Coral scientists trying to stop stony coral disease from ravaging Florida and Caribbean reefs have a rare bit of good news.
Corals infected with the disease in a lab had an immune response in some genes. In simple terms, that means the corals can fight back.
“It's like, 'OK, they are responding,'” said Nikki Traylor-Knowles, lead author of a study published last month in "Frontiers of Marine Science" and assistant professor at the University of Miami’s Rosenstiel School. “Now we can start to investigate those genes more closely. Before we just had no idea. We were guessing.”
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Stony coral disease first appeared off Virginia Key in 2014, at the same time PortMiami was being dredged to make way for massive, new Panamax ships. The disease quickly spread across the Florida reefs, alarming scientists already battling warmer oceans and disease to save reefs which provide a powerful barrier to hurricanes and storm surge. Florida's reef is also the only inshore tract in the continental United States.
The new disease has since moved into the Caribbean, as far west as the Windward Islands and south to Mexico, infecting 21 species of boulder coral that play a key part in building reefs.
Because it moved so quickly and lethally, scientists focused most of their efforts on trying to stop the disease or rescuing enough healthy coral to begin breeding programs.
That left a gap in “understanding, from the coral perspective, how is it reacting? Why are we seeing this drastic outcome?” Knowles said.
“Are they even having an immune response? Is it that there's just nothing? Their immune system isn't working and so maybe that's why this is happening.”
Scientists know the disease is highly contagious and is carried in water. But they still don’t know what causes it, Knowles said.
“What's the pathogen? What's the bacteria? What's the virus?” she said. “Is it an environmental issue? Is it a combination of all of these?"
Complicating the matter: Scientists know little about the inner workings of coral, that feed off algae that live inside them.
“The immune system itself is just complex. We know that they have a lot more genes for certain immune genes than even, in some cases, humans,” she said.
For the experiment, UM students working with scientists from Mote Marine Laboratory in Sarasota and the Smithsonian Marine Station in Fort Pierce collected both healthy and sick corals. Healthy great star coral and mountainous star coral were collected ahead of the infection beginning in April and July in Key West and Looe Key and in February, from the Dry Tortugas. The disease hit the remote islands in June.
Sick coral collected from infected reefs were then used to infect samples from the healthy coral. The last experiment ended in March, just before the COVID-19 pandemic shut down the Smithsonian field station.
Researchers then compared samples from the new infected to their healthy partners from the same genotype. In their analysis, they found many of the genes had a significant response.
“One of the things that’s challenging is we tend to treat them all as just coral. But when you’re actually looking at the genetics, they can be very different and have different needs,” Knowles said. “So it's step one in our, kind of, journey to understanding their total health.”
The hope is that eventually the work can lead to developing biomarkers, like the kinds used in human blood tests to check for high cholesterol or signs of cancer, she said.
“In coral research, it is a lot of doom and gloom. It's hard. I gave a public talk recently and I started crying because as I was talking about it, I was like, 'Oh gosh, this is just so hard.' It's like you're documenting death all the time,” she said.
But with this study, scientists may be able to develop the tools they need before it’s too late.
“We still have a lot of work to do with it. So I don't want to oversell and say that we're anywhere near human medicine,” Knowles said. “But we are really trying to create a toolkit so that we can better diagnose corals and better inform policies and other things to help save them.”
