Why Anti-Viral Drugs are Hard to Come By

This post isn't specifically about hydroxychloroquine or ivermectin, but the craziness over using them as a treatment for COVID made me think that it might be worth a quick explanation as to why they, or any other known drug, are inherently unlikely to be anti-viral therapies.

Let's start with antibiotics--the medicine that you use to fight a bacterial infection. How do they work? Put simply, they work by screwing up the molecular processes of bacteria. They are small molecules that bind to or alter important bacterial enzymes. It's like throwing a wrench (spanner, for the British) into a machine, or a broom stick into the front wheel of a bike. Except, here we are talking about specific interactions between molecules because they have just the right shape and chemical properties. Antibiotics screw up the chemical processes that bacteria need to live and grow. The reason that antibiotics don't also screw YOU up is because bacterial enzymes are different enough from ours that they can be selectively targeted. You don't have peptidoglycan in your cell membrane, for example, and the ribosomes in your cells are a little different than those in bacteria. Thus, scientists have been able to find small chemicals that, at the right concentration, can kill bacteria and not you [1].  The same applies to parasites. This general concept is called selective toxicity.

So how come there aren't more anti-viral medicines? Why is it that a doctor will diagnose you with a virus and then usually say there's not much you can do but manage the symptoms? The answer is that selective toxicity is much harder to achieve with viruses. That is because viruses mostly commandeer your cellular machinery for their own purpose. They do use some of their own enzymes, but there aren't that many targets to go after. This is further complicated by the fact that there are dozens of viruses that can infect people, each with different enzymes, and even if you could find a small drug molecule to screw up that enzyme, the virus has a decent chance of evolving resistance. Also, you usually don't know that you are infected with a virus until you develop symptoms, and by then an anti-viral probably isn't going to do much for you anyway (unless it is a chronic infection). Simply put, it is hard to screw up a virus without screwing up your own cells too. That's just the science side of it; the economics of drug development are a whole additional dimension to the issue. So for the most part it is up to the immune system to deal with viruses, hence the importance of vaccination.

So the idea that some random drug that is good for something else would also just happen to specifically inhibit some part of the SARS-CoV-2 replication cycle is just inherently unlikely. Not impossible, but really unlikely. And just because something works in cell culture does not mean it will work in you. Cell culture is a starting point, not proof of efficacy!

But maybe we don't need the drug to specifically target the virus. Maybe it can just perturb some cellular process enough that the virus has a hard time reproducing while the immune system ramps up to take care of it. That's a theortical possibility, but if the drug isn't screwing up your cellular processes enough to cause you some really unpleasant side effects, then it probably isn't doing much of anything to stop the virus either.

In summary, unless approved by regulatory authorities, you should be very skeptical of claims that an existing drug also happens to be an anti-viral. The same goes for any kind of dietary supplement or non-FDA approved therapy. Remember, it takes chemcial sharpshooting to kill a virus without killing you. If you take a drug that isn't approved as an anti-viral, you are probably shooting the wrong target.

Notes
1. The drug, of course, has no idea what it is supposed to target. It just follows the laws of physics and chemistry.