How the history of statistics may have prevented virologists from discovering the origin of Sars Cov 2
Sir Ronald Fisher developed statistics from a foundation begun by Galton, Pearson and others and did so by establishing methods of partitioning variances based on hypothetically infinite populations. This move was questioned by Pearson who criticized it as unnecessary given that the only case in which he felt such a formulation might be useful, the bivariate normal distribution, other techniques could be applied instead. History sided with Fisher and not with Pearson and thus the criticism leveled during the 20s and 30s no matter how well-founded disappeared from cognizance. I contend that this shift in the practice of statistics with respect to regression etc. along with rise of Mendelian genetics resulted in a practice of evolutionary biology such that virologists became prevented from being able to identify reliably the origin of viruses and in particular Sars Cov 2.
The major issue in recovering the origin of Sars Cov2 for instance is being able to distinguish human artificial manipulations of its genome from naturally occurring evolution of its sequence. Statistically this is not an easy task and there are a variety of means to attempt to approach a resolution of the differences. Unfortunately, because there are so very few variants of and mutations in this virus, it is rather difficult to achieve confidence in results that depend on the such samples from the hypothetical population these genomes are supposed to be a part of.
Another path towards a resolution of the issues involved is not to work first and foremost with genotypic differences but to establish instead phenotypic taxonomies, from which genotypic stock variants are classified within. Woodger (1945. “On Biological Transformations.” W.E. Le Gros Clark and P.B. Medawar (eds.) Essays on Growth and Form, presented to D’ Arcy Wentworth Thompson. Oxford: Oxford University Press, pp.95–120) described a logic that relates for multicellular oganisms — zygotes, embryology and taxonomy and this could be applied to viruses such that the impossibilities noted in the irreversibilities of embryological development could establish where and when a man-made manipulation has appeared in an other wise homogenous populations of like kind variants of the same genotypic constitution in the original 1911 etc. sense of Johannsen https://www.journals.uchicago.edu/doi/abs/10.1086/279202
Because history did not incline towards Pearson’s suggestions pre-Mendelian wise, evolutionary ideas derived from distinctions of organismal genotypes and phenotypes have inhibited the conceptual repertoire of theoretical biologists such that virologists have not had specific concepts available to help them deal with describing, defining and discriminating viruses that are man-made from those that have evolved in nature.
Pearson sought instead to base an understanding of the population from which the variants may be statistically associated on the correlation of “organs” but because virologists have only had the notion of the gene as handed them from Mendelians they have not had access to this older biometric intuition which could show that viral ‘organs’ exist for instance as much in the biophysics of non-coding as well as coding regions. The current notion of science’s viral phenotype is depauperate and statistically inaccessible to the degree the older intuition could lead one to think if the notion of homotype and organic correlation of Pearson were reintegrated into evolutionary virology.
In this way the simple swapping of any given viral ORF by mankind could lead to recoverable distortions in the statistical phenotype of said virus as taxonomized regardless of the evolution of the discontinuities through which an otherwise continuous motion continues. This kind of geometric complexification of genealogies into quasi-species cladogeneses has been missing in general because along with the historical developments in statistics that Fisher wrought, came a deprecation of the older Galtonian notion of ancestral influence and potential non-Mendelian transmissions of heredity. It is not clear if evolution produces heredity or if heredity preexists evolution but regardless of how the vital unit is defined going forward, if man is manipulating genotypes then either way it will produce a discontinuity in an otherwise continuously natural process. It is only a matter of distinguishing the distortions the human artificial manipulation and selection causes from the natural discontinuities that genotypes divide out of phenotypes.
Undoubtedly there will be a virologist or two who claim that this is all being taken into account but they will not be doing so based on phenotypes from which genotypes are classed but rather from genotypic differences further differentiated. That path may lead to results but I see no a priori reason why it must, especially if humans try very hard to leave no marks of their manipulations and they stay ahead of the latest knowledge in virology that links the genotypic constitution of virus to it’s expressivity into the range of possible hosts it may find itself niched within.
Because of this reasoning presented above I do not understand why Dr. Fauci continues to complain that an attack on him is an attack on science. If it is not he who is supposed to lead us towards an integrated understanding of the origin of the pandemic then who is? If I am correct about the history of virology with evolutionary theory then it is only going to be someone of his stature who can make the necessary directives to engage virologists towards a reintegration of the history of the statistics of the phenotype and genotype and he should do so regardless of the norm of reaction coming from the public. I hope we will find out that everything I suggest above has already been considered and is nothing but water under the bridge between the disciplines. Given what I have seen in the press over the past month I am not holding my breath.
