When did you first hear about the new coronavirus? It probably crept into your consciousness, and then, in what seems like overnight, it changed your life.
I heard about it during the first week in January. Scientists in China reported on a new coronavirus that was causing an illness that looked like a respiratory disease we'd seen before called SARS. It belonged to the coronavirus family, which includes four members that cause the common cold, and two others that are more dangerous but rare - SARS and MERS. I didn't think much of it other than a vague sense of unease, because this was a new virus, related to SARS, which I knew had killed people back in 2003.
I then went to a meeting in Rotterdam of virologists and immunologists. This was part of an EU-funded programme training PhD students across Europe at the interface between immunology and virology. An area that now seems so important, but which at the time was just another scientific gathering.
There were SARS experts there, and one of them, Frank van Kuppeveld from Utrecht, said this new virus was definitely one to watch, because it was new, and we didn't know much about it at all.
He reminded us it came from a family with two members that were real bad asses - SARS and MERS. We didn't talk about it for very long.
My mind increasingly turned back to when I first became interested in immunology. It was in the 1980s and all the talk was of a mystery illness called Acquired Immunodeficiency Syndrome (AIDS) that attacked the immune system. It took four years to find the virus that causes AIDS, named HIV. It took a matter of weeks to find the virus that causes Covid-19, named SARS-CoV2, which illustrates how far science has advanced since the 1980s. Let's hope it advances us all the way to the finish line against SARs-CoV2.
May: The Wuhan acrobatic troupe rehearse for a live online performance this week, as life with the virus goes on. Photo: Getty Images
In February, many hoped it would be like its relative SARS. SARS was quickly contained, with around 8,000 cases and 774 deaths. But the number of cases of Covid-19 began to grow in China, and it began to rapidly spread outside China. But still, some said it looked somewhat like the flu, and so nothing to be especially frightened of.
Then in March, at another gathering of immunologists, this time in the US, a group of us were having a post-conference drink. A lot of our conversation was now about this new virus.
Another of my scientific collaborators, Eicke Latz from Bonn, said he'd been talking to a colleague of his - someone who had actually discovered SARS. He'd told him that 70pc of the world's population would become infected. We all stopped talking and I said: "Can you say that again?" The mortality rate from SARS was around 10pc. So if it was like that, 7pc of the world's population might die. This would be over 300,000 Irish people. I gulped. I hoped it was just exaggerated bar talk.
It began to spread around the world. It quickly became clear that this wasn't like the flu. It was more contagious, and probably dangerous because we had limited, if any, immunity to it. Another reason to die. We now know a lot about this virus. Eminent virologists are calling it "extraordinarily unusual" and "something I have never seen in my 20 years of studying viruses" and that's from a flu expert.
Probably the most important thing is people without symptoms can be infectious. Unlike in SARS, which mainly affects the lungs, SARS-CoV2 can infect the nose and throat as well. So, here was a difference. If SARS-CoV2 doesn't make it to your lungs it causes a mild disease, like the common cold or even show no symptoms at all. If it gets into your lungs, it causes a more severe disease and the symptoms become obvious. SARS-CoV2 is, therefore, a bit like a common cold coronavirus having a baby with the SARS virus. That baby can be like one if its parents and cause a cold, or can be like the other parent and cause lung disease, which might actually kill you. New to science. But a very important finding, because if you have the mild form, you can still spread it.
May: The Wuhan acrobatic troupe in rehearsal. Photo: Getty Images
How do you identify a murderer if there are no clues? How do you stop a disease spreading when many of those with it (as high as 50pc) can spread it without knowing it? This is one reason why it spread like wildfire. Because we had no immunity, we were like lambs to the slaughter.
The main way to contain it is to test, test, test. Everyone should wear masks in public. This is why the instructions on masks had to change. The previous advice was to wear a mask if you had a cough, because the cough droplets containing the virus would be trapped in the mask. But when we learnt that you can spread the virus without symptoms, and even by just speaking, it made sense for everyone to wear a mask, and it still does. The science worked: it changed our view on masks (although disturbingly many in Ireland still aren't wearing them).
Clusters of infection happen in confined spaces where people shout a lot. This is a reason why meat factories are especially problematic. They are noisy places and the workers all live together. Same for choirs and pubs - crowds together, singing or shouting.
Other features began to be noticed. Covid-19 makes you feel exhausted. Flu does, too, but Covid-19 might be worse. And viral fatigue syndrome, which means you have symptoms like fatigue for weeks after clearing the virus, is also a prominent feature of Covid-19. Even patients with mild disease can suffer with this.
Doctors also noticed another troubling symptom. Blood clotting. Again, other viruses will do this, but it might be more common in Covid-19. This can be lethal and cause organs to fail, leading to death. Doctors, therefore, watch for this closely. Clotting can also cause 'Covid Toe' which is where a clot occurs in the feet, cutting off blood supply to the toes which look like they have had frost bite. In very rare cases, children can suffer from a related problem that looks like something called Kawasaki syndrome, where blood vessels become badly damaged. Again, doctors are now on the lookout for that.
Finally, patients have something called 'Happy Hypoxia' where their blood isn't able to carry the right amount of oxygen, effectively suffocating them. Doctors are learning new things every day about Covid-19, and trying to treat their patients as best they can.
There are still things we don't know. Can you become reinfected? Possibly not, but we need more evidence. Will it be possible to vaccinate against Covid-19? Again, we don't know, but there are hopeful signs. Will there be an anti-viral drug? One called Remdesivir looks promising, but again we wait for the trials. Will we manage symptoms with powerful anti-inflammatory drugs? Again, several are being tested, including in my own lab.
In March, Frank van Kuppeveld contacted me and said we should collaborate, as he remembered my talk in Rotterdam about a new anti-inflammatory chemical our own bodies make which had also been shown to kill viruses. I said 'yes' immediately, and my lab is now back in action working on it. A long shot as our work is only beginning, but worth a try. Collaboration is everything when it comes to good science, since two heads are better than one.
It is now the month of May, a lifetime since the meeting I was at in Rotterdam. And we stand in awe of this virus. Like all viruses, it is very smart. This means there are, as American politician Donald Rumsfeld famously said, unknown unknowns. No one imagined happy hypoxia or Kawasaki Syndrome. Rumsfeld also said: "You go to war with the army you have, not the army you might wish to have." We have an army of scientists and healthcare workers fighting this virus with all their might. And if every one of us plays our part, together we will win. That's one thing I definitely know.
Luke O'Neill is professor of biochemistry in the School of Biochemistry and Immunology at Trinity College Dublin