Non-structural protein (NSXx)
Spike (S)
Membrane protein (M)
Nucleo protein (N)
Envelope protein (E)
Hypothetical protein - Open Reading
Frame (NS10): It is not clear yet if it is a protein
CoVid-19 is causing the biggest pandemic in recent times, hitting the whole world. Currently, there are many scientists groups actively working to understand the biology of the virus responsible for this disease, SARS-CoV-2. So far, what we know about how the genome / proteome of the virus is organised can be summarised in this schema. Two major proteins are transcribed into two poly-proteins: R1a and R1ab that later self-precess to render a set of different non-structural proteins (NSP1 to NSP16). The S Glycoprotein forms the typical spikes in coronaviruses and is also responsible for recognition and attachment to the host cell surface. A set of auxiliary proteins are still under study and some (ORF10) have not even been characterised and remain as hypothetical.
Spike protein, trimeric complex S1-S2-S2': Attaches the virion to the cell membrane by interacting with host receptor, initiating the infection. Binding to human ACE2 receptor and internalization of the virus into the endosomes of the host cell induces conformational changes in the Spike glycoprotein. Uses also human TMPRSS2 for priming in human lung cells which is an essential step for viral entry. Proteolysis by cathepsin CTSL may unmask the fusion peptide of S2 and activate membranes fusion within endosomes.
Part of Replicase polyprotein 1a and 1ab. Responsible for the cleavages located at the N-terminus of the replicase polyprotein. In addition, PL-PRO possesses a deubiquitinating/deISGylating activity and processes both 'Lys-48'- and 'Lys-63'-linked polyubiquitin chains from cellular substrates. Participates together with nsp4 in the assembly of virally-induced cytoplasmic double-membrane vesicles necessary for viral replication. Antagonizes innate immune induction of type I interferon by blocking the phosphorylation, dimerization and subsequent nuclear translocation of host IRF3. Prevents also host NF-kappa-B signaling
