As was expected, we are seeing a possible mutation to weaker strains like in the last SARS spread.
https://jvi.asm.org/content/jvi/early/2020/04/30/JVI.00711-20.full.pdf
https://jvi.asm.org/content/jvi/early/2020/04/30/JVI.00711-20.full.pdf
https://medicalxpress.com/news/2020-05-scientific-team-unique-mutation-coronavirus.htmlLike SARS -CoV, the SARS -CoV -2 genome encodes multiple open reading frames in the 3' 53 region. We found that the SARS -CoV -2 AZ -ASU2923 genome has a n 81 nucleotide deletion in 54 the ORF7a gene resulting in a 27 amino -acid in -frame deletion (Figure 2B ). The SARS -CoV 55 ORF7a ortholog is a viral antagonist of host restriction factor BST -2/Tetherin and induces 56 apoptosis (11 -14) . Based on the SARS -CoV ORF7a structure (15), the 27 -aa deletion in SARS - 57 CoV -2 ORF7a maps to the putative signal peptide (partial) and first two beta strands. To 58 validate the deletion, we performed RT -PCR using primers spanning the region and verified by 59 Sanger sequencing the amplicons (Figure 2C). Similar deletions in SARS -CoV -2 genomes are 60 emerging, notably in the ORF8 gene (16) that may potentially reduce virus fitness (17). Hence, 61 further experiments are needed to determine the functional consequences of the ORF7a 62 deletion. 63 Collectively, although global NGS efforts indicate that SARS -CoV -2 genomes are relatively 64 stable, dynamic mutations can be selected in symptomatic individuals.
Vaccines are targeting the spike protein which doesn't change."One of the reasons why this mutation is of interest is because it mirrors a large deletion that arose in the 2003 SARS outbreak," said Lim, an assistant professor at ASU's Biodesign Institute. During the middle and late phases of the SARS epidemic, SARS-CoV accumulated mutations that attenuated the virus. Scientists believe that a weakened virus that causes less severe disease may have a selective advantage if it is able to spread efficiently through populations by people who are infected unknowingly.