It is tough to catch a target when you don’t know what its next move will be. It is even tougher when the target itself doesn’t know its next move. The unpredictability of RNA virus is what makes them resistant to antiviral drugs. Since every copy the viruses make of themselves is inaccurate, at least to some degree, the antiviral drugs do not know what to search for. It is like a police officer chasing someone based on a description, but the criminal dumps his coat in the trash and gives his hat to a stranger. For example, the only way to go after a disease like HIV is to pump a patient full of different types of drugs to try and wipe out hiding places, thus backing the disease into a corner.

So what do you do if you can’t fight an RNA virus? You could try attacking the host cells. The only problem with that is keeping the host safe while you do it. It’s not really a cure if it kills you. Ribosomes, however, may hold the key to cornering fatal viruses like rabies. Proceedings of the National Academy of Sciences published results on November 19th that are promising.

Ribosomes have always been believed to sort of be on autopilot just doing their thing, which happens to be making proteins. Amy Lee and Shawn Whelan are challenging that role and claim that ribosomes translate specific proteins which would connect them with virus replication. The study involved examining how mRNAs (messenger RNAs) are translated into proteins by host cells that are infected with RNA viruses. The pair discovered a particular protein on the surface of ribosomes that is crucial to virus RNA translation, but is irrelevant to most mRNAs. It is named rpL40. Targeting this protein could inhibit RNA virus reproduction without hurting host cell’s ability to produce good proteins.

At the present time, there is no treatment for the deadly virus, rabies. This is being presented as the first possible way to counteract that fatal virus. Initial screening using the vesicular stomatitis virus, a relative of rabies, showed that while the virus relied heavily on the rpL40 protein, only about 7 percent of mRNAs did. The class of virus that relies most heavily on this protein also includes the measles virus.

While there are no drugs yet to target rpL40, a number of research groups are now exploring this theory developed by Lee and Whelan.