COVID-19 Insights from OIST - What makes it so difficult to treat viral infections?
A host of bacterial diseases like cholera, tuberculosis, typhoid fever, some ulcers, respiratory infections, or food poisoning are today treated with antibiotics. These drugs remain an incredibly valuable weapon, and in recent human history they have helped save millions of lives.
Viruses, however, are much harder to treat. What makes them so different?
Firstly, they are a lot smaller than bacteria. To observe a virus, you need a powerful electron microscope.
Let us assume that a cell in our body is 0.05mm wide. Bacteria are ten times smaller. A virus is five hundred times more tiny.
Inside each virus there is genetic material with a chemical structure different from genetic material in human cells. This is wrapped in a lipid envelope – a simple fatty layer. A virus is structurally uncomplicated, but devastatingly effective. It is, essentially, a piece of genetic information with a single goal – to multiply itself.
Scientists do not consider viruses to be living beings. Our reasoning for this is that a virus cannot grow, feed or multiply on its own. If we deny viruses access to resources inside our body, they die. Other kinds of microbes can metabolize and reproduce independently, but a virus requires a host – either bacteria, animal or plant cells. They rely on the machinery provided by a host to thrive and replicate.
This makes them extremely hard to destroy once they are inside our body. Antiviral drugs could kill a virus, but they might also kill the cells which host them. Finding treatments which destroy the virus – but not the human cell which harbors it – is extremely difficult.
This challenge was overlooked recently by President Trump, whose suggestion of injecting or swallowing disinfecting chemicals to wipe out the virus overlooked the fact that doing so might also wipe out the patient. The President later claimed his remark was sarcastic, aimed at those who attack him on a regular basis.
When it comes to truly effective modes of attack, a virus has few equals. Experts calculate as many as 400,000 deaths from COVID-19 in Japan if no countermeasures are taken. This miniscule structure has succeeded in inflicting global havoc.
Why now? We understand that viruses have been present for many billions of years within the cells of wild animals, and bats are thought to be their most likely host from which COVID19 virus emerged. But the machinery of viruses like COVID-19 is imperfect. When a virus multiplies, mutations can arise. Mutations are small changes in the genetic material of the virus. These alterations can lead by chance to new properties such as being able now to not only infect bats but humans.
We believe mutant strains infected people in Wuhan, and, from there, spread across the globe.
An infected person will shed copious amounts of virus during the first week or so. Whenever they cough or sneeze, or even just exhale virus-laden droplets, there is a risk that someone else breathes them in. Once this happens, the virus has found a welcome new home in the lining of our nose.
COVID-19 cannot invade every cell of the human body. It contains an ‘S protein’ which works like a key in search of the correct lock. Protein molecules in our body called ‘ACE2 receptors’, which help regulate blood pressure, provide the lock the key is looking for. The virus binds to these receptors, rendering tissue cells vulnerable to COVID-19 infection. Once it has entered the cell, the virus hijacks its machinery, making myriad copies of itself, and then invading new cells. If our immune system does not fight back successfully during this initial phase, the COVID-19 virus can march down the windpipe, attack the lungs, and become deadly.
By Dr. Peter Gruss, President/CEO, Okinawa Institute of Science and Technology Graduate University (OIST)
The Japanese translation of this article was published on May 10, 2020 in the Ryukyu Shimpo newspaper under the title "新型コロナOISTによる洞察 宿主破壊の危険も なぜウイルスの治療は難しいのか".