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The outbreak of the Coronavirus disease 2019 (COVID-19 for short) has created a global health crisis (Figure 1).

Not only do the high infection rates threaten the survival of millions, but the safety measures necessary to fight it also create a crisis in mental health and erode our sense of well-being.

This course covers introduction to coronavirus pandemic and structural organization of coronavirus.

Figure 1. Global health crisis starting December 2019
Figure 1. Global health crisis starting December 2019

The virus that caused COVID-19 is new to us but it belongs to a family of viruses called Coronavirus.

It was named SARS-CoV-2 by the International Committee on Taxonomy of Viruses on account of its genetic similarity to the SARS virus from 2002-3, although differences in disease spectrum and transmission was noted.

In the 1960s, researchers in the United Kingdom and the United States discovered coronavirus for the first time by isolating two viruses with crown-like structures while researching the common cold in humans.

Later in 1968, the term coronavirus was coined for the entire group causing cold in humans and making animals sick too. Researchers thought that coronaviruses caused only mild symptoms in humans, until the outbreak of severe acute respiratory syndrome (SARS) in 2002.

Coronaviruses (CoVs), enveloped RNA viruses, are characterized by club-like spikes that project from their surface, an unusually large RNA genome, and a unique ability to replicate (Figure 2).

Coronaviruses can cause respiratory or gut-related diseases and, in some cases, neurological illnesses or hepatitis.

Coronaviruses have deadly dynamism as they frequently recombine, swapping chunks of their RNA with other coronaviruses.

Scientists are finding out that the SARS-CoV-2 virus has evolved an array of adaptations that make it much more lethal for humans than the any other coronavirus.

Figure 2. A coronavirus
Figure 2. A coronavirus

Unlike other forms, SARS-CoV-2 can readily attack human cells at multiple points, with the lungs and the throat being the main targets (Figure 3).

Once inside the body, the virus makes use of diverse resources and becomes severely lethal.

How exactly it kills, whether it will evolve into something more lethal, and what it can reveal about the next outbreak is still uncertain.

Figure 3. Coronavirus attacking lung with severe pneumonia and disintegrating it
Figure 3. Coronavirus attacking the lung with severe pneumonia and disintegrating it

Structural Organization

The name “coronavirus,” coined in 1968, is derived from the “corona”-like or crown-like morphology  observed in these viruses in the electron microscope.

Coronavirus virions are spherical in shape. The most prominent feature of coronaviruses is the club-shape spike projections on the surface of the virion.

The surface spikes or peplomers of these viruses, have been variously described as club‐like, pear‐shaped, or petal‐shaped.

These virions  have an average diameter of 100–160 nm (Figure 4).

Figure 4. Structure of a coronavirus virion
Figure 4. Structure of a coronavirus virion

The coronavirus family contains 11 recognized species, which are divided into five groups based on the antigenic structure of N and M peplomer protein (Spike).

The genomes of all coronaviruses have a similar structure. They contain the replicase gene, which encodes multiple enzymatic activities.

The genome RNA is complexed with the basic nucleocapsid (N) protein to form a helical capsid found within the viral membrane (Figure 5).

The membranes of all coronaviruses contain at least three viral proteins, as listed below:

  1. Spike (S), the type I glycoprotein that forms the peplomers on the virion surface. This give the virus its corona- or crown-like morphology seen under the electron microscope
  2. The membrane (M) protein, a protein that spans the membrane three times and has a short N-terminal ectodomain and a cytoplasmic tail
  3. Small membrane protein (E), a highly hydrophobic protein
Figure 5. A virion
Figure 5. A virion

For virion replication to begin, the spike proteins first bind to specific host cell surface receptors that are embedded in the host cell membrane.

This process is called host-cell recognition. In the case of SARS-CoV, this receptor is angiotensin-converting enzyme 2 (ACE2).

ACE2 is a regular cellular protein that happens to be used by the virus to gain entry to the cell.

It has been confirmed that the new coronavirus SARS-CoV-2 also binds to ACE-2 and structurally resembles SARS-CoV (Figure 6).

Figure 6. The spike protein (red) mediates the coronavirus entry into host cells. It binds to the angiotensin converting enzyme 2 (blue) through its S1 subunit and then fuses viral and host membranes through the S2 subunits. Source: PDB entry 6cs2
Figure 6. The spike protein (red) mediates the coronavirus entry into host cells