Rabid about rabies – why me?

Rabid about rabies – why me?

As a neurobiologist, I’ve been interested and intrigued about rage, emotions, & rabies for many years.  But without a clear model to work on, there’s never been an experimental approach to use to study rage.  As I mentioned earlier, the most promising model, septal rage, disappears after a short time leaving us with nothing to interrogate.  In terms of treating rabies, there is a very good prophylactic and post-exposure (but pre-infection) vaccine that vastly reduces the chance of infection.  So, there isn’t a huge (in comparison to, say, Alzheimer’s disease) patient population demanding the time and resources of academic or pharmaceutical researchers.  So, I’ve worked on many other projects and neuropsychiatric disorders.

For me, that all came to a crashing halt in 2005 when a boy, Zachary Jones, died from rabies just a few miles from where I live!  He was bitten in his sleep by a rabid bat.  To him, it was just a dead bat on the floor and he may not even have noticed the bite; certainly nothing to tell his parents about.  When the symptoms of rabies infection appeared, it was too late to save him.  Even though the best treatment, the Milwaukee protocol, was used, there really is nothing we can do to treat rabies infection.  Zachary died. 

That made me mad!  How could we have let this happen with all the modern tools and treatments that medicine and neurobiology have to offer?  Of course, at the time I was engaged in more immediate projects and still had no idea of how to engage rabies.  But, I began to re-read and read more about the rabies virus.  I found that its unique properties do make it amenable to understanding.  There is a straight-forward series of studies that will identify the rabies receptor.  I tried to garner interest within Pharma, but no one was interested enough to listen.  Neuroscience research groups, often made up of younger investigators who have never read about how the Papez circuit was discovered, if they’ve even heard of the Papez circuit at all, said that rabies is an infectious disease, so I needed to talk with the infectious disease or immunology department.  And the infectious disease/immunology departments said, that rabies only kills about 50,000 people a year, while HIV, etc., kill many, many more, and we don’t have the resources to work on all the viral diseases.  As a lone pharmaceutical researcher, without academic ties, I don’t have much access to government grants either. 

New treatments for rabies infection are important, and treatments that would block the effects of the virus after infection are critical.  But, in addition, and in some ways more critical is to understand and find treatments for human lyssants, for outbursts of rage that disable so many victims and hurt so many others.  Rage attacks come through many neuropsychiatric disorders as I’ve noted in earlier blogs.  But, as we have no central, biological understanding of rage, they are shoved into a vast array of disorders where they are a secondary, comorbid condition without any hope of treatment.  And then there’s simply the fact that lyssantic behavior is a normal part of being human and control of it a vital part of becoming an adult member of social society.  As long as we don’t know where rage comes from, we will continue to depict it as supernatural vampires and werewolves; creatures, feelings, and behaviors apparently beyond our control.  As long as we use that excuse, we won’t really become the humans that we actually are.

For all these reasons, I am rabid about discovering the target, the receptor, by which the rabies virus releases our inner lyssant, and why I’m determined that we better understand ourselves, and better protect ourselves from the virus and from ourselves when necessary.  We have the tools and reagents to discover the rabies receptor.  The path forward is straight-forward, but it is not inexpensive.  Help me!