Like other coronaviruses, the genome of SARS-CoV-2 contains ten or more open reading frames (ORFs) encoding some 29 proteins. Roughly two thirds of the viral RNA are contained within the first two, called ORF1a and ORF1b.  These are translated into two large non-structural polypeptides (NSPS) that are then cleaved into multiple smaller NSPS.  Based on the functions of their SARS-CoV and MERS-CoV homologs, the NSPS are thought to hijack the membrane structures of the host rough endoplasmic reticulum, rearranging them into double-membrane vesicles (DMVs) wherein viral transcription takes place.  The other one-third of the viral genome contains ORFs for the 4 principal structural proteins: spike (S-protein), nucleocapsid (N-protein), envelope (E-protein), and membrane (M-protein), along with several accessory proteins with as yet unclear functions.
The S-protein represents the key to viral entry into the host cell. First, the virus’s S-protein’s receptor binding domain (RBD) on the S1 domain attaches to the cell surface protein angiotensin-converting enzyme (ACE2). Subsequently, the S-protein’s S2 domain engages the type II transmembrane protease (TMPRSS2) to accomplish a crucial cleavage step known as priming, which allows fusion of the S-protein with the cell membrane. 
Inside the cell, the virus converts intracellular membrane structures into DMVs which serve as factories for viral RNA replication, transcription, and virus particle assembly.  As the viral particles are built, nascent N-proteins insert into the host membrane, forming a nucleocapsid structure. Finally, the virus particle-containing vesicles fuse with the plasma membrane and mature virions are released. 
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