On his fascination with the small and lethal
I keep, almost reflexively, reading dribs and drabs on filoviruses—that extremely odd and tiny virus family including only Ebola and Marburg—the hemorrhagic fever viruses.
Dunno what it is about me. Always had this fascination with the small and extremely deadly. I used to (I kid you not) have posters of space-filling models of some of the more alarming organochlorines in my room in university—including, of course, the uber-nasty 2,3,7,8-tetrachlorodibenzo-p-dioxin.
In my defense, that is an awfully pretty molecule—easily, with its two big aromatic rings and the two oxygen bridges, far prettier even than the lovely caffeine molecule in the background of this page. Really must see about ray-tracing one.
Getting back to the filoviruses: I'm not so sure I want a poster of those on my wall. Impressive little things, I guess, but so not pretty, in so many ways.
Intriguing, though, all the same. Let's see: negative stranded RNA, replication strategy as yet poorly understood (unlike certain other viruses using the same essential genetic structure), pleomorphic (meaning they come in all sorts of shapes and sizes), with overlapping genes (meaning, oddly, certain regions of RNA within the virus genome code for more parts of more than one peptide—a feature not unique to the family—there are actually regions like that even in human genomes). Their primary target seems to be the macrophages (important cells in the host's immune system).
And, of course, they liquify your insides.
Researchers are still working on just how it is they do that1. Found this paper suggesting a mechanism: essentially, the thought is the macrophages and monocytes (white blood cells) disperse the virus through the body, and it's the combined destruction of these and the endothelial cells (the cells making up the insides of blood vessels) that creates the final, messy liquification of the host. Some of the endothelial cells are lysed (broken open; it's a thing all viruses do to cells in order to replicate themselves), which greatly weakens the walls of the blood vessels, and when all the monocytes and macrophages are themselves lysed by the viruses within them, a lot of terribly toxic stuff gets dumped into the circulatory system—breaking down whatever integrity the blood vessels had left.
At which point, things melt. Messily.
In a word: yikes.
In other news, that Marburg outbreak in Angola is now the most lethal of the Marburgs. 127 confirmed dead, out of 132 infections, as yet.
The good news: the WHO say they think it's controllable.
Crossin' my fingers for them.
1 Actually, now that I look at it, it appears that, really, confidence that this is the essential mechanism seems quite high now. See Nature's article, new today.
Dunno what it is about me. Always had this fascination with the small and extremely deadly. I used to (I kid you not) have posters of space-filling models of some of the more alarming organochlorines in my room in university—including, of course, the uber-nasty 2,3,7,8-tetrachlorodibenzo-p-dioxin.
In my defense, that is an awfully pretty molecule—easily, with its two big aromatic rings and the two oxygen bridges, far prettier even than the lovely caffeine molecule in the background of this page. Really must see about ray-tracing one.
Getting back to the filoviruses: I'm not so sure I want a poster of those on my wall. Impressive little things, I guess, but so not pretty, in so many ways.
Intriguing, though, all the same. Let's see: negative stranded RNA, replication strategy as yet poorly understood (unlike certain other viruses using the same essential genetic structure), pleomorphic (meaning they come in all sorts of shapes and sizes), with overlapping genes (meaning, oddly, certain regions of RNA within the virus genome code for more parts of more than one peptide—a feature not unique to the family—there are actually regions like that even in human genomes). Their primary target seems to be the macrophages (important cells in the host's immune system).
And, of course, they liquify your insides.
Researchers are still working on just how it is they do that1. Found this paper suggesting a mechanism: essentially, the thought is the macrophages and monocytes (white blood cells) disperse the virus through the body, and it's the combined destruction of these and the endothelial cells (the cells making up the insides of blood vessels) that creates the final, messy liquification of the host. Some of the endothelial cells are lysed (broken open; it's a thing all viruses do to cells in order to replicate themselves), which greatly weakens the walls of the blood vessels, and when all the monocytes and macrophages are themselves lysed by the viruses within them, a lot of terribly toxic stuff gets dumped into the circulatory system—breaking down whatever integrity the blood vessels had left.
At which point, things melt. Messily.
In a word: yikes.
In other news, that Marburg outbreak in Angola is now the most lethal of the Marburgs. 127 confirmed dead, out of 132 infections, as yet.
The good news: the WHO say they think it's controllable.
Crossin' my fingers for them.
1 Actually, now that I look at it, it appears that, really, confidence that this is the essential mechanism seems quite high now. See Nature's article, new today.
posted by AJM at 11:04 a.m. (Permanent Link)
