Answering big questions about the new flu and SARS-CoV-2 viral variants

An immunology perspective on the influenza "subclade K" variant and the SARS-CoV-2 "Cicada" variant

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Madeline McCurry-Schmidt

Science Writer

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A colorized microscopy image showing influenza virus in orange, with a teal background. The virus looks like roundish blobs.
Colorized transmission electron micrograph of influenza A virus particles, colorized gold, isolated from a patient sample and then propagated in cell culture. Credit: NIAID

LA JOLLA, CA—We’re keeping an eye on new influenza and SARS-CoV-2 viral variants. Here’s what we know about those viruses—and your immune system’s ability to fight back.

What is the influenza “subclade K” variant?

According to the U.S. Centers for Disease Control and Prevention (CDC), the majority of influenza cases this flu season appear to have been caused by a mutated form of influenza virus called the “subclade K” variant. This trend has raised concerns that we might be dealing with a more infectious or severe form of influenza, or a “super flu.”

Fortunately, there’s no evidence that this influenza variant poses an increased risk to public health. 

The flu remains a very serious disease for many people, especially infants and the elderly; however, CDC data show that the spread of the subclade K variant has not resulted in more severe cases or deaths than other recent flu seasons.

Where did this new influenza variant come from?

Influenza virus spreads through the body by making many, many copies of itself. Each time the virus copies itself, there’s a small chance that the virus’s genetic sequence could include an error—a mutation. 

Tens of millions of people are infected with influenza virus each year in the United States alone. This means influenza virus has many opportunities to mutate as it spreads through a population. 

Over time, a virus can accumulate enough mutations that it starts to look a little different from its ancestors. Scientists call this phenomenon “viral drift.” Annual flu shots are designed to help our immune cells keep up with viral drift.

The subclade K variant is the result of viral drift. The label “subclade” means the virus is simply a member of the influenza A (H3N2) subgroup, a common seasonal influenza virus.

Not a “super flu”

Microscopy images showing influenza viruses and a nearby cell in shades of blue.
Electron micrograph of 1918 H1N1 influenza virus particles near a cell. Credit: NIAID

Our immune cells can recognize influenza subclade K variant, explains La Jolla Institute for Immunology (LJI) Professor Alessandro Sette, Dr.Biol.Sci. “We’re seeing a drift here, not a shift,” says Sette. “The impact is much more limited.”

A “shift” comes when we encounter an unfamiliar viral subgroup (not a subclade). For example, the 1918-1920 influenza pandemic was caused by an H1N1 “avian” influenza virus. The H1N1 subtype had more significant mutations, and these mutations helped it evade human antibodies and immune cells.

In contrast, many people today have already experienced an influenza A (H3N2) infection at some point in their lives. Annual vaccines also provide immunity against influenza A (H3N2) viruses. 

This year’s annual flu shot even helped immune cells fight the influenza subclade K variant. In a study published in March 2026, scientists reported that the 2025–2026 seasonal influenza vaccine prompted many individuals to produce antibodies that recognized the subclade K variant.

You are protected by an ‘immunity wall’

It’s important to remember that vaccinated people can still get sick. Vaccines save lives by dramatically reducing the risk that an infection will turn into a life-threatening illness.

“If you have a new viral variant and you experience mild symptomatology, that doesn’t mean that the vaccine doesn’t work,” says LJI Research Assistant Professor Alba Grifoni, Ph.D. “The vaccine was designed to prevent you from having to go to the hospital.”

“The immune system has multiple ways to combat infection,” adds Sette. “Even if a virus escapes our antibodies and causes infection, our immunity wall protects us from severe disease.”

This “immunity wall” includes hard-working T cells, which recognize infected cells and destroy them. “T cells can limit infection and limit severe disease,” Sette says.

What is the SARS-CoV-2 “Cicada” variant?

This transmission electron microscope image shows SARS-CoV-2—also known as 2019-nCoV, the virus that causes COVID-19. Virus particles are shown emerging from the surface of a cell cultured in the lab. The spikes on the outer edge of the virus particles give coronaviruses their name, crown-like. Image captured and colorized at Rocky Mountain Laboratories in Hamilton, Montana. Credit: NIAID

In 2024, researchers in South Africa discovered a variant of SARS-CoV-2, the virus that causes COVID-19. This viral variant has been detected in the United States more frequently in the last several months. 

