Curing Ebola: Why I, a Diabetic, Care

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In the May 29 issue of The Lancet, a group of scientist announced that they cured ebola in six macaque monkeys.

Child of the nineties that I am, that seems phenomenal to me. The future is now! I admittedly have never seen the movie Outbreak; my mother said it would be too scary for me at the time, and given that I have to leave the room for many of the scenes in Dexter, I’m inclined to agree. But, I did read the book that Outbreak was based on– The Hot Zone, by Richard Preston– so I got a good sense of the collective fear of ebola that swept the nation at the time the movie came out.

For those of you unfamiliar with the story, ebola is a highly contagious virus, with some strains (specifically the Zaire ebola virus) having up to 90% mortality rates in humans. Symptoms of infection manifest rapidly and viciously– hemorrhagic fever, vomiting, diarrhea, bleeding, and so on.  The Hot Zone is a (mostly) factual account of the events surrounding the discovery of ebola-infected primates in a corporate research facility in Virginia. The book is categorized as a “non-fiction thriller,” full of the suspense that comes with the threat of an extremely fatal airborne outbreak from Africa. And, vivid in my tween memory of the book, there are plenty of gruesome details of ebola infection in humans, complete with people hemorrhaging from every orifice and sexy female scientists.

So, to me, and I imagine many others whose imaginations were captured in the mid-nineties by ebola-epidemic narratives, curing ebola is a big deal– one more scary viral vector of death one step closer to being eliminated.

But, as a diabetic, I am not just pleased that the researchers were successful; I am fascinated by how they did what they did, because it is a fabulous example of how molecular biology and proteomics have changed the way medicine and disease elimination work in our modern world.

So what exactly did the scientists do? They designed and synthesized several different segments of RNA (ribonucleic acid, a string of nucleotides similar to DNA that builds amino acids and assembles proteins in the body). The idea was to use these segments of RNA as interruptors in the replication process of the ebola virus; the short segments of RNA that the scientists made, called small interfering RNA (siRNA), would latch on to the virus’s own RNA at key points. This small bit of interference by the siRNA, if located correctly, would effectively prevent the virus RNA from building its own proteins and from self-replicating.

The scientists narrowed down their set of siRNA candidates in _in vitro_ tests (that is, outside of any living organism, on lab slides). They selected three siRNA segments, each of which targeted a different protein key to the correct functioning of the virus, and then gathered nine macaque monkeys to begin non-human tests. The monkeys were each infected with the deadly Zaire ebola virus, which is nearly 100% lethal in macaques. One monkey, the control, was given no treatment; three were given a dose of the special anti-ebola siRNA cocktail that the scientists had synthesized right after they were infected, plus another dose on each of days 1, 3, 5, and 7 after the initial infection; one monkey, the second control, was given a cocktail of other siRNA strands, not specifically targeted against the ebola proteins; and the final four monkeys were given a dose of the anti-ebola siRNA cocktail after infection, plus another dose on each of the seven days following the infection.

The results? The control monkey, as expected, showed all the symptoms of hemorrhaging fever and was dead by day 6. The second control monkey, which received the non-specific siRNA, made it to day 10, but it too died. Of the three monkeys given four days of post-infection doses, all three showed severe symptoms– fever, rash, depression, lymphopenia, bleeding– but only one actually died. And the remaining monkeys? Lived. All of them. They showed symptoms of ebola, but their symptoms were less severe than the control moneys. By day 14, all six surviving monkeys were free of traces of the virus in their blood. By day 40, all six surviving monkeys were symptom-free and healthy. (And by day 43, all six surviving monkeys were euthanized. The lesson here is that the life of a lab monkey sucks, but we’ll save that discussion for another time.)

With only nine subjects, this study is intended to serve as a proof-of-concept study and as a preliminary to further research towards drug development. But the promise is clear, both for the ebola virus and for medicine in general. This very small-scale manipulation of molecular biology, one nucleotide at a time, opens new doors for protein and genome function control, both for virus containment and for diseases like diabetes, where we want to change and control aspects of cellular and protein interaction– namely, the immune system’s interaction with insulin and other metabolic agents, as well as the endocrine system’s production of insulin and related proteins.

In other words, what we understand, we are in a position to change, and we are in a position to change, we are in a position to fix. In this case, a group of researchers moved towards fixing ebola, and in many studies around the world, researchers are using similar tools and techniques to gain a greater understanding of the small-scale workings if type 1 and type 2 diabetes, so that one day I will be able to write a post titled, “Curing Diabetes: Take that, Mother Nature!”

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