To your first point: my intuition is that ACE2 is far too small for the genome to pass through itself. ACE2 is an enzyme that’s bound to the membrane—it actually just cleaves angiotensin 1 to angiotensin 2 (hence ‘angiotensin cleavage enzyme, ACE2). It does pass through the membrane, but it’s not really a ‘channel’—it is simply localised to the cell membrane, and acts on substances extracellularly.
Enveloped viruses can enter cells in many ways (principles of virology chapter 5 is really excellent for this, if you’re interested). It seems that SARS-CoV (the original outbreak) enters cells primarily how it is implied above—simple, direct membrane fusion mediated by the ACE2 receptor. There is some speculation that it may under some circumstances be endocytosed (taken into the cell in a separate sphere of membrane) and then break free of the endosome (the bubble) in a pH-dependent way. Obviously this is further complicated by the fact that this is SARS-CoV-2 that we’re really interested in, so I thought it would be best to leave it blank. You’re right in thinking this process is similar to SER budding, though.
To your second point: I wasn’t actually sure! I’ve done some research, but honestly I’m still not as confident about this as about the rest. As far as I can tell, for most viruses nucleocapsid shedding is either mediated by substances or organelles inside the cytoplasm—ribosomes in particular, apparently, bind to the capsids of some viruses and destabilise them—or is part of the process of receptor binding. Some viruses, for instance, seem to be able to leave their nucleocapsid behind with their envelope so it coats one side of the cell membrane.
Sorry I can’t give a better answer, hope it helps!
To your first point: my intuition is that ACE2 is far too small for the genome to pass through itself. ACE2 is an enzyme that’s bound to the membrane—it actually just cleaves angiotensin 1 to angiotensin 2 (hence ‘angiotensin cleavage enzyme, ACE2). It does pass through the membrane, but it’s not really a ‘channel’—it is simply localised to the cell membrane, and acts on substances extracellularly.
Enveloped viruses can enter cells in many ways (principles of virology chapter 5 is really excellent for this, if you’re interested). It seems that SARS-CoV (the original outbreak) enters cells primarily how it is implied above—simple, direct membrane fusion mediated by the ACE2 receptor. There is some speculation that it may under some circumstances be endocytosed (taken into the cell in a separate sphere of membrane) and then break free of the endosome (the bubble) in a pH-dependent way. Obviously this is further complicated by the fact that this is SARS-CoV-2 that we’re really interested in, so I thought it would be best to leave it blank. You’re right in thinking this process is similar to SER budding, though.
To your second point: I wasn’t actually sure! I’ve done some research, but honestly I’m still not as confident about this as about the rest. As far as I can tell, for most viruses nucleocapsid shedding is either mediated by substances or organelles inside the cytoplasm—ribosomes in particular, apparently, bind to the capsids of some viruses and destabilise them—or is part of the process of receptor binding. Some viruses, for instance, seem to be able to leave their nucleocapsid behind with their envelope so it coats one side of the cell membrane.
Sorry I can’t give a better answer, hope it helps!