Courtesy of Bailey Willett '20

Preventing pandemics | Willett’s research focuses on vaccines.

October 9, 2018

Student Spotlight on Bailey Willett ’20: Combating Antigenic Drift in Influenza Viruses

Print More

In 2009, the world saw the first influenza pandemic in more than forty years in the form of the H1N1 strain. Although response to this variant was fast and a vaccine quickly developed, the fight against influenza hasn’t ended. Bailey Willett ’20 continues to be a part of this fight as a Cornell undergraduate researcher working to combat the new strains of influenza that appear every year.

Willett works alongside graduate student David Buchholz in the Aguilar-Carreno Lab of Microbiology and Immunology doing research concerning antigenic drift, one of influenza’s greatest hidden weapons.

According to the Centers for Disease Control, antigenic drift is an abrupt change in the glycoprotein receptor makeup of the virus. Since the body’s antibodies recognize viruses by these glycoprotein receptors, antigenic drift can be highly dangerous in the hands of a rapidly developing virus like influenza, which can produce multiple new strains per year.

“There haven’t been as effective flu vaccines, just because how much antigenic shift there can be in influenza between the main glycoproteins, neuraminidase and hemagglutinin,” Willett said, referring to the main proteins associated with influenza.

This is also the reason why someone can contract the flu multiple times, or contract it after getting a flu shot, because the body can contract a strain of the virus which it hasn’t yet developed antibodies against.

Willett’s research involves the formation of virus-like particles, which have the glycoprotein receptors of a strain of the virus on the outside, but have none of the virus’ infectious properties, carried via genetic material contained inside it. Since it looks like a virus from the outside, the cells to which they are introduced will develop antibodies against them, without the risk of actually having an infection.

Willett is specifically looking at how to produce virus-like particles that use the neuraminidase glycoprotein instead of the hemagglutinin glycoprotein. According to Willett, she does this by producing the viral DNA in a bacterial culture and transfecting a specific type of cell found in human embryonic kidneys called 293 T cells with this DNA. After that it starts producing the virus-like particles with a specific glycoprotein makeup. They can then use these particles in live trials with mice to see how much of the virus is needed to induce a response from the mice’s immune system.

“Being able to see how little [of the vaccine] we would need is really important for vaccines because we don’t want to overexpose a human,” says Willett. “We want the highest amount of response we can get for immunity with the least amount that we can inject as part of the vaccine.”

Willett is also hoping that the mice trials can help with investigating the possibility of immunity using these virus-like particles, since these particles are fitted with multiple receptors which could possibly lead the immune system to develop antibodies to multiple strains at once with a single vaccine.

Willett’s research into influenza can also help with research into more rare diseases which are harder to model. One example is the Nipah virus, a highly virulent disease whose properties still remain murky. Although not much is known about it, the fact that it, like influenza, is respiratory disease and has the same structure, means that influenza research could very well contribute to our body of knowledge on these rarer diseases like Nipah and how to combat them.

Through her work, Willett hopes to provide insight into how the influenza vaccines of the future might protect against influenza pandemics, and ultimately protect generations of children and adults from the ever-changing influenza virus.