SARS-CoV-2 is a single-segmented, double-stranded RNA virus. There are no genes being "collected", just two complementary RNA strands that are replicated direct

SARS-CoV-2 is a single-segmented, double-stranded RNA virus. There are no genes being "collected", just two complementary RNA strands that are replicated directly from source RNA and wound into a packed structure by helicases. Gene deletions are extraordinarily uncommon for most viruses, because viruses don't generally carry around entire non-essential genes. SNPs and small indels are indeed common, and because the genome is well-annotated, many of them can be characterized into synonymous, non-synonymous structurally significant/insignificant, frameshift, or non-coding mutations. In the case where a mutation appears to disrupt a gene through a frameshift or structurally significant mutation, further evidence is needed (like multiple independent isolates) that the mutation is not a sequencing artifact. In the case of the link that OP posted (http://cov-glue.cvr.gla.ac.uk/#/deletion http://cov-glue.cvr.gla.ac.uk/#/deletion), only non-frameshifting deletions in coding regions are listed. Most deletions listed are one- or two- codon deletions observed in multiple isolates, which is good evidence. Aside from the terminology issues, OP's claim that some of these deletions may result in an attenuated virus is plausible, subject to further analysis of the structural effect of these mutations (which can be modeled in silico). I don't think it would be useful to "go and visit the people who were infected with each of the different deletion strains and investigate what was their clinical outcome" as OP suggests, since that would be confounded by many factors. Trying to isolate live attenuated virus from the human population in this way carries a lot of risks and potential ethical issues, and amounts to a very low-throughput, difficult screen. The far higher throughput, better researched method that labs are prepared to do is to infect an animal (possibly genetically engineered to be more human-like in its molecular machinery) and wait for the virus to evolve to target that animal, which will make it less virulent in human. However, for SARS-CoV-2 this is especially tricky because of how explosively fast its replication cycle is. Most vaccine trials for coronavirus are working on presenting the human immune system with pieces of the virus instead of live attenuated virus. I would encourage everyone in this thread to read the scientific literature on this, which is abundant and freely available, for example this review: https://www.nature.com/articles/nrd.2015.37.pdf https://www.nature.com/articles/nrd.2015.37.pdf