A Brief History of Ebola, Part 1

Title shamelessly cribbed from A Brief History of Time, by Stephen Hawking. (Read it if you haven’t, it’s a great book.)

 

So by now everybody and their dog has at least heard of the Ebola outbreak in Africa. Now, I see that there’s a whole bunch of misinformation going around, and a despairingly large number of FUCKING RETARDS who think that Ebola, motherfucking EBOLA isn’t kind of a big deal. On the flipside, we have the alarmists and tinfoil hat conspiracy theorists. They should be lined up and shot as well.

Or, maybe these people should be given everything they want (in regards to Ebola), and be volunteered to go into the hot zone to test experimental vaccines. Yeah, that’s a more productive use for them. Better than animal testing, at least!

 

But I digress.

 

I’m not here to write about which societal strata should be up against the wall first (vaccine scaremongers, you’re up), I’m here to write about possibly my most favouritest virus in the whole wide world: Ebola.

I’ll be telling you exactly how it was discovered, what it is, how it kills, and why we should be worried, but not too worried about the scale of the latest outbreak.

 

Part 1: Ebolavirus

First things first: What’s a virus? To paraphrase a quote, “A virus is a string of bad news wrapped in a protein shell.”

There’s a very big distinction between bacteria and viruses, chief of which is the fact that bacteria can replicate on their own, and a virus must infect a host cell to replicate.

Viruses are tiny, smaller than the smallest bacterium – most are around the order of a few hundreds of nanometres in diameter. They don’t have cytoplasm or cellular organelles, nor do they contain a nucleus, but they do have a strand of either DNA or RNA, encoding all of their vital proteins.

Most importantly, very few viral infections are amenable to drug therapy. Ebola especially, with its striking lethality and, until now, mostly unknown pathobiology.

 

The first cases of Ebola haemorrhagic fever were seen in 1976, with simultaneous outbreaks in Nzara, Sudan, and in Yambuku, Democratic Republic of Congo (then known as Zaire). By this time, Marburg haemorrhagic fever was already known of, with 31 cases in Germany and Yugoslavia in 1967. Both of these diseases are now known to be caused by members of viral family Filoviridae, but in separate genus.1

 

Transmission of the virus is by contact with infected bodily fluids – patients are contagious as long as their secretions contain the virus. This can be as long as seven weeks after they recover.

Now, some are worried about spread of Ebola and associated viruses by aerosol. This is actually a danger, although not as immediate as some are concerned it could be. A related Filovirus, Reston ebolavirus (RESTV) was seen to bud from alveolar linings in infected monkeys, leading to the fear that it was transmissible by aerosol. This proved to be realised when the virus jumped the species gap, with no contact with the infected animals by humans.

Fortunately, RESTV does NOT cause serious illness in humans. Still, it drives home the point that the current strains causing the 2014 epidemic have the possibility of mutating to be conducive to aerosol spread. Scary stuff, but take heart in the fact that family Filoviridae viruses have very low rates of mutation, around 1/100th the rate of influenza.

 

Ebola haemorrhagic fever disease progression can vary considerably, with onset of initial symptoms between 2 and 21 days after infection. The disease runs its course typically over 14 to 21 days. Infection initially presents with nonspecific flu-like symptoms such as fever, myalgia (muscle pain), and malaise. As the infection progresses, patients exhibit severe bleeding and coagulation abnormalities, including gastrointestinal bleeding, rash, and a range of haematological irregularities.

Just to drive the point home of how appallingly deadly a virus Ebola is, here are some rather graphic descriptions from the initial 1967 Democratic Republic of Congo outbreak.

 

“…Blood was oozing from needle puncture sites, from any part of the skin that had been penetrated, and in some cases from their noses, gums, from the bowels and in some women from the wombs.”2

“I started interviewing people who had recovered… …They had suffered a total desquamation. They had shed the skin of their hands and feet, the hair from their heads, even their nails.”2

“I had no place to lay my instruments, so they stuck out of a bucket of formalin like a porcupine. I had to kneel down to do it [an autopsy] on the grass. Then it started to rain. If I pricked myself through my gloves or my rain-soaked gown, I was as good as dead. I opened the guy up – just made a cut and his abdominal fluid oozed this red serous fluid, his liver was like a purple water balloon filled with blood. As soon as I cut it, it was bulging – the normal tissues seemed to have melted away.”2

 

Ebola virus is deadly for a number of reasons, chief among them the unusually high rate of replication, which results in the infected cell’s protein manufacture machinery being overwhelmed. The full picture of how the virus and the host immune system interact to produce the staggering lethality associated with Ebolavirus infection is still not fully known, but differing host immune responses have been seen to confer an effect on survival.3

 

Further outbreaks have resulted in the discovery of a total of five different ebolavirus species:

  • Bundibugyo ebolavirus (BDBV)
  • Zaire ebolavirus (EBOV)
  • Reston ebolavirus (RESTV)
  • Sudan ebolavirus (SUDV)
  • Taï Forest ebolavirus (TAFV).

Lethality of these species ranged from 31-90%, where significant data were available.

 

The 1967 outbreaks burnt themselves out quickly, with modest barrier and quarantine regulations enough to contain the spread.

 

In part two, I’ll discuss the current outbreak, and more recent advanced in the study and treatment of ebolavirus.

 

Stay angry and limit contact with BSL-4 pathogens, my friends.

EbolaBooze selfie

 

  1. Sanchez, A., A. S. Khan, S. R. Zaki, G. J. Nabel, T. G. Ksiazek, and C. J. Peters. 2001. Filoviridae: Marburg and Ebola viruses, p. 1279-1304. In D. M. Knipe and P. M. Howley (ed.), Fields virology. Lippincott, Williams & Wilkins, Philadelphia, Pa.
  1. Ryan F. 1996, Virus X. HarperCollinsPublishers Hammersmith, London.
  1. Baize, S., E. M. Leroy, M.-C. Georges-Courbot, M. Capron, J. Lansoud-Soukate, P. Debre, S. P. Fisher-Hoch, J. B. McCormick, and A. J. Georges. 1999. Defective humoral responses and extensive intravascular apoptosis are associated with fatal outcome in Ebola virus-infected patients. Nat. Med. 5:423-426.

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