In a comprehensive new study published today in the journal Cell Host and Microbe, the University of Wisconsin-Madison’s Yoshihiro Kawaoka and a team of researchers have set the stage for an entirely different approach. They have revealed methods for thwarting the hijackers by shutting down the cellular machinery they need, like cutting the fuel line on a bank robber’s getaway car.
When this got translated by Popular Mechanics we get the headline
Potential New Flu Treatment Would Starve the Virus, Limiting Resistance
which is the text blogged by Instapundit. This caught my eye because “starve the virus” is an odd claim since a virus is only metabolically active in the host, and the metabolites it uses are generally things the host needs too. From what I can tell from the abstract (apparently we don’t get on-campus Cell Host and Microbe here), the study is a large scale interactome to identify host proteins that coimmunoprecipitate with influenza proteins. Some of these were validated as affecting virus growth in culture by doing siRNA knockdowns. I’m not sure whether they then showed that known drug inhibitors also affected virus growth.
Here’s my guess about what happened:
- The researcher told a UW PR person that the study catalogs host proteins that might be needed by influenza to propagate itself, and points out that resistance to drugs that target the host can’t easily arise in the virus.
- The UW PR person tries to come up with something that is not part of a bank robber and comes up with a getaway car.
- Continuing the analogy, the UW writer picks an essential part in the getaway car: the fuel line.
- The Popular Mechanics headline writer saw “fuel” and thought the study was about reducing fuel for the virus
- We get the headline suggesting that the study is about starving viruses.
Of course, if the virus is a bank robber, the host cell is not the getaway car; it’s the bank. Inhibiting virus infection with drugs that target host proteins is not like cutting the fuel line in the getaway car; it’s more like preventing bank robberies by killing bank tellers. And it’s not just killing the tellers in the bank that’s being robbed, it’s killing all the tellers in all the banks in the community, whether they are being robbed or not. Maybe that’s a reasonable strategy if the tellers are really nonessential in an age of ATMs. But that analogy is a lot less attractive.
The abstract mentions two potential “targets”, GBF1 and JAK1. I’m not sure how promising those are in terms of being therapeutic targets, based on the phenotypes of mouse knockouts.