Every morning Hector Aguillar-Carreno wakes up, greets his family and then descends the stairs to his basement to work. He’ll be there for several hours, give or take a meal break. He'll stay in that room with his childrens artwork and his monitor before him trying to lead his team to one of the most desired answers of our time: what will stop coronavirus?

Aguillar-Carreno is a professor in the School of Veterinary Medicine at Cornell University where he researches virology, glycoproteins, vaccines, antivirals and now the novel coronavirus. He and his team of 12 students have been studying the coronavirus since they received approval to research potential vaccines and antivirals in March. 

When the pandemic hit and forced New York into lockdown, Aguillar-Carreno said that he immediately sought out a permit for his team to keep working in their lab. Unfortunately, due to strict social-distancing guidelines, only four of them were granted access to the lab. They decided on having two graduate students, one post-doctoral student and a lab technician take over access to the lab with Aguillar-Carreno’s oversight via Zoom, while the rest conducted research outside.

Carreno said he hasn’t stepped foot in the lab since mid-March, but that hasn’t halted progress. Aguillar-Carreno’s days are full. Between individual and group meetings, overseeing lab work, discussing the progress of research, writing proposals for grants and filling out applications and teaching his two children, he said he averages at least 50 hours of labor a week, but he’s impassioned about the work.

Even before the pandemic had touched within the borders of the U.S., before the coronavirus that causes COVID-19 had exploded in any country for that matter, Aguillar-Carreno and his team were already working on a method to combat it, albeit in a different form. Before the pandemic, he and his team had been researching influenza in hopes of perfecting the efficiency of the regular flu vaccine. 

It wasn’t groundbreaking work. He described it as redesigning the wheel to include grooves; a minor adjustment that makes a noticeable difference when you want it to. Similarly, their improved approach is a method of killing the virus that would also preserve the protein structure of the virus. It was a method already used in vaccination development: deactivate the virus, implant it into a host and wait for the host to develop a natural immune response, but it wasn’t absolutely effective. 

By this point the concept of a virus is commonplace: a golf ball with about 25–30 flathead nails sticking out of it so that it resembles a cartoon porcupine, only with spikes not so randomly arranged. The arrangement of the spikes matters, said Aguillar-Carreno, and when one of the nails/spikes is damaged or broken it’s not the same, according to our bodies. 

 “The way the influenza virus is killed to be used in vaccines destroys the virus enough that it is no longer in an optimum condition to keep developing with, it’s broken down a little,” Aguillar-Carreno said. ”That’s why the vaccines we have against influenza right now are effective, but not fully effective. It doesn’t leave the virus in its native structure well-enough.” 

He said he has high hopes that the group’s method would be effective in developing a vaccine or drug against the COVID-19 virus, but he pointed out that it’s limited to only one viral strain at a time, which can slow progress.

“Viruses multiply rapidly, some more rapidly than others, like the coronavirus,” he said. He suggested that like the flu, the best option is another method he’s currently developing—a multivalent response that is capable of providing immunity against more than one virus at a time and focuses on “building” the virus, as opposed to “killing” it, which is the case in the first approach. 

In a recent study, the team experimented on hamsters to see if they could generate an immunity. They combined glycoproteins from nipah, hendra and ebola virus, each a zootropic virus transmitted by bats that have a high mortality when transmitted to humans, into one viral particle. This meant taking spikes from each of the individual viruses and arranging them together to create something relatively new. If it worked the hamsters would be immune against all three deadly viruses. The results that followed were successful: The hamsters demonstrated an immunity to the three viruses. Further plans for this research method are still way off into the future, said Aguillar-Carreno, but the team is feeling optimistic.

“We’re really excited about this method,” Aguillar-Carreno said. We’re hoping to do something similar with SARS and coronavirus, if we get the chance.”

He said although support is relatively slow, especially during years without a major health concern, he’s confident that the world should see an answer in the coming year.  

“I think it is possible that we will have something that works before 2021, but whatever it is will have to be mass produced and we must keep that in mind,” Aguillar-Carreno said. “If it is a drug it will be easier to mass produce, but if it is a vaccine it will be harder to mass produce because it has to be made for everyone.”

As for Aguillar-Carreno, in the morning when the sun rays creep across his floor, he will head back down to his basement to work; in the afternoon while his children are learning the elementaries of science, he will be on Zoom directing his assistants through lab activities; and then he will write down what they find and he’ll read through the latest data. And maybe they’ll save the world.