Being down with the flu is a common letdown that bars people from doing their daily activities and attending to important events. While drinking water, getting lots of rest and antivirals help, people can't help but wonder why flu viruses just keep on coming back. A new study was finally able to identify the reason: these viruses perform hijacking tactics during the infection process.
Researchers from Imperial College London found how flu viruses seize control of the cell machinery when they infect the body. The discovery is said to be a stepping stone toward developing more effective antiviral treatments.
Senior author of the study Wendy Barclay said that all human flu viruses originated from birds. Humans are lucky because these viruses cannot clone themselves inside the body and thus cannot be transferred instantly from birds to people.
How do people get infected with flu viruses then?
When the virus mutates in numerous ways, it changes features and is finally able to enter the human cell to replicate inside via some form of a hijacking process. Once this invasion becomes successful, illness occurs.
"Up until now, we haven't understood why the bird flu virus has to change in order to hijack the human cell machinery," said Barclay. "Our research showed this is all due to a cell protein called ANP32A."
ANP32A is a protein found in mammalian cells that acts as an accomplice in the infective process. The protein helps the virus form copies of itself once it gets inside the host cell. ANP32A does not serve any function for bird flu viruses unless it has a particular mutation.
To be able to single out the "hijacker," the researchers used both mammalian (hamster) and bird (chicken) species in an experiment. They particularly studied hamster cells that have traces of chicken DNA in them and tested whether the virus would be able to replicate inside.
With the understanding that bird flu viruses cannot normally infect mammalian cells, the researchers figured out that any hamster cell that would allow a virus to replicate inside it must contain the culprit.
After identifying which hamster cells allowed the virus to replicate, the experts determined which chicken genes exist in the mammalian cells to finally detect the protein.
The researchers found that the same protein also exists in birds, only the mammalian version is shorter. This is why bird flu viruses cannot just use the mammalian protein to infect the body unless they adapt to its length through mutation.
Additional investigation also confirmed that ANP32A also plays a vital role in seasonal flu viruses that replicate in human cells.
Now, the researchers are keen to develop more effective antiviral treatments based on their study findings.
"Our experiments also showed that removing this host protein from cells stopped virus infection, suggesting it is very important for the virus," said lead author Jason Long. The next step is to study therapies that may hinder this particular virus-cell interaction, which may subsequently stop viral attacks.
Pandemics and seasonal flu viruses affect about 800 million individuals every year. Being able to develop more effective treatments may help alleviate this global health problem and provide comfort to millions of people.
The study was published in the journal Nature on Thursday, Jan. 7.
