Why Don’t We Take Antivirals?
We take antibiotics for bacterial infections. Why aren’t we taking antivirals for the flu?
If we’re talking about total number of lives saved, antibiotics are likely one of the greatest discoveries ever made.
Since the first half of the twentieth century, when they were discovered (remember famous penicillin?), life expectancy has risen by nearly thirty years. The most common cause of death has shifted from communicable diseases (smallpox, typhoid fever, plague, tuberculosis) to non-communicable diseases (heart attack, stroke, diabetes, and cancer).
Much of this can be directly attributed to antibiotics.
An antibiotic is, to use simple terms, any substance that kills bacteria. Many antibiotics, like the penicillin compound that was the first discovered, are naturally produced by other creatures. (Penicillin is made naturally by Penicillium mold, used to kill bacteria so that the slower-growing mold could spread.)
These drugs can be lifesavers — if your illness is caused by a bacterium.
But what about diseases caused by viruses? Aside from the current COVID-19 global pandemic, we deal with plenty of other nasty viruses. HIV, influenza, and the common cold are all caused by viruses.
We do have a series of drugs called antivirals, which can be used to help prevent viral infections. But why aren’t these as common as antibiotics? Why do we go for vaccination instead of antiviral drugs?
Here’s how antivirals work, and why we don’t go to them as our first choice like we do with antibiotics.
It is Hard to Kill That Which is Already Dead
Bacteria are decidedly alive. They eat, they can reproduce through the exchange of genetic material, and they exhibit most other qualities of life.
Viruses, on the other hand? It’s a matter of open debate.
Viruses can only reproduce through hijacking of a cell’s machinery — they can’t make more copies of themselves on their own. This means that, if left to sit on their own, they’re pretty much inert. They don’t move, they don’t show metabolic activity, and they don’t make more copies of themselves.
This also makes them hard to kill.
Many antibiotics work by either attacking the cell wall of bacteria, or by interfering with their metabolism, blocking certain vital processes that the bacteria need to perform to reproduce. Break apart the cell wall, and the bacteria literally falls apart. Interrupt the processes that the bacterium needs to reproduce, and they’re literally stuck, like jamming s stick into the spokes of a bike.
But for viruses? They don’t have a cell wall, just a protein coat that surrounds their DNA instructions. They don’t have any metabolic processes to interrupt, since they use the machinery of their prey.
Instead, we have to use more specialized, more targeted approaches. We can’t just use a method that works on all viruses; we need to build more specific treatments that only work on specific types of viruses.
How We Kill Viruses
Viruses go through a set of stages when they infect a host:
- The virus attaches to a host cell.
- The virus releases its genetic material (DNA or RNA) into the host cell.
- The virus makes more copies of itself, using the cell’s own machinery.
- Those copies assemble into new viruses.
- The new viruses are released (or burst free) to spread to additional cells.
If we disrupt one or more of these stages, we can stop the spread of the virus.
We’ve found a few ways to do so, including:
- We can build specific proteins that bind to the outside of the virus’s shell, so that it can’t attach to (and infiltrate) host cells.
- We can interfere with the binding of the virus to host cells.
- We can block the virus’s shell from opening, even after they’ve attached to a host cell.
- We can block the activation of the genetic material inside the virus, so it can’t be used to make more copies of viral components.
- We can build pieces of cell machinery that will specifically cut viral sequences, chopping their genetic material into bits.
- We can target and specifically kill the host cells that have been hijacked by viruses, killing them before they can release their payload of new viruses.
These are all valid methods, for some viruses — but because the composition of different viruses varies so widely, a treatment that works on one type of virus won’t necessarily work on others.
This means that most antivirals are “one virus, one treatment” — they only work on the specific virus that they’re built to fight.
Are There Broad-Spectrum Antivirals?
For a bacterial infection, doctors may prescribe broad-spectrum antibiotics — that is, antibiotics with a mechanism that works on a wide range of different bacteria.
Are there, similarly, broad-spectrum antivirals?
There are a few. Most, with names like favipiravir, cidofovir, and ribavirin, work by targeting the viral polymerase, a specific viral protein that helps make copies of the viral genetic material. These treatments are “broad-spectrum” in that they work on multiple different classes of viruses, but none of them are truly effective for all viruses. Cidofovir, for example, works on viruses that are based around DNA, but doesn’t work on viruses based on RNA.
This means that, for a viral treatment, we usually need to have an antiviral that is specifically focused on that particular strain or type of virus. Think about how a lock requires a specific key.
There’s a strong drive among researchers to search for that fabled broad-spectrum antiviral that will work on a huge range of viruses — but we may never find it. There’s just too much variety among different viruses, how they work and what they’re comprised of, for us to ever have a single treatment that can stop the spread of any virus.
When Should I Take an Antiviral?
All of this raises a question: when are antivirals worth taking?
There are two main reasons to consider an antiviral:
- For dangerous/deadly viral diseases;
- If you are in a population at high risk of death or lasting injury from a virus (elderly, immunocompromised, etc.).
Antivirals can help lessen the length of time that you are sick from a disease, but usually won’t completely cure the disease. For example, there are antivirals for the flu — but they will only shorten the time spent feeling ill from the flu by about a day, and they must be taken right after the initial infection to work.
Antivirals are used in situations like in nursing homes, when people may be too weak to survive a course of the flu.
Similarly, with diseases like HIV, there are antiviral treatments — but they aren’t a cure. They can help lessen the viral load, and prevent someone who is HIV positive from passing the disease on to others, but they won’t cure the disease or fully eradicate the virus.
The other concern with antivirals is, just like how bacteria can mutate to become resistant to antibiotics, some viruses may mutate to the point where the antiviral no longer has any effect.
This is dangerous — it removes a vital tool that we may use to help our most vulnerable populations avoid dying from virus-based diseases.
So, why don’t we take antivirals for virus-based diseases, the same way that we take antibiotics for bacterial infections?
The first reason is that, unlike broad-spectrum antibiotics, there are no true broad-spectrum antivirals. Most antivirals only work on specific viruses, and you’d first need a test to determine which virus is infecting you before you could determine which antiviral to take to treat it.
Second, antivirals won’t be an instant cure for virus-based diseases. They may not even be a cure at all; they reduce the severity of the viral infection, but they won’t eliminate the virus from your system. For some diseases, like HIV, antivirals will lessen the number of viruses present but won’t get rid of the virus entirely.
Finally, we want to preserve our antivirals for the most vulnerable members of our population — the immunocompromised, the very young, and the elderly. These people may not be able to fight off a virus without some extra help from antivirals. If we use them with carte blanche on all members of our population, the virus may develop resistance.
We’re still searching for that fabled broad-spectrum antiviral, but for now, we’ll need to focus on the more effective weapon in our arsenal: vaccinations against virus-based diseases.





