After working as a doctor in an Ebola-stricken nation, Ian Crozier felt like he had something in his left eye. He was right: a live, replicating reservoir of the Ebola virus.
According to a story in the New York Times, Crozier had contracted Ebola while working with the World Health Organization in Sierra Leone in late 2014. By October, his symptoms had abated and his blood tested negative for the virus, so he left Emory University Hospital to go home.
Two months later, he was back. He described his symptoms to fellow physicians: his eye burned, he was sensitive to light, his vision, normally 20/15, had changed to 20/20 (by the height of the inflammation, it had blurred to 20/400), and he had the sensation of something in his eye. The pressure inside his left eye was much higher than normal, which threatened his vision. Doctors diagnosed Crozier with uveitis, a severe inflammation in the eye, but when they sampled his aqueous humour (the fluid inside the eye), they were shocked by the cause of the inflammation: Ebola.
Tests revealed that the virus wasn’t present in Crozier’s tears or on the outer surface of his eye, just lurking inside it. His eye had become a reservoir for the virus. Viral reservoirs happen when a virus finds its way into a part of the body that is usually pretty isolated from the immune system. Once there, the virus goes on replicating, but it usually doesn’t spill over to the rest of the body, since reservoirs are, by definition, isolated from the rest of the body. It’s like finding the only quiet room at a party and deciding to just hang out there, except that you’re filling the room with a deadly virus.
The eyes are shielded from the immune system, because immune responses like inflammation could do serious damage to the delicate mechanisms of vision. This makes the eyes an ideal reservoir location. The testes are similarly protected, and researchers think that’s why Ebola can still turn up in semen for several months after a patient’s blood is free of the virus.
Crozier’s case is the first time doctors have seen an Ebola reservoir in an eye, and it emphasises how little we really know about the aftermath of the disease. The New England Journal of Medicine reported on his case in detail, with Crozier as a co-author of the article.
It’s not clear how common cases like Crozier’s might be. According to the NEMJ article, a survey of 85 survivors in Libera found that 40 per cent had eye problems similar to Crozier’s early symptoms: pain, blind spots, and blurred vision. However, researchers aren’t sure how many of those patients actually have uveitis. Of the cases that do turn out to have uveitis, it may be hard to determine which patients have reservoirs of Ebola in their eyes and which have other viral infections, let in by weakened immune systems. In fact, that’s what doctors thought had happened to Crozier at first, the New York Times reported.
Reservoirs are more common in patients with Herpesvirus. Doctors also know that something similar happened to at least one patient with Marburg, a virus related to Ebola. The patient’s blood had tested negative for the virus, but it turned up in his eye three months after his first signs of the disease. Two weeks later, his eye was also virus-free. That was in 1975, and it’s still not clear how often this happens with either Marburg or Ebola.
In Crozier’s case, after treatment with an experimental anti-viral drug and steroids to fight the inflammation, the Ebolavirus in his eyes finally cleared up, three months after he first reported his symptoms. For Ebola survivors in West Africa, such outcomes may remain elusive until viral reservoirs are better understood.
Image: New England Journal of Medicine