Very different 🦠: “2019-nCoV S binds ACE2 with higher affinity than SARS-CoV S; We tested several SARS-CoV RBD-specific monoclonal antibodies and found that they do not have appreciable binding to 2019-nCoV S, suggesting antibody cross-reactivity limited” science.sciencemag.org/content/early/…
2) Interesting tidbits: “2019-nCoV S... most notable variation arising from an insertion in the S1/S2 protease cleavage site that results in an “RRAR” furin recognition site in 2019-nCoV (19), rather than the single arginine in SARS-CoV (fig. S5) (20–23).” What does this mean?...
3) furin site cont’d... “Notably, in influenza viruses, amino acid insertions that create a polybasic furin site in a related position in influenza hemagglutinin proteins are often found in highly virulent avian and human influenza viruses (24).” 🤔
4) Also “The high affinity of 2019-nCoV S for human ACE2 may contribute to the apparent ease with which 2019-nCoV can spread from human-to-human (1), however, additional studies are needed to investigate this possibility.”
5) “The overall structural homology and shared receptor usage between SARS-CoV S and 2019-nCoV S prompted us to test published SARS-CoV RBD-directed monoclonal antibodies (mAbs) for cross-reactivity to the 2019-nCoV RBD” ==> they wanted to test it old SARS antibodies could work.
6) “Despite the relatively high degree of structural homology between the 2019-nCoV RBD and the SARS-CoV RBD, no binding to the 2019-nCoV RBD could be detected for any of the three mAbs at the concentration tested” ==> old SARS antibodies didn’t work at all somehow.
7) “the lack of observed binding suggests that SARS-directed mAbs will not necessarily be cross-reactive and that future antibody isolation and therapeutic design efforts will benefit from using 2019-nCoV S proteins as probes” ==> sounds like have to start a vaccine from scratch.
