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  • Kurt Williamson headshot
    A sobering second look:  Virologist Kurt Williamson reconsiders the COVID-19 outbreak after the viral disease reaches global pandemic stage.  Photo by Stephen Salpukas
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Back in February, virologist Kurt Williamson, an associate professor in William & Mary’s Department of Biology, answered questions about COVID-19 and the virus that causes the disease when the outbreak was beginning to spread. We asked him to take another look at the coronavirus pandemic.

This story is part of W&M News' Faculty on Topic series – Ed.

Our first Q & A was in mid-February. How closely has the COVID-19 outbreak conformed to your expectations at that time?

Honestly, things have gone much worse than I had hoped at that time. My expectations were that this would be broader in scope than the 2003 SARS outbreak, spreading to more countries and infecting more individuals globally. This outbreak had potential to get very bad very quickly, but my optimistic hope back then was that we could get in front of it, do more mitigation – that we wouldn’t see things get as bad as they are now.

A lot of people are surprised — and some are skeptical — that scientists can tell that the coronavirus cases in New York came from Europe, and not China. Can you explain the science here?

Viruses with RNA genomes, like this coronavirus, mutate at a predictable rate. This mutation rate comes from the enzyme the virus uses to copy its RNA genome to make more viruses. The copying enzyme makes mistakes at an average rate of 1 mistake per 10,000 nucleotides copied. We can basically track these mistakes to piece together how and where different mutations came from.

You can think of this like scribe copying a manuscript. Before the printing press, people had to copy documents by hand, and scribes would do this laborious task. Let’s say our scribe is copying away, and he makes a mistake – let’s say, in the sentence he’s copying, the word was supposed to be “cat” and he accidentally writes “rat.” Now you have a mistake.

He sends this manuscript, mistake and all, out of his office for others to read and copy. Anyone who makes a copy of this manuscript will retain the word “rat” instead of “cat.” And future copies of this copy all have the rat-for-cat substitution.

Let’s say a different scribe working in a different office is working on the same manuscript, but she copies “bat” instead of “cat.” Now all of the subsequent copies coming from her office have the bat-for-cat substitution. If we can get our hands on as many copies of this manuscript as possible, we can compare all the copies and look for changes: this one has “cat” in this sentence.

Another one has “rat” in the same position in the same sentence. Yet another has “bat’ in the same position in the same sentence. By tracing which office the manuscript came from, and when that copy was made, we can figure out which errors came from what locations and when. We can often determine the original wording, too – the source.

Turning back to the virus: if we collect many samples of virus from different people, and we know where and when the samples were taken, we can compare the nucleotide sequence of the virus genomes (the manuscript contents) and look for changes. We can link these changes to specific locations and times.

Vaccine vs. cure: From a virologist’s point of view, which is most likely to come first?

There really is no cure for diseases caused by viruses. Bacterial infections may be cured because antibiotics will kill off the bacteria that are causing the disease. Viruses do not respond to antibiotics, but we have antiviral drugs that work with varying degrees of success. Most antiviral drugs try to exploit some molecular function that the virus needs, but our cells don't. There have been many promising candidates over the years, but very few antiviral drugs have panned out the way we hoped they might have from the early clinical trials results.

There is a lot of buzz right now about tests of an antiviral drug by Gilead Sciences. But here’s the thing: historically, the most successful antivirals have been anti-retroviral drugs for individuals living with HIV and drugs like acyclovir (Valtrex) for suppressing herpes simplex.

The most successful have been anti-retroviral drugs for individuals living with HIV and drugs like acyclovir (Valtrex) for suppressing herpes simplex. Neither of these drugs cure the infection – they only help people control the infection so that they can live a mostly normal life.

This is an important point. We have few, if any, therapies that will stop a virus in its tracks. Most of our treatments for severe viral infection are what is called “supportive therapy” – you try to keep people alive and stable while their immune systems do battle with the virus. And we hope that the person’s immune system wins out in the end. This is a hard reality, and it is one that is important for people to understand.

This is also why prevention is our frontline defense for viruses. Vaccines are the ultimate in prevention. Vaccines expose individuals to viruses, or often pieces of a virus, in a safe and controlled way. This allows their immune systems to develop protective antibodies against that virus without getting the disease caused by the virus.

Then, once you have protective antibodies, if you are exposed to the actual virus out there in your daily routine, your immune system is ready to go. You can fight it off. In the absence of a vaccine that grants protective immunity, the specific outcome for an individual who acquires a viral infection is up to chance.

Scientists and medical experts have a great deal of experience with other coronaviruses. How closely is this novel one sticking to the coronavirus playbook?

There are coronaviruses that have been infecting humans for probably more than a century. These coronaviruses cause mild, cold-like symptoms and are rarely a problem in terms of hospitalizations and deaths.

This current outbreak, and previous coronavirus outbreaks (like SARS in 2003), have been what are called spillover events, where the virus jumps from an animal reservoir into a human host – and then spreads from there. Many epidemiologists and disease ecologists tend to think about spillover as a case where, initially, the virus is not that good at replicating in the human host. But it gets better and better as it moves through more and more humans, because the virus is mutating and evolving the whole time.

Every time new virus copies are made, selection is acting so that sequence variants that are good at replicating in human cells (as opposed to the previous animal host cells) – those sequence variants make the most offspring. So the virus gets better and better at infecting humans and being transmitted human to human.

This was not the case for this current outbreak. A recent analysis of coronaviruses harbored by bats has shown that many of these viruses already have the capability to infect human cells. In other words, this transition period of getting better at infecting humans didn’t exist.

The virus could move from animal reservoir species to humans and immediately take off and spread in the human population. This is a major change in the “playbook” so to speak, and in our understanding of spillover and zoonotic disease.

There is a lot of speculation about a possibly man-made origin of SARS-CoV-2. From your knowledge of coronaviruses, what is the likelihood that this one is engineered?

In addressing this question, there is a lot of overlap with the previous question about how this current pandemic is similar or different from other coronavirus outbreaks. Again, it has been shown that hundreds of types of coronaviruses are harbored by bats and some of these coronaviruses already have the capability to infect human cells.  

This strongly suggests that natural animal reservoirs exist, and when humans come into contact with these reservoir species, viral infections can be transmitted.  Further, the large group of genetically related but distinct viruses carried by the bats suggests these viruses arose through mutation, drift and selection (processes of evolution), rather than by a directed process like engineering.

We are hearing a lot about dates at which COVID-19 is expected to peak. Is it likely to ever go away?

At this point, the virus is spreading, unchecked, across the globe. Social distancing is working to slow the spread. But the vast majority of the human population has not yet been exposed and has no protective immunity.

We would have to completely stop the chain of transmission everywhere, simultaneously. As long as a few infected individuals remain, this whole thing can be triggered off again. This is another hard reality, but it is likely that this virus is here to stay. This makes it all the more important that a safe, effective vaccine be developed and distributed as soon as possible. And, I would add, it also will be important for people to actually get vaccinated once it’s available.

Thoughts going forward?

A pandemic like this could have occurred with SARS, MERS or any number of previous coronavirus outbreaks in the human population. Part of the reason why these previous jumps by coronavirus into the human population haven’t exploded the way this one has is just luck. 

As we’re seeing right now, we can’t rely on good luck to carry the day for global public health or the global economy. It is dangerous folly to think this is the last pandemic, or even the last coronavirus pandemic, we’re likely to face.

We need to prepare for the next one, so we’ll have on hand everything we need, from PPE and ventilators to well-understood legislative and public-policy tools. This also includes sustained budgeting for teams of experts and related staff, as well as for continuing research and development efforts.