A Primer on and Conversation About the Biology and Evolution of COVID-19

— Written By

[Following is an excerpt of a comprehensive discussion with NC State scientists and other subject-matter experts conducted by NC State Applied Ecology Professor Rob Dunn. We highly recommend you read the full article from NC State News.]

Many words have been written (or at least typed) about coronavirus SARS-CoV-2, the virus that causes COVID-19. Yet, for as much as its story has dominated news cycles and changed all of our lives, very little is being said about its biology and, specifically, its evolution. The virus is an example of the real-time consequences and dynamics of rapid evolution. It evolved, anew, in China and spread country to country, changing the world as it did. It has a power far greater than its size, a power that makes more sense in light of evolutionary biology.

To provide a little more context for current discussions of the consequences of the virus SARS-CoV-2, NC State Applied Ecology Professor Rob Dunn (RRD) sat down with Tom Gilbert (TG) from the Center for Evolutionary Hologenomics, Katia Koelle (KK) from Emory University, Julie Casani (JC), Matt Koci (MK), and David Rasmussen (DR) from NC State, and Sergios-Orestis Kolokotronis (SOK) from SUNY to talk about the virus. Or rather he sat down with them, virtually, practicing good physical distancing practices.

The following conversation reflects a series of emails back and forth among the participants in response to Rob’s questions. Thanks to Olivia Sanchez Dunn for help editing the text for clarity.

Terms bold and italicized are included in the glossary at the end of the article.

The Basics

RRD: What makes a coronavirus different from any other virus?

TG: Very philosophical question, Rob! But at the most basic, there are something like 150 identified families of viruses, and the Cornaviridae are one of these families. Defined as “enveloped, positive-sense, single-stranded RNA viruses with a genome of 26–32 kilobases in length.” That is to say they have an envelope-like covering. They are based on RNA not DNA. And they are, although small compared to bacteria, large for a virus. Until recently the most famous Cornaviridae was SARS.*

Families are a key unit in the classification of viruses as they are based on and define the overall structure of a virus, e.g., what its genome is based on (DNA, RNA, single or double stranded etc), how big its genome is and what genes it contains, and what the outside of the virus looks like (enveloped, protein shell). Other famous RNA viruses from other families include HIV (within the family Retroviridae), Influenza A (within family Orthomyxoviridae), Ebola (within family Mononegavirales), Measles (within family Paramyxoviridae) and the common cold Adenoviruses (within family Adenoviridae).

RRD: How many kinds of viruses are there on Earth? What proportion are unknown?

TG: Err….150 families 🙂 I imagine the answer is enormous. If you assume each species has its own unique pool of viruses…and there are millions (hundreds of millions) of unique kinds of multicellular organisms that can be hosts…that is a very big number!

RRD: And that doesn’t even include the viruses that attack bacteria, bacteriophages, right?

TG: Right.

Origins and Evolution

RRD: What do we know about the origin of this SARS-CoV-2 virus that causes Covid-19? Which viruses is it most similar to? Based on what?

TG: It is a fairly close genetic relative to SARS, and the most closely related known viruses are coronaviruses found in bats. Bats are famous carriers of pathogens, as their immune system doesn’t react as strongly to pathogens as, say, ours, so infected bats often don’t have strong symptoms (as far as we can tell). There are interesting ideas on why this may be, related to the high amount of cell damage bats experience as flying animals. If their bodies over reacted to this, they’d kill themselves. So they had to evolve to tone down how they react to such damage, and this extends also to pathogens. They seem to cope fine with a belly full of viral baggage.

That bat coronaviruses are the closest relatives found so far to SARS-CoV-2 doesn’t mean it came directly from them. It more than likely jumped from bats to an intermediate host. One strong suspect being pangolins.

RRD: Is SARS-CoV-2  predicted to become more or less virulent as it spreads? Why?

TG: Tough question. From an evolutionary point of view…to survive the virus needs to maximise its spread and persist. If it kills too fast…it won’t get transmitted. If, however, it evolves so that it reduces its rate of replication in an individual human, there will be so little of the virus in the nasty things we spread to each other (snot, spit, other…), it won’t transmit. An “ideal” form (ideal from the perspective of the virus) would be perhaps like the common cold…it makes you feel a bit crappy, but not enough to put you in bed (thus avoiding others). It makes you sneeze and dribble, so as to pass it to others. But it doesn’t kill you which allows you to continue to sneeze, dribble and spread. Note that at this point it may already be ideal…as it doesn’t kill most people, and it certainly doesn’t kill the best people for spreading it (active young people and kids who get much more around than the elderly and infirm. So I would actually be surprised if it became much different from how it is now. There’s just not much to select on to stop it being pathogenic to the elderly/infirm.

DR: One of the reasons SARS-CoV-2 is particularly deadly is that the inflammation it causes in the lungs gives rise to pneumonia-like symptoms. This is largely self-inflicted harm arising from our own inflammatory response. It is not clear that causing such pneumonia-like symptoms in any way benefits the virus and may even reduce its transmission potential by rendering infected individuals less mobile. It’s therefore possible that there will be selection on the virus to trigger a less aggressive immune response in the lungs. But it may also be that the immune response is more under the control of the host than the virus. This certainly seems to be the case in mice where there is tremendous genetic variation among different mice strains in their immune response to SARs-like coronaviruses.

RRD: The ideal virus would make its host more social too, less willing to oblige efforts at social distancing.

TG: To continue…  if it jumps from humans into yet another species alongside us (and it clearly has no problems jumping fairly large distances…even if it wasn’t directly from a bat to humans but via an intermediate…) then this could also change its rate of evolution. And possibly make it more, or less, virulent/pathogenic. To both whatever the new host species is, and new future host species, but also if it jumps back into humans.

RRD: What should we be paying attention to with regard to the biology of the virus? What are the unknowns?

TG: Will it/strains of it mutate in ways that will negate the efficacy of the diagnostic tests? Or affect the efficacy of vaccines?

RRD: Oh jeez, I hadn’t thought about the possibility that strains could evolve in such a way as to become undetectable.

MK: It is still early, but for me the big question is what does immunity to these viruses look like. How long does it last? There are several coronaviruses we all see every year. They cause the common cold. Each year we get infected by more or less the same viruses because our immunity to these viruses only lasts about 6 months. Will it be the same for SARS-CoV-2? Or maybe we’ll still get infected by SARS-CoV-2 but the next time it will just be cold.

You can read the full article from NC State News.

Who Are We?

  • TG is Tom Gilbert: Tom studies hologenomics, namely how microbes and their hosts work as one, at the University of Copenhagen’s GLOBE Institute.
  • KK is Katia Koelle: Katia studies the evolution and spread of viruses, with a special focus on influenza. She is based at Emory University.
  • DR is David Rasmussen: David develops computational methods for studying infectious disease epidemiology and viral evolution. He is based at North Carolina State University.
  • SOK is Sergios-Orestis Kolokotronis: Sergios studies the molecular evolution and ecology of infectious disease systems. He is based at SUNY Downstate Health Sciences University in Brooklyn and the American Museum of Natural History in New York.
  • RRD is Rob Dunn: Rob studies the biology of species associated with humans. He is based in the Department of Applied Ecology at North Carolina State University and the Center for Evolutionary Hologenomics at the University of Copenhagen.
  • JC is Julie Casani: Julie has experience leading statewide (Maryland and North Carolina, USA) response to public health emergencies. She teaches global health at NC State University.
  • MK is Matt Koci: Matt is a virologist and immunologist working on host-microbe interactions in birds. He is based at NC State University.

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