Just recently, a report was published giving hope and closure to many. We all remember just years ago when the Ebola Virus was an overwhelming threat and scare to one and all. This careless virus, causing internal bleeding and organ failure, claimed over 11,000 deaths and 29,000 infected victims in it's most dominant massacre during 2014-2015. It seemed a looming death, with no cure. However, researchers believe they have found a way to stop the Ebola Virus dead in it's own tracks. The classic Trojan Horse.
The Ebola Virus is a sneaky, and clever virus. In order to actually infect us and multiply, they must attach to a host cell. They can do so by entering a cell's lysosome. Once inside, they use the material in the lysosome to burst free, and enter into the cell's cytoplasm, where they can begin to infect and to multiply. By connecting with the NPC1 (Niemann-Pick C1), the Ebola Virus now has control, and can direct the lysosome using it's RNA to break into the cytoplasm.
Because the lysosome are invisible to the immune system, traditional antibodies wouldn't work. For this reason, Dr. Chandran, Dr. Dye, and Jonathan R Lai, devised a clever "Trojan Horse" to get the Ebola Virus to carry it's own destruction into the cell with him. To do this, they created two different antibodies; one to neutralize the virus itself, and the other to target the NPC1. Both of the antibodies contain FVM09, which allows for the two antibodies to ride along side the virus into the lysosome. Once inside, the antibodies are set free, and get to work. One goes after the virus, which is like a key, while the other goes for the NCP1, which is like the lock. With both parts being attacked, it makes it impossible for the Ebola Virus to actually attach to the lysosome, and break free into the cytoplasm.
This was tested as scientists injected mice with lethal injections of the virus, in all of it's forms. They waited two days, until finally checking back in on the mice. Unfortunately, the antibody couldn't attach to the NCP1, since the NCP1 in mice differs from in humans. The next step will be to test the idea on non-human primates. (Much closer in structure to humans than mice.)
I really like this article, because in the years 2014-2015, I was living in a different country that was infected greatly with this virus. It's interesting to me that through the biological breakdown of each cell, we can identify what interacts with what, and what we can do to stop that. Biology is so relevant in society, simply because it is the study of life. It makes us, and everything that is, what they are.
-C.W.
What happened to the mice?
ReplyDeleteA. Wardell
the antibodies couldn't connect to the NCP1 so as I understand it the mice stayed sick and fought the virus naturally.
ReplyDeleteK.F
DeleteI think this was one of my favorite topics we learned about in this class. I liked to be able to learn about the specific functions of things inside a cell, and how different diseases affect different organelles. I think it is really exciting how we can understand how something affects a certain function of a cell, and then be able to counter that affect. The coolest part is that most of these solutions happen on a cellular level.
ReplyDeleteThis is extremely interesting, one thing I'm wondering is if the FVM09 had to be added to the virus or if it was added once the mouse was infected? If it was the second part then we could help people who obtain the virus. But if it was the first one then we would have to change the way the virus is.
ReplyDeleteHS