One species jump and then it spread across the globe. Mutations cause SARS-CoV-2 to adapt to the environment and the immune system of the organism that hosts it (i.e. humankind).
As an evolutionary biologist, I can’t remain insensitive to the ongoing discoveries that scientists make about the origin and evolution of the genome of SARS-CoV-2. We’re currently going through a very difficult period, but it’s also an opportunity, hopefully unique, to understand how zoonoses originate and propagate. Just to be clear, because perhaps for some people the term zoonosis is not so well known; it’s about those diseases that pass from animals to humans. There have been many in the past; avian flu, swine flu, rabies and so on.
A team of scholars from Cambridge, England, coordinated by biologist Peter Forster conducted a comparative study called phylogenetic, in which he initially compared 160 sequences of the coronavirus genome and then extended the study to over 1000 sequences.
To perform this study, Forster’s team used algorithms that are used to map the movements of prehistoric human populations; an algorithm quite well known and developed over many years of research and is therefore reliable.
What did the British researchers discover?
In their study, published by a leading international scientific journal, Proceedings of the National Academy of Sciences of the United States of America (PNAS), Cambridge researchers mapped the genetic history of the infection from December 2019 to March 2020 and found that SARS-CoV-2 cleaved into three distinct viral strains. They defined them with a lot of imagination; A, B and C.
The virus was transmitted not from a bat to human, as initially thought, but from a bat to the pangolin and then from this to humans by coming into contact at the (in)famous Wuhan market. For those of you who don’t know, the pangolin is a small mammal, with its body covered with scales and looks like an anteater; a nice little animal and much appreciated on the average Chinese dinner table.
From genetic analysis, researchers have identified a window for species-jumping (i.e. for the transition from pangolin to human, from September 13th to December 7th 2019). This same window is compatible with the findings of an Italian study, published in February 2020).
Back to variants A, B and C. British researchers have identified variant A as the root of the epidemic; the virus strain most similar to that found in both pangolins and bats. Variant B derives from A — from which it’s distinguished by two mutations, and finally there is variant C which is the offspring of B. So far, all logical. The surprise came when Forster’s team mapped the spread of the identified variants. Initially, they thought that they would find variant A very widespread, because it was the first to be passed from animal to human, and then the other variants were less widespread.
The spread of SARS-CoV-2 variants
As it was easy to predict, variant A is present in Wuhan, but isn’t the most common. It is, in fact, variant B that’s more frequently occurring in patients throughout Far East Asia and then spread to Northern Europe, Canada and Brazil.
Variant A is instead, quite prevalent in Australia, Spain and the United States but not in New York — where the most common variant is B and arrived in the Big Apple from Europe — before the closure of airports on March 11th 2020. This difference in the United States is due to the entry routes involved. From Asia, the main entry points are the airports of California; from Europe, the airports of New York and Boston.
Finally, variant C spread to Hong Kong, Singapore and Italy. In Italy, researchers agree that the virus entered in the second half of January via two routes, brought by a German traveler who had been in China shortly before passing through Italy — and another route from Singapore. There were probably two strains introduced, namely B and C, and the latter spread more widely.
What causes the prevalence of the strains?
There are several hypotheses still to be confirmed; however, the most plausible is that SARS-CoV-2 needs to mutate, in order to survive in different parts of the world as confirmed by the fact that the initial mutation rate of the virus is lower. Mutations allow the virus to better adapt to the immune system of the host who obviously tries to fight it.
The ultimate goal of SARS-CoV-2, as with all other viruses, is to survive and propagate, so it must find the right balance between its survival and that of its host (i.e. humans). If it becomes too lethal, it will soon have no more hosts. It’s a mechanism of adaptation and selection well known in nature and to which SARS-CoV-2 clings. In fact, it doesn’t appear that the most recent variants are also the most lethal.
Finally, British scientists call for the use of analysis software in addition to the data already processed, in order to extend the phylogenetic analysis to the new viral sequences that will be made in the future. New analyses will make it possible to predict future outbreaks of SARS-CoV-2 and contain the further spread of the disease worldwide.
This post is also available in: Italiano