing to remember about the evolution of viruses is that natural selection favors forms that propagate better than other types. The good news is that more pathogenic – or dangerous – variants are less likely to spread well. This is because individuals who feel particularly ill tend to self-isolate naturally, reducing the chances of transmission of the virus.
Also the good news is that, because one type of infection provides partial immunity to the others, the rapid spread of omicrons has led to a rapid decline in the delta.
At this point it is expected that the widely spread all-new variant – the so-called form of concern – will remain highly transmissible.
What about the buzz about ‘Deltakron’ and ‘Flurona’?
In early January 2022, researchers in Cyprus reported cases of COVID-19 infection involving sequences of both omicron and delta, referred to as “deltakron”. However, other scientists are speculating that it is nothing more than a laboratory contaminant – an omicron sample contaminated with Delta. While more details are needed, as of now, there is no cause for alarm over this potential hybrid as it is not commonly observed.
And in recent weeks the term “flurona” has emerged, referring to a person who is infected with both the influenza virus and the coronavirus at the same time. While rare, such conditions do occur, and it is important that you reduce your risk by getting both the influenza and COVID-19 vaccines. But it is important to note that fluorona is not a new combination of the flu and coronavirus genomes, making the term a bit inaccurate.
- Sarah Sawyer – Professor of Molecular, Cellular and Developmental Biology, University of Colorado Boulder
- Arturo Barbachano-Guerrero – Postdoctoral Fellow in Virology, University of Colorado Boulder
- Cody Warren – Postdoctoral Fellow in Virology and Immunology, University of Colorado Boulder
This article was first published in The Conversation.