I'm new in the world of blogs, so you should have a bit of patience.
A brief introduction: I have studied viral evolution in the last four years during my PhD, so I want a place to discuss about hot topics in this theme.
Since I'm one of that
Ebola virus in West Africa
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| Ebola virus (EBOV). Image available in Wikipedia. |
Since February, several human cases of Ebola fever were reported from five countries (Guinea, Liberia, Sierra Leone, Nigeria and Senegal). This is the largest known outbreak until now. Despite the obvious concerns about the spreading of this horrible disease that claimed more than 1500 lives, I am very interested about the evolution of this RNA virus that is transmitted mainly by human fluids without a vector. During a large outbreak like this, we can observe the virus "negotiating" with the host defenses. These negotiations aren't so clear but they could be well explained by population genetics and natural selection.
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| West Africa EBOV outbreak. Image available in Wikipedia. |
So finally (Uff!) we will reach the purpose of this blog.
In the past Thursday (August 28), Gire et al. published the paper: "Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak" in Science journal, describing the analysis done with 99 genomes of EBOV. Unfortunately, five authors of this study died before the publication.
Less than three months to obtain 99 genomes!
Per se, these results are very interesting since the author's team was able to sequence almost a hundred of genomes in a short time. This study was practically impossible ten years ago, when a EBOV outbreak happened in south Sudan. Undoubtedly, the advances in sequencing technologies overwhelmingly modified the study of pathogens.
Viral population genetics in real time
In my opinion, the most important results described in this paper were the dynamics of EBOV evolution in the Figure 4. They are not so surprising to someone that works with RNA virus evolution. These viruses has short replication times, large population sizes and high polymerase error rates (In this post we can see a cool discussion about polymerase errors and viral fitness). In this context, EBOV could produce a lot of allele propositions, by mutation, and test the fitness in the host during its infection. Imagine that a viral lineage with a better fitness could spread more than other, so this process could generate a very well fitted virus to spread among humans. It is practically impossible determine if the 'best-fitted' virus will be more virulent or not, since the virus could be transmitted before the start of the symptoms.
My opinion 1: this outbreak could be far of the end, in case that the viral lottery of mutations followed by the ratchet of natural selection find a very well fitted EBOV lineage for humans. If this catastrophe really happens, let's cheer on a low-virulent lineage.
My opinion 2: a proposal of treatment should take the viral evolution into account before start the massive distribution of drugs to avoid the selection of high-virulent ones.
Cheers,
Caio
