Source: Lancet, David Brin, Wikipedia Antigenic Shift, CDC
Written By Brian Wang,

Genetic analysis of the COVID-19 virus shows that it is very similar to a coronavirus in bats but the receptor binding looks like the receptor for SARS. This could happen naturally with slow changes of one in ten thousand sequences each year. This appeared all at once. This gives support to the belief that the Wuhan lab took the bat virus and attached the SARS receptor.

However, this could happen with the mechanism of antigenic shift. While influenza viruses change all the time due to antigenic drift, antigenic shift happens less frequently.

Antigenic shift is the process by which two or more different strains of a virus, or strain of two or more different viruses, combine to form a new subtype having a mixture of the surface antigens of the two or more original strains. The term is often applied specifically to influenza, as that is the best-known example, but the process is also known to occur with other viruses, such as visna virus in sheep. Antigenic shift is a specific case of reassortment or viral shift that confers a phenotypic change.

Antigenic shift is contrasted with antigenic drift, which is the natural mutation over time of known strains of influenza (or other things, in a more general sense) which may lead to a loss of immunity, or in vaccine mismatch. Antigenic drift occurs in all types of influenza including influenza A, influenza B and influenza C. Antigenic shift, however, occurs only in influenza A because it infects more than just humans. Affected species include other mammals and birds, giving influenza A the opportunity for a major reorganization of surface antigens. Influenza B and C principally infect humans, minimizing the chance that a reassortment will change its phenotype drastically

The Lancet published Genomic characterization and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding.

Phylogenetic analysis revealed that 2019-nCoV fell within the subgenus Sarbecovirus of the genus Betacoronavirus, with a relatively long branch length to its closest relatives bat-SL-CoVZC45 and bat-SL-CoVZXC21, and was genetically distinct from SARS-CoV. Notably, homology modeling revealed that 2019-nCoV had a similar receptor-binding domain structure to that of SARS-CoV, despite amino acid variation at some key residues.

As a typical RNA virus, the average evolutionary rate (antigenic drift) for coronaviruses is roughly one in ten-thousand nucleotide substitutions per site per year, with mutations arising during every replication cycle. It is, therefore, striking that the sequences of 2019-nCoV from different patients described here were almost identical, with greater than 99·9% sequence identity. This finding suggests that 2019-nCoV originated from one source within a very short period and was detected relatively rapidly. However, as the virus transmits to more individuals, constant surveillance of mutations arising is needed.

Phylogenetic analysis showed that bat-derived coronaviruses fell within all five subgenera of the genus Betacoronavirus.