What’s the hold-up? “The difficulty is that those [flu] viruses don’t have the protein attachments that can actually attach to cells in the upper airway. They have to develop attachments to do that,” Schaffner says. So even if a virus were exhaled, it would need to lodge onto something in another person’s cells that are already prepared for it in the upper airway. “Since the virus doesn’t have attachment factors that can work in the upper airway, it’s very rare for it to go human to human, and then it almost always stops and doesn’t get to a third person,” Schaffner notes. Similarly for Ebola, the virus would have to develop attachments that would allow it to easily attach receptors in the upper respiratory pathway — something that neither it (nor any of its viral cousins) has been known to do in the wild.
And yet Ebola already spreads very easily without such mutations. The delicate lock-and-key protein–virus fit required for the virus to successfully latch onto and replicate in the airway has not developed because there is no evolutionary pressure for it to do so; it simply would not be an efficient option. Epidemiologists can take some comfort in that.
As the virus continues to circulate through west Africa, it may like any other pathogen continue to acquire genetic mutations. So far, however, there is no indication that Ebola is mutating in a way that could allow it to make the leap from becoming transmissible via contact with body fluids (as it is now) to become a germ that could be transmitted by breathing the same air, according to WHO. With Ebola, “I don’t think we have the information at this time to know what the real risk is but it is probably not zero,” says Ebola expert Thomas Geisbert, a virologist at The University of Texas Medical Branch at Galveston.