In order to aid in their adaptation to their new hosts, bird flu viruses may carry a small hint of home.
Typically, viruses only infect specific kinds of hosts. Many viruses that infect humans, for example, do not infect other species. However, influenza viruses frequently appear to spread from birds to other animals. The H1N1 “swine flu” spread from birds to pigs and then to humans in 2009, igniting a pandemic (SN: 12/18/09). As of right now, birds, marine mammals, and a few other animals are being affected by and dying from an outbreak of avian influenza worldwide (SN: 1/25/24). Nobody is certain if the flu virus will ever infect humans or if it will be able to spread quickly enough to start a pandemic.
Scientists were unsure of how the viruses invade the cells of other species, despite several reports of human infection with bird flu viruses. One of the initial stages that avian influenza viruses take to adapt and infect humans and other animals is revealed by a recent study.
Researchers at the Chinese Academy of Agricultural Sciences in Harbin and colleagues have found that avian influenza viruses tuck proteins that aid in reproduction inside their viral particles. According to a study published on January 31 in Science Advances, the reproductive aids known as ANP32 proteins may facilitate the spread of flu viruses from birds to mammals.
The discovery might make it easier for scientists to identify and forecast which flu viruses are most likely to start a pandemic.
Molecular virologist Wendy Barclay of Imperial College London explains that viruses “don’t carry everything with them that they need, and they just hijack things that are already inside the cell” in order to aid in their replication after they infect a host. Scientists were aware that the viruses have polymerases, which are basic reproduction machinery. However, that might not be sufficient to prove an infection.
To enable the invaders to swiftly replicate themselves, the viruses must seize control of host proteins. Among these are the ANP32 proteins, which facilitate the assembly of other proteins to build the polymerase copy machines.
Barclay, who was not involved in the experiment, argues that the modern flu virus needs this assistance in order to replicate itself inside any host cell quickly enough to avoid being overwhelmed by our immune system and shutting down.
Using electron microscopes to study avian influenza proteins within mammalian cells, the researchers discovered that certain virus particles included traces of bird ANP32. The researchers found that the protein is most likely bound to the viral polymerase and bundled into the viral particle with the rest of the replication machinery. More helper protein is integrated into viruses in proportion to the strength of the interaction between the polymerase and ANP32 proteins.
How avian influenza viruses, which differ from those of humans in terms of their ANP32 proteins, were able to cling to and utilize these proteins in human and other mammalian cells has long been a mystery. Scientists speculated that some flu viruses might already have alterations that would enable viral polymerases to interact with ANP32 proteins in mammals.
However, the current research indicates that flu viruses do not always need to bind human ANP32 proteins right away because they can pack their own bird versions of the proteins. Alternatively, the virus can replicate once inside a human or other animal cell using the avian ANP32 protein. According to Barclay, “this first foothold might allow the virus to replicate just enough to make a few mutations.”
The polymerase in birds may then be able to interact with ANP32 proteins in mammals as a result of some of those changes. The researchers discovered that when viruses carrying the bird version of ANP32 were produced in human cells or in mice, they were more likely to acquire such adaptive changes. “This clarifies how avian viruses—which ought to be incapable of proliferating in human cells—can actually do so and develop to engage with human ANP32,” says Ohio State University College of Medicine in Columbus viral immunologist Jacob Yount, who was not associated with the study.
According to Barclay, if the results hold up to additional research, scientists could be able to identify which viruses have a higher propensity to start a pandemic based on how strongly they interact with ANP32. “It’s possible that certain bird flu viruses are more adept than others at transferring the ANP from chickens or ducks into human cells.” “Those are the ones who enter and take hold more quickly than others who might have a weaker interaction, and they can proceed with their evolutionary process more readily.”
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