Should You Be Mortally Afraid of Viruses Mutating Into Airborne Forms?
What would it take for Ebola or any other virus that spreads through contact with bodily fluids to become airborne? This was a central talking point in 2014, when there was a debate about whether or not Ebola was about to make the leap and become an airborne pathogen. It’s a really scary thought to think that a mere sneeze could potentially sentence you to death. Of course, the story created paranoia amongst the members of the population. But how likely is it for a virus to become airborne, and is your time better spent worrying about meteors colliding with the Earth?
The Quest to Understand Viruses
I’ll begin by giving you a little background on what a virus is, because it’s important to understand what a virus is and how it replicates in order to understand how a virus could become airborne.
The discovery of viruses began in 1892 when the scientist Ivanoski noticed something peculiar one day. Ivanoski, who was experimenting with tobacco leaves infected with the tobacco mosaic virus, observed that after crushing infected tobacco leaves into an extract and passing it through a Chamberland filter-candle the extract still remained infectious.
This was a strange occurrence because the Chamberland filter-candle should have trapped all the bacteria that were in the extract. As important as this discovery was, Ivanoski would wrongly conclude that the source of the infection was a toxin because it appeared to be soluble.
Flash forward to 1898 when a scientist by the name of Beijerinck would prove in no uncertain terms that the infectious agent was not simply, very small bacteria. He placed the filtered, bacteria-free extract in agar gel and noticed that the infectious agent migrated, a feat that would be impossible for bacteria to accomplish. He would later name the agent 'contagium vivum fluidum' or contagious living fluid.
Humans would have to wait another 32 years when the electron microscope was invented before they could see with their own eyes what Ivanoski had stumbled upon so many years ago.
What is a Virus?
So, umm, when are you going to tell me what a virus is? Hold on just a sec, I’m getting there.
Basically, a virus is a piece of DNA or RNA that’s encapsulated by a protein coat and/or a lipid membrane. Viruses come in a variety of shapes and sizes, from spheres covered with spike-like protrusions to a shape oddly reminiscent of the Apollo lunar lander. Whether or not a virus is alive is a subject of debate amongst scientists, with some saying that it is while others don't believe it's alive in the truest sense of the word. The smallest virus particle has just enough genetic material to encode only four proteins while the largest can encode 100-200 proteins.
Infecting Cells 101
Viruses are incapable of reproducing by themselves, and it is for this reason that viruses cannot function outside a cell. So what does it do? It infects a cell and hijacks its DNA replication and protein synthesis machinery to reproduce new virus particles. They do this using one of two methods: the lytic cycle or the lysogenic cycle.
Both cycles begin with the virus particles attaching themselves, by way of proteins on their surfaces, to the receptors on the surface of their target cells followed by the insertion of their RNA or DNA into the host cell. Under normal circumstances, nutrients and cell-signaling molecules bind to these receptors, and both the receptor and the attached molecule are taken into the cell. Viruses trick host cells into granting them access by placing proteins on their surface that have shapes that are complementary to the binding site of their receptors.
Soon after gaining entry into the host, the virus unpacks its viral nucleic acid. The virus, unable to produce new virus particles on its own, elicits the help of the host DNA and protein synthesis machinery that then produces new virus nucleic acid and proteins. At this point, these molecules are lying freely in the cell cytoplasm like pieces of a puzzle yet to be put together. So the many pieces are assembled and packaged into a protein coat, and when they become too numerous for the cell to contain, the host cell bursts open, spilling the new virus particles into their surroundings.
Some viruses, however, are surrounded by a lipid membrane, one that is not synthesized when the host cell’s cellular machinery is hijacked. So what does it do? It rewards its host for its hospitality by stealing its cell membrane.
Yes, you heard that right; it actually steals the cell membrane. Once the viral nucleic acid and proteins assemble themselves, they move to the host’s cell membrane and make their escape. In the process of doing so, they take with them pieces of the cell’s membrane, which then surrounds the viral protein coat, and presto a new virus particle is born. Eventually, the constant departure of virus particles leaves the cell membrane less than stable and so the cells lyses and dies.
In order to not sound like a stuck record by repeating what was said before, I’ll just say that the virus attaches itself to the host cell and inserts its viral nucleic acid. But like a good sleeper agent the virus doesn’t attack at once. No, it inserts its viral nucleic acid into the host DNA where it remains dormant and waits, sometimes maybe for years, to be activated before it wreaks havoc on its host. All that time spent waiting and nothing really to show for it? Well, the wait isn’t exactly in vain, for you see, every time the host cell divides and its DNA is replicated the viral nucleic acid replicates alongside it.
So eventually when it does become active there are already many daughter cells with copies of the viral nucleic acid present, all ripe for the picking. So who are these sleeper agents? One such virus that utilizes this method of reproduction is HIV; it’s why persons infected with the virus can go years without displaying symptoms. Once activated, the viral nucleic acid excises itself from the host DNA and uses the cell’s machinery to make new viral DNA or RNA and proteins.
I have a feeling you know how the rest of the story goes, so can I move on? I’ll take that as a yes.
What Adaptations Would a Virus Need to Become Airborne?
The proteins on the surface of a virus have shapes that are complementary to the binding site of specific receptors. If those receptors aren’t present on the surface of a cell it cannot infect that cell. Since all cells don’t carry the same types of receptors on their surface, the types of cells a virus can infect is limited. We call this tropism or the determining factor that decides whether or not a virus is free to infect a cell.
Viruses that aren’t airborne would most likely not have a tropism for the cells that line the respiratory tract. Why is this significant? Because airborne viruses that spread from human to human or animal to animal do so when a new host inhales droplets that were left in the air or on the surface of an object after an infected host sneezed or coughed. And guess what’s in those droplets? Yes, you guessed right, virus particles. Where do they come from? Well, from the lining of the respiratory tract of an infected host that’s teeming with the little invaders. With this in mind, the first step a virus would have to take in order to become infectious as an airborne virus would be to change the structure of the proteins on its surface, so that it would be able to attach to the receptors of the cells that line the respiratory tract.
How would a virus go about changing its structure? The answer is easy: through a series of mutations. Mutations are the agents of change in a population. They provide the genetic diversity that’s necessary for natural selection to cause evolution. Note that those mutations are completely random, and they do not in themselves cause a species to evolve. It’s natural selection that decides which genes are carried across to the next generation. If a specific version of a gene confers an advantage to the organism that possesses it, then that gene will eventually become the most dominant version in the population. So what do we know about the way viruses mutate?
We know that mutations are introduced into the genome of a virus when there are errors in copying viral nucleic acid. And some viruses, RNA viruses, are more prone to errors during the replication process. Thus RNA viruses mutate at a much faster rate than DNA viruses. We also know that for a virus to change in a way that would allow it to infect cells of the respiratory system many mutations would be required. All of which would have to happen in a specific sequence, and since mutations happen randomly, the likelihood of these mutations occurring and occurring in the sequence that’s required is actually slim.
But let’s imagine that these mutations did happen, then what?
Well, the mutations would have to increase the survivability of the virus in comparison to the alternative in order for it to become the most dominant form. Viruses that are not airborne have evolved means of transmission that are already quite efficient, so the selective pressure for a virus to change its mode of transmission and become airborne is actually low. And those aren’t the only hurdles that must be overcome.
Due to an experiment that was done by Fouchier and Kawaoka, we know that even if a virus were to mutate and become airborne it could lose its ability to kill. To put it simply, there is a low probability that a virus would mutate and become airborne because so many things must go right for that to happen, and there is no evolutionary impetus for a virus to do that.