Good news! However, how the SARS-CoV-1 virus was released from the Institute of Virology in Wuhan (a dual use research institute at the time), China will not be answered, I suspect.
"A key step in the origin of many pandemics occurs when an animal-borne virus infects humans and then evolves to spread more efficiently from person to person. That is why scientists and physicians keep a close watch on viruses that could jump from animals to humans, such as emerging strains of avian flu and bat coronaviruses, as well as viruses that have already crossed into humans but, for now, spread poorly among people, such as hantavirus and Ebola.
Researchers have now recreated in a test tube, within just a few months, the evolutionary path the coronavirus followed during the COVID-19 pandemic – from the original Wuhan strain to the emergence of the highly contagious Omicron variants. ..."
From the abstract:
"In vitro protein evolution can provide powerful insights into the amino acid sequences that underlie key biological functions.
Here, we use this to explore the evolutionary trajectories of the SARS-CoV-2 spike protein receptor-binding motif (RBM) binding the human angiotensin-converting enzyme 2 (ACE2), an essential first step in viral infection.
Applying stringent selection pressures starting from the Wuhan or another non-Omicron variant protein-coding sequence results in rapid convergence towards Omicron characteristic mutations and its sub-lineages.
Conversely, under mild selection, only some Omicron-like mutations are selected, however at lower frequencies and with incomplete representation.
Stringent selection results in fewer, but dominant, non-synonymous mutations mirroring Omicron mutations and their variations within its sub-lineages.
Notably, initiating evolution from Omicron itself results in maintenance of Omicron-defining mutations under both conditions.
This evolutionary pattern parallels global SARS-CoV-2 mutation trends as well as in silico simulations, emphasizing the critical role of receptor-binding constraints in shaping viral adaptation.
Mutations primarily associated with immune evasion are not selected by in vitro evolution.
Our findings demonstrate the predictive capacity of in vitro evolution, suggesting Omicron RBM to be the humanized binding motif, emerging from high-stringency selection, superimposed on milder background pressures."
Stringent selection drives convergence toward omicron-like SARS-CoV-2 receptor-binding motifs (open access)
Fig. 1: High-throughput yeast display evolution of SARS-CoV-2 RBD under defined selection pressures.
Fig. 3: Mutation accumulation following in vitro evolution in comparison to SARS-CoV-2.
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