“The belief that the structure of a protein causes a biological function arises from a misunderstanding of the notion of causality, which is a relation between successive events and not between a structure and an event. A biological event such as a binding reaction cannot be the inevitable consequence of something that is not an event, such as the structure of a molecule.”
Metaphor @Nick Hudson. In order to produce reverse swing you rough up one side of a cricket ball. This “causes” the ball to move in the air. However the ball only actually moves in the air when delivered through the action of the bowler. There are complex interactions with air humidity involved. You can’t really predict which delivery will actually swing, even though you are using the same ball. So you can’t say that roughing up the ball “causes” reverse swing.
The implication being that studying the configuration of the spike protein does not permit statements to be made regarding causality. The author of this statement opposed reductionist thinking in all its forms
What happened in 2012 was that the ICTV (International Comitee on Taxonomy of Viruses) changed the definition of a species from polythetic to monophylitic. @Heike Brunner. @Nick Hudson @Gabor This sounds like an esoteric, semantic and philosophical issue. However it is not. The change was vehemently opposed by the older generation of virologists on the grounds that the wide range of possible properties that were previously used when defining species (and as a consequence also applied to variants) were being ignored in favour of a definition based only on a genetic sequence and that required monophyly (i.e. a defined sequence from which other members of the species were derived). Prior to this change it was meaningless to even search for “the origin of”the virus“. Van Regenmortel defines a”virus" as an individual entity that can be considered to belong to a named class, but stresses that assigning a virus to a classification is not the same as defining the class. As coronaviruses are known to engage in horizontal gene transfers (recombination) the new definition is particularly inappropriate. If I were a lawyer I would constantly be asking all those involved in testing and vaccine development to define what it is they are testing for and what it is that vaccines prevent. Until they answer this question we are appear to be going around in circles. When they do answer it we will know that we are going around in circles.
The first document produced by the ICTV regarding nomenclature stated .. “In terms of taxonomy, SARS-CoV-2 is (just) another virus in the species Severe acute respiratory syndrome-related coronavirus” (Gorbalenya et al. 2020)
By “just another virus” they meant that it was a sequence that fell within the pre-defined class of entities falling under the definition of the species SARS. So the “origin” debate does not concern the species. It concerns the sequence (i.e. the “virus”). Which is an “inviduum” as @Nick Hudson has stated. On this definition “the virus” could not have been circulating prior to the publication of the first Wuhan sequence, but the species pre-dated it.
It might also explain why computer programmers get this wrong. In object oriented programming (OOP) an object is an instance of a class. It inherits all the classes properties, including data and code. So it is tempting to think of a “virus” as “just” an instance of the viral “species”. I suspect many scientists instinctively do this, without even reflecting further. However this is actually wrong. The class is in fact defined by the collective properties of the instances that are used to define it. This is still implicit even under the 2012 ICTV definition of a viral species, although not stated clearly anymore. Although inheritance does occur, inheritance does not rely on the species definition to determine an original “type” class. And when horizontal gene transfers occur information is inherited across classes, making the concept of “cookie cutting” from the original class incorrect.
More from Van Regenmortel, master of viral taxonomy “Classifying objects is a human prerogative based on the capacity of the mind to conceptualize and recognize the presence of similar properties in individual objects. Properties and classes are related abstract entities: when a property is ascribed to an object, the object thereby becomes a member of a particular class defined by that property. If a virus has a positive strand RNA genome, it becomes automatically a member of the class of positive strand RNA viruses. Classifying viruses consists in inventing taxonomic classes and allocating individual viruses to these classes so that similar viral agents are grouped together.”… OK that’s actually quite clear. So I have a question. If the overriding defining property of SARS-CoV-2, which is the motivation for producing immunity through developing mRNA vaccines, is infection though binding to ACE2 .. Why do we not define a class of coronaviruses that uses the ACE2 receptor as belonging to a single species?
If this sounds like an absurd idea based on current sequence data, provide another motivation for picking out the spike protein as the defining characteristic of the virus that was the putative origin of all the sequences that are being picked up globally by PCR tests.
Presuming that your answer is that multiple coronaviruses belonging to additional genera were circulating in both animal and human populations all with similar properties with respect to receptor bindings, then additional properties of the entities known as SARS-Cov-2 must therefore define their class membership. In which case the uniqueness of the furin cleavage site must be defined with respect to the probability of its co-occurence along with these additional properties. In which case the lab origin theory should not be focussed only on the spike proteins. If it then just comes down to numerical comparisons of base pair similarities, then any other part of the genomic sequence has identical importance. But this is clearly also absurd as the focus must be on conserved sequences under purifying selection. Which pushes the argument back onto the spike! I simply can’t resolve this in my head.
If recombination and horizontal gene transmission occurs (as we know it does) should we be basing phylogenies on some defined segments of the viral genome rather than the entire sequence? If so, how does this relate to pathogenesis?