The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the seventh known coronavirus type to infect humans. While four cause the common cold, the more troubling viruses – SARS-CoV, MERS-CoV (Middle East respiratory syndrome coronavirus) and now SARS-CoV-2 – can cause severe symptoms and death.1 
SARS-CoV-2 comprises a single RNA strand within a capsule covered with glycosylated spikes, or S proteins. One of the subunits of S proteins recognises and binds to angiotensin-converting enzyme 2 (ACE-2) receptors on host cells, while the other main subunit causes the virus and cell membrane to fuse, allowing the viral RNA into the host cell cytoplasm. A coating of polysaccharides ‘camouflages’ the S proteins so they evade the host’s immune surveillance system during entry.1 
S proteins are the main antigen component of the viral structural proteins and are responsible for stimulating the host’s immune response, hence the focus on them in developing a vaccine. However, other mechanisms might offer alternative approaches. Ways to stimulate neutralising antibodies (NAbs) directly, or to develop monoclonal antibodies or other compounds to prevent S proteins binding to ACE-2 receptors and/or competitively inhibit the fusion process may emerge.1 
Existing vaccines for other diseases, such as the BCG vaccine for preventing tuberculosis, are also being studied for anti-Covid-19 activity.2