Yes, it binds to ACE2 receptors more strongly, but once you're infected it's about one order of magnitude less severe.
To note, receptor affinity is not the only mechanism by which infectivity is modulated. You would already expect that a virus that is ten times less severe would spread more easily, and SARS was already able to spread efficiently through air at great distances, so it seems likely that me that receptor affinity is stronger but that other mechanism are weaker. This would explain the fact that it is less severe and not much more infectious.
To note, receptor affinity is not the only mechanism by which infectivity is modulated. You would already expect that a virus that is ten times less severe would spread more easily, and SARS was already able to spread efficiently through air at great distances, so it seems likely that me that receptor affinity is stronger but that other mechanism are weaker. This would explain the fact that it is less severe and not much more infectious.