New Hampshire may have just exited another severe flu season, but fresh research from the University of Vermont may have unlocked the possibilities of new ways to prevent or treat the common viral disease.
Dr. Emily Bruce, assistant professor of microbiology and molecular genetics at UVM who led the team doing the research, said the aim was to better understand how influenza viruses infect cells.
“I describe [viruses] to my kids as pirates that have to hijack a pirate ship in order to get where they’re going and do what they want to do, but they don’t have a ship of their own,” she said.
In this analogy, the pirate ship is the human cell. Viruses need to hijack the cells of a host so that they can replicate and reproduce, because they lack the biological machinery to do so on their own.
When someone has the flu, that means that a strain of the influenza virus has entered their body and found a way to get inside some cells. There, the virus takes over the cell to replicate itself, and then exits the cell to float around and find more cells to take over, and so on.
The human body has an immune system that activates and fights back against the virus with white blood cells and antibodies, but this conflict is what generates the physical symptoms of the illness, like a stuffy nose or a fever.
Bruce and her team studied the methods that viruses use to gain entry into our cells. She said viruses use something similar to a lock-and-key style method, where viruses have a “key” on their surface which allows them to enter any cell that has a matching “lock” on the cell surface. This lock and key match is one of the major factors determining whether a virus can get into and infect a certain cell.
For a long time, scientists thought that on a general level, many types of cells had a lock on their surface that was broadly used by many different types of flu viruses — a molecule called a sialic acid.
But it turns out, that’s not true. Bruce studied the two most common strains of flu that circulate through humans during flu season: subtypes H1N1 and H3N2. Her team found that the two strains of influenza A infected human cells in two different ways, with H3N2 viruses requiring something more specific than just sialic acids to enter cells.
“That was really surprising to us because we were operating under the assumption that all of the influenza viruses went in the same way,” Bruce said. “The data we have now shows that it is some specific receptor that is being used by one of those two kinds of flu that circulate every year.”
The next steps for Bruce’s research team is to figure out exactly which specific molecule is needed for the virus to hijack cells, but this new insight into how different types of flu attack our cells opens the door to the possibility of new preventative methods and treatments.
“One of the reasons that it’s hard to target that step of viral entry is that sialic acids are on so many things, and they’re expressed so broadly that it’s something hard to block,” Bruce said. “But if it turns out that these H3N2 viruses enter through a very specific mechanism, it’s possible that maybe that thing is something that you can target with a drug without as many side effects, or maybe it leads to some other piece of information that we don’t understand yet that lets us design a better strategy.”
More research is necessary before any applicable clinical research changes the way doctors treat the flu, Bruce said. Yet, the possibilities of where influenza prevention and treatment could go are vast.
