Recently, a paper describing the sequencing of many samples from patients in Sierra Leone with Ebola was published in Science by Gire et al.:
There have been many headlines referring to this paper with variants of this phrase: “Ebola rapidly mutating!” The meaning and implications of such statements is not always clear due to an incomplete understanding of evolution. Therefore, I think it is worth defining some terms and explaining how viruses evolve generally and how Ebola may be evolving specifically.
First, I should like to clarify the difference between the rate at which mutations occur and the rate at which mutations are observed. Mutations are changes in the genetic sequence. They can occur for several reasons including mistakes which occur during replication of viruses. The rates at which these mutations occur thus depend in part on how accurately enzymes copy genetic sequence. This mutation rate is unlikely to change for a given species unless there is a change in the enzymes involved in copying genetic material. This is a very rare occurence. However, changes in the rate at which mutations are observed is much more common because another important force, selection, affects this process.
Many mutations occur but are never observed. How can this be? If a mutation occurs which is deleterious, it will decrease the likelihood that an organism will survive. Such mutations are common in viruses. However, although unfavorable mutations have always been occuring in Ebola, they were unlikely to be observed because the individual viruses which possesed them did not produce many additional viruses. We say that such viruses were selected against.
One of the key concepts of evolution is that selection can change. If the environment of an organism changes, then what constitutes a “bad” mutation, from the viewpoint of the organism, can also change. For a virus, the host is the environment. If the host for Ebola changes from, say, a fruitbat, to a human, then the environment has changed and the effect of a mutation on the ability of the virus to survive and replicate may change. In fact, a mutation which was selected against in fruitbats may be selected for in humans if it helps the virus survive in its new environment – humans. This will lead to a change in observed mutations in viruses which have colonised a new host even if the rate at which mutations actually occur has not changed.
Thus far, this has been a relatively academic discussion. But now we come to the public health implications of the Science paper. One interpretation of these results is that Ebola is adapting to its new host, humans, by acquiring new genetic sequences which allow it to replicate and spread person to person more effectively. Indeed, given that the virus has apparently been spreading human to human since December 2013, it would be surprising if this were not occuring.
In the past, Ebola would spread from its animal host to humans, pass human to human a few times, and then die out. It never had a chance to adapt to humans. The current outbreak is different. Because Ebola now has had many “passages” through the novel human environment, it has had many more opportunities to adapt to humans. This may be reflected in some of the changes in genetic sequence observed in the Science paper. It may also be reflected in changes in the ability of the virus to replicate and spread in humans. People who expect Ebola to remain unchanging in its new human host are ignoring evolution. If mutations can occur which will allow the virus to spread more efficiently in humans, then, given enough time, such mutations will occur.
Ebola was an animal virus.
It is becoming a human virus.