In 2005 a landmark paper was published, Characterization of the Reconstructed 1918 Spanish Influenza Pandemic Virus, with authors including virologists Terrence Tumpey and Jeffery K. Taubenberger. It was notable in that it was the result of dogged sleuthing which at last provided enough long sought viral genome to sequence the 1918 influenza.
Genomic RNA of the 1918 virus was recovered from archived formalin-fixed lung autopsy materials and from frozen, unfixed lung tissues from an Alaskan influenza victim who was buried in permafrost in November of 1918. The complete coding sequences of all eight viral RNA segments have now been determined, and analysis of these sequences has provided insights into the nature and origin of this pathogen.
Without samples from that one permafrost frozen victim, and a few pathology slides, we would have nothing at all. In contrast, the GISAID Covid database has a staggering eleven million genome sequence submissions. Nothing in history comes remotely close to this genetic scrutiny of evolution in real time. While the Sanford Carter influenza paper promoting Genetic Entropy was incoherent and rife with error, the pandemic has made a further mockery of those ideas. As covid has come up in a few threads recently, I thought it may be time to dedicate a topic to have the forum explore the implications of lessons learned to GE and ID. To prime this:
One - extinction is not due to Genetic Entropy.
Carter Sanford on H1N1: A new look at an old virus: patterns of mutation accumulation in the human H1N1 influenza virus since 1918
These extinctions appear to be due to a continuous accumulation of mutations.
Clades do not just fade away and go extinct due to Genetic Entropy; they are squeezed out by successive mutant strains which are more adapted to circumvent rising host immunity. The essence of GE is that downstream generations will suffer the relentless accumulation of slightly deleterious mutations resulting in fitness decline and ultimate extinction. SARS-CoV-2 has progressed as a clear counter-example, in that existing strains have been successively out-competed by their more fit descendents. This was true of H1N1 influenza as well, but given influenzaâs multi stranded mix and match propensity to frequent recombination, GE proponents pitched the appeal that fitness was refreshed from contributions from natural reservoirs. SARS-CoV-2 recombination has been between circulating strains.
Generally, the virus has trended from high infectivity to unprecedented infectivity, so in that respect the gain in fitness has been both relative and absolute. Eventually, caseloads and severity will drop off, and we may be seeing some of that, but that will be due to the build in herd resistance and the viral response to host adaptation, and not any accumulation of mutation.