First diagnosed in December 2019 in Wuhan, China, the coronavirus disease (COVID-19) has emerged as a worldwide pandemic. COVID-19 can result in mild flu-like symptoms for some younger people, but for the elderly and patients with underlying pre-existing respiratory conditions, potentially fatal dyspnea and acute respiratory distress syndrome may develop. COVID-19 is caused by a novel beta-coronavirus that has been named, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

Like other coronaviruses (order: Nidovirales, subfamily: Coronaviridae, family: Coronavirinae), SARS-CoV-2 is an envelope virus containing a single-stranded positive-sense RNA genome with a length of 30 kilobases (kb) – one of largest genomes among RNA viruses.[1] SARS-CoV-2 has been named because the RNA genome is about 82% identical to the original SARS-CoV (sometimes named SARS-CoV-1) and both viruses belong to the same Betacoronavirus genus.

The SARS-CoV-2 genome encodes four major structural proteins: (1) Nucleocapsid (N), (2) Membrane (M), (3) Envelope (E), and the (4) Spike (S) protein. Among the four coronavirus structural proteins, the spike (S) and the nucleocapsid (N) are the main immunogens (Figure 1). The spikes are composed of three identical spike proteins (i.e., homo-trimeric structure) and have a triangle shape when viewed from the top (Figure 2). The spike (S) protein is a class I virus fusion protein[2] that facilitates (a) attachment of the virus to the host cell surface, (b) cell entry, and (c) sometimes cell-cell fusion.