Achilles' Heel of Ebola, Rabies, and Measles Exposed
Researchers have recently discovered what looks to be the exotic mechanism that allows the Ebola virus to replicate in its host, spreading to the point that it becomes a deadly infection. Understanding this could open up new treatment options that help victims of measles and even rabies as well.
One of the reasons that Ebola has been so difficult to treat and contain as it continues to ravage west Africa, is that we know very little about it. Much like rabies - arguably the most deadly infection in the world - Ebola lives a particularly short life in the human body, either being defeated by modern medicine or killing its victim in short order.
This means that researchers have very little time to observe the virus in action, as doctors simultaneously struggle to save their patient.
It's no wonder then, that up until now, experts had only a faint idea of how Ebola does its damage.
However, according to a study recently published in the journal PLOS Computational Biology, that mystery is finally being tackled, where virologists have found a "fundamental mechanism" used by illnesses of the nonsegmented negative-strand (NNS) RNA virus family.
This family includes Ebola, rabies, childhood respiratory syncytial virus (RSV), and even - strangely enough - measles.
After observing how NNS RNAs functions in livestock, the authors of this latest work were able to launch 20,000 computer simulations, assessing different possible ways the virus could be replicating. One key mechanism was highlighted again and again, leading to the researchers' current conclusion.
They propose that the viruses use a "sliding mechanism" that allows viral polymerases to transcribe and change cellular code, turning cells into virus factories (see caption above). In contrast, most viruses simply boast guided polymerase, which easily detaches from the virus inside an infected cell and then finds the right end of RNA to start replication.
"The proposed sliding mechanism is a fundamental new mechanism specific to the NNS RNA viruses that can be a target for antiviral drugs in the future," senior study author Saveez Saffarian explained in a statement.
By interfering with replication, a viral infection can be stopped in its tracks, unable to spread to new cells and cause more harm.
However, the virologist adds that the creation of such drugs would take at least a decade, meaning that they "unfortunately would not have an impact on the current Ebola epidemic."
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