A New Discovery at UNC Brings Up an Ongoing Debate about Virus Research
May 6, 2016
Researchers at UNC-Chapel Hill recently announced their discovery of a new virus, SHC014-CoV.
SHC014-CoV is in the family of coronaviruses; fast-acting viruses that usually cause upper respiratory symptoms like runny nose, sore throat and sometimes fever, but can be more severe. SARS (Severe Acute Respiratory Syndrome) and MERS (Middle East Respiratory Syndrome) are both caused by coronaviruses.
Normally, the discovery of a new virus is not particularly earthshattering. While learning about new viruses is obviously important, virologists estimate there may be 320,000 or more viruses on Earth that can infect mammals, including as many as 5,000 coronaviruses.
According to UNC professor of epidemiology Ralph Baric, who is senior author of an article in the journal "Nature Medicine" describing the new virus, SHC014-CoV is special because of both what it can do, and the restrictions that researchers have when studying it.
SHC014-CoV has the ability to jump directly from its host species, Chinese horseshoe bats, to humans without mutating, a somewhat rare feat in the coronavirus family.
Viruses rely on their outer shells to infect their hosts in very specific places, and coronaviruses are no different. The outer shells attack either a protein or the cell membranes of their host. Once that attack is complete, they inject their genetic material into the host cell, hijack the cell’s replication machinery and make as many copies of themselves as they can before the cell dies (click here for a more in-depth explanation of viral life cycle).
The trick with coronaviruses is the attack part. The outer shell has to make very precise chemical bonds to access the interior of the cell. This makes attacking multiple species very difficult, as bat proteins and bat cell membranes are just a little different from human ones, which are different from dog ones, etc. The differences are subtle, but they are usually enough to keep the outer shell from attacking more than one species.
Of course, viruses jump from species to species all the time. Spanish flu and swine flu make their home in other species and hop into humans. The difference between those viruses and this new one is that Spanish flu and swine flu required a mutation to jump or “spill over” into humans, while SHC014-CoV can make that jump as it is.
What separates coronaviruses from others is they have a spiky head on their outer shell (corona is Latin for crown) and you can tell different coronaviruses apart by the shape and chemical makeup of their crowns.
Baric and his colleagues found that both natural and synthetic versions of SHC014-CoV could infect both human airway cells in a test tube and mice. More alarming, however, was that antibody and vaccine treatments used against the virus that causes SARS, had little to no effect on the new virus. The same specificity that can prevent one virus from attacking multiple species is in this case working against researchers. SHC014-CoV is just different enough to where the medicines and vaccines we use to block SARS-CoV don’t recognize the new virus.
The discovery of this new virus also comes at a time when a specific type of viral research called “gain-of-function” or GOF has been on hold by order of the U.S. Department of Health and Human Services since late 2014. Gain-of-function or GOF research is currently a huge topic for debate in the virology community.
The most basic way to describe GOF research is that scientists genetically engineer viruses to make them more transmissible (easier to pass from one person to the next), more pathogenic (more prone to multiply inside and interact with a host) or both: a valuable research tool, but possibly dangerous. Here's why.
Genetic engineering is more or less targeted mutation. Mutations happen every day when the enzymes that copy our DNA make a mistake. Sometimes mutations do nothing and sometimes they cause a malady that really hurts an organism. But every once in a while a mutation comes along that makes an organism better at surviving than non-mutants. The first organism can pass the mutation onto her kids, and their kids and a few hundred generations later everyone has the mutation.
In big organisms like humans, this process takes millions of years, but viruses reproduce so fast that a life-altering mutation can spread in decades, years or even months if it has enough of an advantage. What a virus does or what it can infect can completely change in a year.
Gain-of-function research uses genetic engineering to artificially speed this process. The logic is that, for example, a deadly bird flu that’s attacking a lot of birds could possibly evolve to spill over in humans, so if scientists tinker with the bird flu and enable it to do this, they can study exactly what that mutated virus looks like and how it works. Then with that knowledge, the scientists can develop plans to treat for and vaccinate against it.
The same logic applies to viruses that spread quickly but don’t have really bad symptoms or viruses that don’t spread particularly well between humans. Crank them up to 11 in a safe, controlled lab setting and scientists can figure out what to do about them before they get to 11 naturally and cause a pandemic.
If you’re troubled by the idea that scientists are making more potent viruses, you’re not alone. The main argument against GOF research is just how safe and controlled it is.
That’s not to say research organizations are not careful to the point of paranoia about protecting dangerous pathogens. They certainly are, but all it takes is one mistake or even a malicious act to release a virus that is engineered to spread fast and hit hard. Critics of GOF worry it might be a pandemic waiting to happen.
It is a scary thought; one that a stunning class of B-movies ("Resident Evil," "28 Days Later," "Planet Terror," "I am Legend," "The Crazies," etc.) has taken full advantage of. And unfortunately, having these engineered viruses around is an occupational hazard of GOF research until the scientists involved figure out how to stop the viruses they’ve made.
So on the one hand, you have a tool that allows you to get out in front of viruses and learn how to stop them before they reach a really dangerous level outside the lab. On the other hand, in order to properly use this tool, you have to create that danger inside the lab.
The question up for debate right now is whether the benefits are worth the risk.
That’s the question the U.S. Department of Health and Human Services and the National Science Advisory Board for Biosecurity is weighing right now. They have paused funding on GOF studies for SARS, MERS and influenza viruses, while they analyze the risks and benefits.
But until they reach a conclusion, and that conclusion becomes policy, GOF research for SARS, MERS and influenza will remain mothballed, and researchers like Ralph Baric and his team will attempt find other ways to get out in front of SHC014-CoV and its brethren.
— Daniel Lane
Daniel Lane covers science, engineering, medicine and the environment in North Carolina.