The Ebola Outbreak of 2013-2016: Why So Deadly?

The outbreak of Ebola Virus Disease in West Africa was the biggest outbreak of the disease we’ve yet to encounter. It killed more people than the previous 25 outbreaks combined and arose in a region of Africa that had never seen Ebola before. The big questions scientists are still asking is why West Africa, why now, and why did it affect so many people?

There are five strands of ebolavirus, the main one to have affected central and western Africa is the Zaire strand – simply known as “the” Ebola virus. It’s a zoonotic disease, which means it can be transmitted from animals to humans. An essential part to understanding a zoonotic disease is knowing which animal is its reservoir host; which we do not when it comes to Ebola. Looking at where the human (and non-human primate) outbreaks occur, we know it must be an animal whose habitat spans across the whole of sub-Saharan Africa. There has been speculation that this animal is the fruit bat, however there has not been a successful isolation of the virus from the blood of the animal itself.

Ebola virus is a single stranded RNA virus, which only codes for seven proteins. Because of this nature, it has a high mutation rate (relative to DNA viruses). This is because the protein that aids the replication of the RNA lacks the ability to recognise damage done to the sequence that encodes the proteins. Despite this, Ebola virus was considered to have a relatively stable mutation rate –  so the virus seen at the beginning of the epidemic hadn’t changed vastly since the virus found in the first ever Ebola outbreak; in fact, they were 97% similar. This evidence only considered the virus strand found at the onset of the outbreak, but noticing how this recent epidemic covered approximately two years with over 28,000 cases, we later discover mutation could possibly have played a larger role than previously suspected.

Two articles released in Cell in 2016 focused on the virus strands after the onset, revealing a particular mutation that occurred some three months after the first case in December 2013. Found in the form of a change in the molecule that the virus uses to hijack cells, this mutant increased infectivity in human cells and may have been a contributing factor in the mortality of Ebola. By March of 2014, the virus had split into two distinct lineages (separated on the basis of this particular mutation). One of the articles used pseudoviruses to infect human and bat cell lines. They found the mutation to have increased infectivity to human cells but decreased to bat cells. The reports found subsequent mutations aided the virus also. There is now a possibility that the virus itself adapted to the human body, to better thrive in the given environment.

Although compelling evidence, neither group of researchers had access to a biosafety level 4 laboratory (hence the use of pseudoviruses) and the latter experiment was tested on cell lines, so we can only assume how the virus would act inside the patient. The following question of whether this affects how Ebola fatally attacks its victims is still being asked, and it would perhaps be reaching to assume to what scale this mutation affected people in West Africa. It is still widely considered that the sheer scale of the 2013-2016 outbreak is explained by arrival of Ebola in heavily populated urban cities, in countries that had incredibly weak health institutions.

So to answer my initial question simply – we do not know. There are many theories behind why over 11,ooo had died in this epidemic, and not all of them are solely biological. The World Health Organisation in particular fell victim to criticism that they didn’t (or rather couldn’t) respond to the outbreak in a controlled and methodical fashion. Anthropologist Paul Farmer described Liberia, Sierra Leone and Guinea as “public health deserts”, with the lack of health professionals and poor facilities, were the main reasons so many people died.

 

Sources & extra links

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