Hi, I’m BET HA N Y QU I N TON I’m in Upper Sixth and am studying Biology, Chemistry and Spanish, though I also studied maths last year. Having attended many Moncrieff-Jones talks over the years I was very excited to be able to present one of my own. I loved having a variety of age groups attend my talk, and the challenge of making my talk interesting for those studying science at 6th form level, but yet accessible for those preGCSE pupils. I hope you enjoy reading my article!
Rabies is a very curious disease indeed. I am sure that many people reading this magazine will have at least heard of it certainly a few times in their lives, but why is this? Many other less ‘famous’ diseases kill far more people each year, so why is it that we place rabies on a pedestal? I first decided to research rabies when I was reading a Biological Sciences Review magazine, which briefly outlined how rabies worked – that it not only is transmitted in the saliva, but that it also damages the host’s brain so that the animal is more likely to bite, thus more likely to pass on this virus to another organism. All I could think was what amazing biology that must be. And hence, this article – finding the truth behind the extraordinary ‘life’ of this virus, and if it really does deserve the fame it has.
The virus itself is classified as; Mononegrivales, Rhabodoviridae, Lyssavirus, Rabies – which means that it has non-segmented negative RNA, is bullet shaped, and causes encephalitis (swelling of the brain). The structure is simple – its outer-most ‘membrane’ is that of its original host. When budding, it cases itself with a bit of ‘stolen’
membrane from the host cell. Underneath this is the Matrix protein which retains the structure of the virus, is bound to the glycoproteins used for entry into foreign cells, and encases the ribonucleocapsid. (The matrix also has been proved by many studies to have an enormous impact into the quantity of budding rabies viruses – a 500,000 fold decrease in the number of budded viruses was shown when they had no matrix, opposed to only a 30 fold decrease when no glycoproteins were present). There is much speculation as to why there is even a nuclecocapsid (protein) at all, however there are two suggested theories; to keep the RNA molecule stable, so it doesn’t react or get broken down (mRNA lasts for 20 minutes in a normal cell), or to prevent the single strand of RNA from hydrogen bonding to itself. If this happened another enzyme would have to be used to break these bonds which could form in many different places and combinations, taking time and using energy. Finally, there are two further proteins (the rabies genome codes for 5 proteins in total), L and P. The L protein is the polymerase enzyme which binds each RNA nucleotide together and the P (phosophoprotein) appears to activate, or act as a coenzyme, to the L protein.
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