It just has RNA that can be transcribed directly by the host ribosome.
youtu.be/oCelMyMtRCk?t=167 mentions that they get their lipid layer from the Golgi complex of the host, where they replicate.
www.youtube.com/watch?v=zvuYJTL90J8&t=166s The Coronavirus Replication Cycle by Kevin Tokoph (2020)
COVID happens in two stages:
  • viral infection
  • inflammatory phase, where the body takes over, and sometimes harms itself. It seems that people are not generally contagious at this point?
This distinction is one of the reasons why separating the virus name (SARS-CoV-2) from the disease makes sense: the disease is much broader than the viral infection.
Why is it there such a clear separation of phases?
Why do people with mild symptoms go on to die? It is a great mystery.
Ciro Santilli's theory is that COVID is extremely effective at avoiding immune response. Then, in people where this is effective, things reach a point where there is so much virus, that the body notices and moves on to take a more drastic approach. This is compatible with the virus killing older people more, as they have weaker immunes systems. This is however incompatible with the fact that people don't seem to be contagious after the viral phase is over...
There are a few possibilities:
Genes at: www.ncbi.nlm.nih.gov/nuccore/MN908947.3 TODO protein list on a database?
50-200 nanometers in diameter.
www.youtube.com/watch?v=6DxlkxA82FM COVID-19 Symposium: Entry of Coronavirus into Cells | Dr. Paul Bates
Interaction points:
Video 1.
Model of Membrane Fusion by SARS CoV-2 Spike Protein by clarafi (2020)
Source.
Some are named after the encoded protein. Others that are not as clean are just orfXXX for open reading frame XXX.
Largest gene, polyprotein that contains SARS-CoV-2 non-structural proteins 1 to 11.
Envelope.
Membrane.
Spike.
Nucleocapsid phosphoprotein, sticks to the RNA inside.
www.nature.com/articles/s41467-020-20768-y mentions functions:
  • helps pack the viral RNA into the capsule
  • also has a side function in immune suppression
These are also required for test tube replication.
Protease that cuts up ORF1ab. Note that it is also present in ORF1ab.
The RdRp, since this is a Positive-strand RNA virus.
Unlike SARS-CoV-2 non-structural protein, these are not needed for test tube reproduction. They must therefore be for host modulation.
Integrates its RNA genome into the host genome.
Sounds complicated! The advantage is likely as in HIV: once inside the cell, it can remain hidden far away from the cell surface, but still infections.
Converts RNA to DNA, i.e. the inverse of transcription. Found in viruses such as Retrovirus, which includes e.g. HIV.

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