Updated: Apr 21, 2020
I guess you can all guess what this one is about. Up until this point, I've been cautious - perhaps overly cautious, as scientists are wont to be - about writing a Microbial Mondays post about the SARS-Coronavirus-2 (or SARS-CoV-2 for short), the virus which causes COVID-19. The reason for my caution was that there simply wasn't a lot of scientific literature available that I could read on the virus. Usually when I pick a Microbial Mondays topic, I read for hours and hours before I start writing, to make sure that I'm passing on good, well-researched information to you. Luckily, due to a massive effort from scientists around the world, a few months down the line there is an abundance of solid scientific publications about this virus.
So let's jump in.
So what is this virus, anyways? As you might know already, SARS-CoV-2 is related to the original Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) that caused the infamous SARS outbreak in 2003, and the Middle Eastern Respiratory Syndrome Coronavirus (MERS-CoV) that caused a 2012 outbreak. However, the coronavirus family is composed of quite a varied bunch.
Coronaviruses can cause everything from mild colds, to severe intestinal inflammation, to deadly respiratory infections, and in many different animals, including, of course, humans. In fact, before the 2003 SARS outbreak, scientists thought that coronaviruses only caused severe diseases in non-human animals. For example, cows and pigs can get brutal diarrhea and intestinal inflammation from certain coronaviruses, and cats can die from a coronavirus called Feline Infectious Peritonitis Virus (FIPV), which causes massive inflammation around their intestines, pancreas, and stomach. Meanwhile, humans seemed to have gotten off easy - the only recorded result of human infection with coronaviruses back then was the measly common cold. In a lecture during my master degree, I remember a coronavirus expert saying that before 2003, his research wasn't taken very seriously and it was tricky getting funding for research to prevent "the sniffles". Well, that's sure changed.
These newer coronaviruses that cause SARS, MERS, and COVID-19 are similar to other human coronaviruses in that they infect the respiratory tract (i.e. the road air travels along to get in and out of your lungs), but different in the extent to which they damage the cells along that tract. Scientists think that at least part of the reason that SARS-CoV-2 is so deadly is that it both destroys the cells in your lungs, making it difficult to breathe without a respirator to help, and also causes massive inflammation throughout the body. This massive inflammation is also the reason why people with pre-existing conditions like cardiovascular disease should be extra careful. When you have cardiovascular disease, your body is already in a sort of generally inflamed condition, which makes it easier for the virus to tip the scales against you.
On top of all this, SARS-CoV-2 is also nasty in that it doesn't only seem to attack your lungs, but also other organs, from the heart to the gut. All of this together means that when you get it bad, you're in the hospital for a pretty long time. This long hospital stay, together with the fact that the virus spreads between humans very easily, has contributed to the horror stories you may have heard from Italy. There just haven't been enough hospital beds to care for the very many, very sick people.
So, what are scientists doing about all of this? We do have some tricks up our sleeves, luckily. One of the many strategies that we are making use, at least in the interim period before a vaccine is developed, relies on the fact that viruses rely on us. That's right: on their own, without our cells, viruses can't do much. To replicate, they need to hijack bits and pieces of us humans (or whatever other animal or plant they've infected) to do the work. In other words, viruses snatch the tiny machines within our cells, and make those machines work for them. So, smart as we scientists are (heheh), we thought, why not make that harder for the viruses?
I'll give you an example. One of the ways in which the virus relies on us, is simply to get into the cell. Coronaviruses can't get into the cell all on their own, they have to steal a key first. In the case of SARS-CoV-2, that key is called ACE2. ACE2 is a protein that sits on the surface of many different human cells. The virus basically has to grab on to ACE2 in order to get inside your cells and start off on its intracellular hijacking business. It's kind of like a really fancy doorbell to get into the 'houses' that are your cells. That's where we scientists come in. To confuse the virus, researchers have been working on making versions of ACE2 that are not attached to any cells that we can give to patients. These viruses aren't smart enough to tell the difference between a cell-attached-ACE2 and a floating-around-ACE2, meaning that they'll be ringing doorbells that are not attached to any house, and therefore not getting in anywhere.
The good news doesn't stop there - there are many other ideas like this going around, and scientists are working very hard to combat this virus. It indeed might take a while, since we need to be thorough, but we'll get there.
In the meantime, you can help us by staying home. I know it's boring, but this virus truly depends on humans being social to infect us. Before scientists can develop the best possible antivirals and vaccines for everybody else, the best thing you can do is think like a scientist: outsmart the virus. By staying home.
A very happy, microbial Easter to all of you.