This variant is called SARS-CoV-2 variant BA.3.2, or the “Cicada” variant. Like the subclade K variant, the SARS-CoV-2 variant BA.3.2 is not a new kind of virus. 

This viral variant is a “sublineage,” or a mutated form, of the SARS-CoV-2 Omicron variant. And just like with the subclade K variant, mutations do not equal danger. According to the Global Virus Network, the SARS-CoV-2 variant BA.3.2 poses “no cause for concern.” 

Scientists have found that some of the new mutations on SARS-CoV-2 variant BA.3.2 may allow the virus to escape our antibody defenses. Fortunately, T cells can still recognize the viral infection and step in to prevent severe disease. “T cells are more flexible,” says Grifoni.

The immune system continues to evolve

As viruses mutate, our immune cells evolve to fight back. 

Since 2020, Grifoni, Sette, and LJI Professor Shane Crotty, Ph.D., have published a series of critical studies showing that COVID-19 vaccines—and natural infections—can prompt the body to produce a very special type of T cells. These T cells are “cross-reactive,” which means they can recognize the structural details that different coronaviruses have in common. 

In a 2024 study, LJI scientists showed the immune system’s B cells can also develop the ability to produce “cross-reactive” antibodies against multiple SARS-CoV-2 variants.

And our immune cells never stop learning. Grifoni’s research also suggests that T cells continue to hone their responses to SARS-CoV-2 year after year. “We predicted that every time you have a new variant—because you get exposed to a previous SARS-CoV-2 variant—you are generating a response that is going to help you,” says Grifoni.

How scientists prepare for future outbreaks

Scientists need to monitor emerging viruses and viral variants, even when these pathogens don’t pose a high risk to human health. 

A healthy immune system can fight the current influenza and SARS-CoV-2 variants, but many people are still vulnerable. Infants, the elderly, people with autoimmune disease, and many other conditions can develop severe disease after exposure to these viruses. “The immunocompromised are an exception, because their immune systems don’t work the way you would expect,” says Grifoni.

Every day, LJI scientists work to keep us all healthy. Their goal is to help us fight back—quickly—should we encounter a newly emerged virus or a viral variant of concern.

Grifoni and Sette have received funding from the National Institutes of Health’s National Institute of Allergy and Infectious Diseases (NIAID) and from the Coalition for Epidemic Preparedness (CEPI) to pursue “universal” vaccines. These vaccines would prepare the immune system to fight entire viral families.

For example, LJI studies suggest a “pan-coronavirus” vaccine could harness cross-reactive T cells to combat many SARS-CoV-2 variants at once, as well as any related coronaviruses that might emerge in the future.

Vaccine innovation on the horizon

LJI scientists are also taking a closer look at how we administer vaccines. Crotty is studying how intranasal vaccines (given through a puff of mist in the nose) can help us build stronger immune cell protection.

This is a brand new field of immunology. In 2024, the Crotty Lab was the first to show it is possible to measure immune responses in the nasal passages, using a deep swabbing method that captures hidden immune cells in the tissues above the throat.

Using this method, Crotty and his colleagues have found that our upper airways are home to armies of virus-fighting B cells and T cells. Their new research suggests intranasal vaccines could train these protective immune cells to fight respiratory viruses, such as influenza and SARS-CoV-2, before these viruses can reach the lungs.

“It would be a real innovation to make vaccines that work in the tissues where these infections happen,” says Crotty.

Learn more:

LJI Center for Vaccine Innovation

About La Jolla Institute

La Jolla Institute for Immunology (LJI) was founded in 1988 as an independent, nonprofit research organization. LJI is based in San Diego, CA, and is home to world-class scientists solely focused on immunology. LJI scientists are harnessing the power of the immune system to defeat cancer, autoimmune, infectious, and neurodegenerative diseases.

Our breakthroughs in immunology make life without disease possible. Visit lji.org for more information.

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