Different mechanisms allow viruses to enter our cells. By mimicking host molecules, viruses gain entry into cells and evade the immune response. The S-protein of SARS-CoV-2 can bind to the human angiotensin-converting enzyme 2 (ACE2) by wearing the disguise of a particular epithelial sodium channel (ENaC-α) in humans \cite{Yan2020,Lan_2020}. To exert its function, ENaC-α binds to ACE2 and is recognized and cut by a specialized protein called transmembrane protease serine 2 (TMPRSS2). The site at which TMPRSS2 cuts ENaC-α is identical to a small part of the S-protein of SARS-CoV-2. Given the high structural similarity between the S-protein and our own ENaC-α, both the ACE2 and TMPRSS2 cannot discriminate between the virus and our molecules and allows viral particles to enter our cells \cite{Anand_2020,33116300}.
Once inside our cells, the viral particle disassembles and releases its RNA. The viral RNA serves as a manual for our ribosomes to produce the components required to generate more viral particles. The first viral protein that our cells synthesize is called replicase, and it makes thousands of copies of the viral RNA. These thousands of viral RNA copies are used to produce more viral components and assemble thousands of new viral particles that will be released by the infected cell upon its death. The newly generated viruses are ready to infect thousands of cells and start a new cycle of infection, replication, and dissemination \cite{coronavirus,animation}.