A micromechanics researcher in Canada used computer modeling to determine how virus size impacts replication rate.
In a paper published in the Journal of the Royal Society Interface, Dr. Mattia Bacca, an assistant professor at the University of British Columbia, proposes that the mechanism by which enveloped viruses like the coronavirus, influenza, hepatitis replicate tends to favor a certain size of virus particles. The findings could be useful in preparing for future pandemics.
“When a virus infiltrates a cell, it forms many copies of itself inside the cell,” says Bacca, whose expertise is the study of extremely tiny structures. “These virus copies assemble into several nuclei, around which the cell membrane starts to wrap itself, forming buds that stick out from the surface of the cell. Eventually the buds are expelled, becoming new virus progeny, ready to infect other cells.”
Spike proteins scattered across the cell surface play a key role in this process, says Bacca, who developed a simple mechanical model of how viruses replicate inside a cell. “They bend the cell membrane into a rounded shape that promotes the formation of the buds. This curvature ultimately controls the optimal size of the virus. Virus particles that are either too small or too large, compared to the optimum, will have a much higher energetic barrier to replication, and thus will take much longer to replicate. In some cases, they will not replicate at all.”
Bacca says the best size for efficient replication seems to be 60 nm to 100 nm in diameter for most viruses. This theory could also partly explain what makes certain viruses more infectious. “A virus could be highly infectious because it is very efficient in replicating,” Bacca says. “Since virus replication commonly takes 10 minutes, while infection takes less than a minute, replication efficiency is more than 10 times more impactful than infection efficiency, across the life cycle of a virus.”
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