On March 22, the World Health Organization announced that Omicron has become the dominant form of the submarine BA.2 SARS-CoV-2, the virus that causes global covid. BA.2 shares many genetic similarities with its close relative BA.1, which has led to a worldwide resurgence of COVID infections in recent months. But BA.2 is 30 percent to 50 percent more contagious than BA.1.
Now, as this latest version of SARS-CoV-2 fills the planet, epidemic-weary people everywhere are asking the same question: Is society destructive to face new viral forms one after another, more contagious than the last?
“We still don’t know the full potential of this virus and we’re going to be able to create a completely new form of it,” said Jeffrey Shaman, an infectious disease model at Columbia University’s School of Public Health. According to Shaman and other scientists, SARS-CoV-2 still has a lot of genetic information about how it infects human cells and skirts the immune system. New variations can emerge from the gradual change in the viral sequence. But heavily modified versions of SARS-CoV-2 that bear little resemblance to their predecessors “also came from blue,” said Ralph Barrick, a virologist at the University of North Carolina at Chapel Hill. “And if any of these variants are better at infecting cells or avoiding immunity than their predecessors, you’ll see an increased transmission over earlier strains.”
Omicron submarines were detected in South Africa at the same time last November. These new and dramatically different versions of SARS-CoV-2 shocked many scientists, who speculated that the next major variant would be increasingly descended from the Delta variant. BA.1 quickly surpassed Delta as the dominant strain in the world, while BA.2 lagged behind, “probably in a rural area where it had no initial chance of spreading,” said Bate Korber, a computational biologist who studied viral disease. At the Los Alamos National Laboratory in Mexico. But as BA.2 enters a larger, more interconnected community, “it starts to move faster.” As it has spread to other countries, BA.2 has exploded across Africa, Europe and Asia and is currently responsible for about 55 percent of all new SARS-CoV-2 infections in the United States, according to the Centers for Disease Control and Prevention.
In all possible cases, BA.1, BA.2, and a third omikron subvariant that has never evolved: BA.36 evolved during chronic infections in a small population of immune-compromised people. Stephen Griffin, a virologist at the University of Leeds School of Medicine in England, said repeated bounces among members of this population may have provided “a training ground for viruses” that allowed SARS-CoV-2 to be investigated and tested. New mutations that spread it more efficiently.
BA.1 has acquired 60 mutations not found in the ancestor SARS-CoV-2 that were first published in Wuhan, China. Among them, 32 genetic mutations are located exclusively in the iconic spike protein of the virus, which targets immune cells and vaccines. BA.2 shares many of the same mutations but has 28 unique genetic mutations of its own, including four spike proteins.
According to Barrick, Omicron is the first SARS-CoV-2 variant to be developed in response to increased immunity in the population – the result of vaccines and earlier infections with other forms of the virus. The earlier variants, alpha, beta, gamma, and delta, initially competed for dominance over how well they infect human cells and efficiently transit between humans. But Omicron has the added advantage of being able to resist the differences that have come before, resulting in an increase in the number of vulnerable people in the population. The difference in neutralizing the antibody response against Omicron, compared to previous variants, is “extensive,” Barik says. Neutral antibodies deviate SARS-CoV-2 from binding to ACE2 receptors, the entry point of the virus into human cells. “We’re talking about a 15- to 50-fold reduction in antibody levels, depending on who runs the ass and how recently you’ve been infected or increased,” Barik said.
Identifying mutations that allow Omicron to “escape” by neutralizing antibodies is now the focus of intense research. At least some mutations affect parts of the spike protein that bind to ACE2. In ancestral viruses, these mutations will interfere with the ability of the bacterium to infect. But Omicron seems to tolerate changes without losing the ability to bind to ACE2. As long as these mutations persist in the virus, “we can expect omicron-like forms to continue to emerge, primarily through increased internal infection rather than immunity,” said Ram Sasisekharan, a biological engineer at the Massachusetts Institute of Technology.
However, infectivity and immunity are also deeply involved and determining their respective roles in the spread of the virus is extremely challenging. This is especially true at the present stage of the epidemic. Dozens of vaccines have been deployed against SARS-CoV-2, and numerous forms of the virus have spread around the world. Infections and vaccines are contributing to an increase in immunity through a striking combination, Barik says, and “it’s becoming annoying and messy for the scientific community.”
Fortunately, the evidence so far indicates that the symptoms caused by BA.2 are not as severe as those caused by BA.1 in vaccinated individuals or those who have previously been infected with SARS-CoV-2, according to Shashishekharan.
BA.1 obviously won against Delta, largely because of its resistance. But to what extent does immunity from previous BA.1 infections protect against BA.2?
Preliminary evidence suggests that re-infection with BA.2 occurs after BA.1 but is rare. “If you’re infected with BA.1, you’ll probably be better protected from BA.2,” Griffin said. “But security is not complete.” Scientists have speculated that places where BA.1 has already reached high levels could avoid further growth of BA.2. The BA.1 peak in South Africa eroded rapidly last December, and BA.2 in that country is “not too much of a problem,” said Juliet Pulium, an epidemiologist who instructs the DSI-NRF Center of Excellence in Epidemiological Modeling and Analysis. Stellenbosch University in South Africa. “The number of our cases is currently very low.”
Experts are carefully tracking BA.2’s trajectory in the United States, where BA.1 also spread widely earlier this year. The incidence of covid in this country has dropped by 35 percent in recent weeks, even as BA.2 has become an influential strain. SARS-CoV-2 infections are on the rise in parts of the United States, including some northeastern states. But whether a national wave will follow is unknown. “We’re in a gray area right now,” Barik said.
Other factors also control BA.2 transmission: vaccine and booster coverage, public health prevention, and the average age of the population all play a role. The dramatic rise in BA.2 cases in Hong Kong has been attributed to the dilemma over vaccines among adults. John Moore, a virologist at Cornell University’s Weill Cornell Medicine College, believes that the relaxation of covid restrictions has led to an increase in BA.2 in European countries and the United Kingdom. “The governments of those countries, especially in the United Kingdom, have said that ‘the covid is over; “Let’s party,” she says. “It’s all a highly contagious variant.”
If there is a silver lining to the successors of the more transmissible variants, it is that they are evolving in tandem with the resistance of the population. Each new variant may cause fewer deaths because more people are able to prevent infections and serious diseases. However, Shaman points out that SARS-CoV-2 is far more responsible for changes than other respiratory viruses we have learned to live with. The contagiousness of the new SARS-CoV-2 variant should eventually hit a plateau, just like the coronaviruses that cause the common cold. But in the meantime, “we don’t know what the next decade will be like with this virus,” Shaman said. “So we have to keep an eye on it.”