Virology:
The virus was identified by Wu et al.(11) and named it WH-Human 1 , and by Zhou et al., simultaneously, who named it 2019-nCoV (12). Later on, the virus name was changed to “SARS-CoV-2” by the Coronavirus Study Group (CSG) of International Committee on Taxonomy of Viruses (ICTV), since it was found to be the sister virus of severe acute respiratory syndrome coronavirus (SARS-CoV)(13). Based on this, the WHO officially announced the virus name as SARS-CoV-2 and the infection as Covid-19 by February 11, 2020 (14).
Coronaviruses belong to the family Coronaviridae  (subfamily Coronavirinae ) and are capable of infecting various wild animals as well as humans where they can cause diseases ranging from mild flu to severe respiratory infections and sometimes fatal complications (13). Among the 6 CoVs which are pathogenic to humans, 4 of them have led to mild respiratory infections, however, the other 2 viruses; SARS and the Middle East respiratory syndrome (MERS) were responsible for epidemics of severe respiratory infections in 2003 and 2012 respectively(15). SARS and MERS have a lower infectivity rate but a higher lethality than SARS-CoV-2 which showed tremendously higher infectivity with apparently lower lethality rate(16).
SARS-CoV-2 is the 7th identified Corona virus and the 3rd zoonotic virus of CoVs that has been transmitted from animals to humans after SARS and MERS (17),(18). In fact, the Chinese horseshoe bats have been proposed to serve as the primary source for SARS-CoV-2. It was reported that SARS-CoV-2 genome has shown around 80% similarity with SARS (19) and nearly all its encoded proteins are homologous with those of SARS(8).
Corona viruses are enveloped single stranded positive sense RNA viruses; their RNA is approximately 30 Kbp. They have a spheroidal shape, their diameter is 80–120 nm and their envelope holds the structural proteins; spike (S), membrane (M), and envelope (E), and they include the nucleocapsid (N) inside the virion which covers the RNA(20).
S is a glycoprotein that projects from the viral membrane, giving it the crown shape and hence the corona virus name, it also helps in the attachment of the virus to different surfaces leading to its high stability and infectivity. Glycoprotein S is composed of 2 subunits: S1 which contains the receptor binding domain (RBD) and also has epitopes that could be recognized by T and B lymphocytes and induce the production of neutralizing antibodies; and S2 which induces the fusion of the virion with the host cell membrane (16).
The surface angiotensin-converting enzyme 2 (ACE2), which is expressed on type-I and -II alveolar cells of the lungs is the main receptor that allows the entrance of SARS-CoV-2 into human host cells. Noteworthy, the expression of ACE2 receptors is not only restricted to the lung cells but their expression on small intestine enterocytes, kidney proximal tubules cells, endothelial cells of arteries and veins, and the arterial smooth muscle was also demonstrated which may explain the extrapulmonary spread of SARS-CoV-2(21). Furthermore, homology modeling showed great degree of structural resemblance between the receptor-binding domains of SARS and SARS-CoV-2(22). However, the degree of affinity of the 2 viruses to their receptors may vary which may be the cause of the higher infectivity and virulence of SARS-CoV-2 in comparison to SARS (23).
Binding between RBD of the virus and its receptor initiates conformational changes of S protein which causes cleavage of S1 and S2 which is a fundamental step that enables S2 to induce the fusion of the virus envelope with the cell membrane followed by the internalization of the viral RNA into the cytoplasm of the host cells by endocytosis(20), (24). Next, the viral RNA acts as a template for the translation of the polyproteins pp1a and pp1b which are then cleaved into 5– 16 non-structural proteins (nsp2-nsp9), which in turn induce reorganization of the membranes to form the vesicles where viral replication and transcription complexes are formed then the assembly of the virions starts and the mature virions are released from the cells by the secretory pathway to infect the neighboring cells (20).
In addition, it was found that entry of the virus in helped by the cellular host type 2 transmembrane serine protease (TMPRSS2) which is expressed on many cell types and has a role in priming the S protein leading to its cleavage at the S1/S2 site to enable fusion of the viral envelope with the host cell membrane. Thus, TMPRSS2 could be a possible biological target in therapies and vaccines strategies and the entry of SARS-CoV-2 into the host cells could be prevented by TMPRSS2 inhibitor (camostat mesylate).  In fact, TMPRS2 inhibitor (camostat mesylate) is already in use in Japan for treatment of pancreatitis which proposes its possible benefit in treating Covid-19 cases(23).