The virus behind COVID-19 mutates and evades immunity. Here’s what that means

As COVID-19 approaches its fourth year, Omicron continues to mutate and become more resistant to immunity, health officials say.

In December, the World Health Organization said that variants derived from Omicron show more capacity to escape our immune system.

“Omicron, the latest worrisome variant, is the most transmissible variant we’ve seen so far, including all the sub-variants that are in circulation,” Maria Van Kerkhove, WHO’s technical lead for COVID-19, said on December 21.

Whether this is enough to spur new waves of infections depends on conditions such as the size and timing of previous Omicron waves, the regional immune landscape and the coverage of vaccinations against COVID-19, the UN Public Health Agency said.

In Canada, population-level differences in immunity and world trends suggest that cases of COVID-19 may increase in the New Year, health officials said last week.

But what does the mutation mean, what doesn’t it mean, and why does evading the immune system matter? Here are some answers based on what we know at this point in the pandemic.

What is a mutation?

A mutation is a change in the genetic code of the COVID-19 virus. Some mutations have no effect. Others lead to changes in proteins that can benefit the virus by making it more transmissible — the ability to pass from one person to another. Or the mutation could be harmful to the virus if your immune system gains an advantage over the pathogen.

The WHO notes that there are currently about 540 Omicron mutations, but only five are “under surveillance” for changes such as mutations or increases in prevalence.

The variants of anxiety show one or more traits compared to the original or legacy version of the virus:

  • It causes more severe disease.
  • Avoid or avoid current vaccines or treatments.

In particular, doctors and scientists are watching for mutations in the spike protein of the virus. This is what the virus uses to grab our cells and then enter them.

A Belgian scientist holds a magnified 3D model of a spike protein (blue) from the virus that causes COVID-19 bound to an antibody (red) in this 2021 photo. The coronavirus uses the spike protein to grab onto our cells. (Bart Beismans/Reuters)

Omicron’s BQ 1.1 subvariant is immunoresistant to the extent that antiviral treatment did not work, Dr. Teresa Tam, Canada’s chief public health officer, said in mid-December.

“We need to monitor the sensitivity of the virus to these drugs,” Tam said.

The genetic sequencing data also suggests that variants with greater immune system resistance are increasing, while BA.5, which dominated in the summer, is decreasing, Tam said.

At a minimum, that means COVID cases will decline more slowly with a higher plateau of infections and hospitalizations as the respiratory virus season winds down, she said.

How does immunity work?

From the virus’ perspective, McMaster University immunology professor Dawn Bowdish said if the virus allows our immune system to fight it off, then it’s game over for the microbe. To survive, progeny Omicron variants like BQ1.1 bypass our immune defenses.

The virus infects hosts to make copies of itself. In the process of using our cells as a virus factory, we get sick.

But not everyone who is exposed to the virus gets sick. As for why, think of the immune system as a medieval castle with various barriers, such as a wall surrounding the building, a moat, and then armed guards.

First, there is an outer wall that protects against invaders. For us, the main barrier to respiratory pathogens is the nose. In the case of COVID-19, what scientists call “mucosal immunity” is located in the nasal passages and pharynx, commonly called the throat.

When a virus approaches, our natural immune response tries to call for help.

“When they [Omicron subvariants] get into your nose, into your mouth, when you first inhale them, they have ways of turning off our natural antiviral immune responses,” said Bowdish, who holds the Canada Research Chair in Aging and Immunity.

After the virus passes through the first protective layer, the antibodies work. Antibodies are proteins that your immune system produces to help fight infection. They also work to protect you from getting sick from the same virus in the future.

Antibodies must “stick” to the virus to be effective, Bowdish said. Weeks after someone has been vaccinated, the immune system produces many antibodies. Even if they don’t stick as well, the sheer number will likely offer protection.

Female scientist in plain clothes.
Dawn Bowdish, an immunologist at McMaster University, says new variants of the virus that causes COVID-19 are good at hiding from antibodies. (Marci Cutler)

The trade-off is that it takes a lot of energy for us to make antibodies that wane or decline over weeks and months.

“In the context of Omicron, it’s well documented that the closer you are to your vaccine, the less likely you are to get the virus, because weeks after you’ve had your vaccine, your antibody levels are extremely high,” said Bowdish.

COVID can evade immunity

But SARS-CoV-2, the virus that causes COVID-19, has other ways to overcome antibody defenses.

“It’s also very good at hiding from these antibodies,” Bowdish said.

Because the Omicron subvariants evade the immune system’s capacity to fully control it, we are more susceptible to re-infections now than with the earlier variants, said Dr. Helen Dekaluwe, an immunologist and clinician scientist.

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Most Canadians were either infected or vaccinated,” said Decoluve, who is also an associate professor at the University of Montreal. “However, we cannot completely block transmission.”

Decalué said antibody levels are an important way to block transmission, but their levels also decline after the first infection.

“If you have your main series of two doses of vaccine and you have your booster with this third [dose]we can see in patients who have been infected [the combination] possibly leading to a better long-term memory of the infection,” she said.

This is because the body’s immune system has been exposed not only to the viral spike protein, but also to others that are important in protecting us from severe illness.

What happens when antibodies don’t protect us?

That’s what Decaluwe and her lab team are investigating: a T-cell response. T-cells, a type of white blood cell that help protect the body from infection, are like the armed guards hurling javelins against the COVID virus from the castle tower.

When antibodies fail to take care of the virus, T cells step in to prevent hospitalization and death from COVID-19 by targeting and destroying virus-infected cells. T-cells do not prevent infection, but they start working after the virus has penetrated.

A medical laboratory technician takes a blood sample for a serology test for COVID-19 on site at the British Columbia Disease Control Laboratory in Vancouver. Antibodies can be measured in a small blood sample, but T cells cannot. (Ben Nelms/CBC)

Dekaluve and her colleagues at the Coronavirus Variants Rapid Response Network (CoVaRR-Net) used whole blood samples from nearly 600 individuals and advanced technology to study T-cell responses.

Decalué said about half of the subjects continued to provide blood samples to help the researchers look at antibodies and other immune cells to determine the quality of their response.

Antibodies are made by another type of immune cell known as B cells.

When the immune defenses in the nose and antibodies are not effective enough to block the infection, then T cells and B cells enter the picture. One of the roles of B cells is to remember an invader to help produce antibodies when re-infected. It’s like the B-cells are armed with a most wanted poster to use their bow and arrows or catapults against Omicron.

Despite the benefits of the immune system and vaccinations, about 50 Canadians a week continue to die from COVID-19. Many of them are over 65 years old

Older people and those with immunocompromising conditions are at increased risk of severe COVID and need protective boosters the most, Decalué said.

Their vulnerability means that medical researchers must continue to monitor for increased immune protection.

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