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Why the New Coronavirus Spreads so Effectively, Explained

Why the New Coronavirus Spreads so Effectively, Explained

A 3D print of a spike protein of SARS-CoV-2, the virus that causes COVID-19, in front of a 3D print of a SARS-CoV-2 virus particle. Caption and photo: niaid/Flickr, CC BY 2.0.

In 1806, the Spanish astronomer José Joaquín de Ferrer observed the fringe-like projections of the Sun’s outer atmosphere that are visible to the naked eye during a total solar eclipse. He described their pattern using the Spanish word for ‘crown’:

It has appeared to me, that the cause of the illumination of the moon … is the irradiation of the solar disk, and this observation may serve to give an idea of the extension of the luminous corona of the Sun.

More than 150 years later, a doctor named D.A.J. Tyrrell noticed while working at the Common Cold Research Unit, Wiltshire, that the electron microscope image of a new virus that caused symptoms similar to the common cold was decorated with closely packed pillar-like projections on its surface – much like the fringes in the solar corona. Dr Tyrrell’s team realised a few other viruses had the same pattern on their surfaces, and decided to call them coronaviruses. The International Committee on Taxonomy of Viruses approved this name in 1975.

Coronaviruses are a group of viruses that use RNA as their genetic material, instead of DNA, the genetic material of nearly all organisms on Earth. And of all RNA viruses, coronaviruses have some of the largest genomes. In the late 20th century and after, coronaviruses have been of relatively little interest to the scientific community because scientists were paying more attention to influenza and HIV. This was in spite of the presence of different coronaviruses that could infect humans (OC43, HKU1, NL63 and 229E). But all of this changed when the coronaviruses that caused severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS) emerged in 2002 and 2012, respectively.

The coronavirus responsible for the SARS outbreak is called SARS-CoV. Scientists suspect it jumped the species barrier twice – from bats to civet cats, and then from civet cats to humans. The MERS virus was found to have jumped from camels to humans.

The coronavirus responsible for the current pandemic is thought to have originated in bats. However, scientists don’t yet know if the cross-species jump happened directly from bats to humans or if there was an intermediate mammal. This virus, previously called the 2019 novel coronavirus, has since been renamed SARS-CoV-2. The genetic materials of SARS-CoV and SARS-CoV-2 are at least 70% alike.

SARS-CoV-2 causes similar but milder symptoms compared to the old SARS virus. However, the current pandemic has evoked a response quite unlike any the world has witnessed in recent times. The devil is in the ~30% difference between SARS-CoV2 and the SARS virus.

All viruses require a receptor protein, which is a biochemical compound on a cell that they can use to enter the cell. So the viruses have a complementary viral protein on their surface that binds to the cell’s receptor protein and rolls out the welcome mat. Once inside, the viruses hijack the cell’s resources to make new viruses.

The complementary viral protein of coronaviruses is called the spike protein, visible as the pillar-like projections on the virus’s surface. The coronaviruses are named so because they are distinguished by the high density of spike proteins. Different coronaviruses use different receptors, but the SARS-CoV and SARS-CoV-2 viruses both use the same protein, called angiotensin converting enzyme 2 (ACE2). Any cell that makes the ACE2 protein – including all cells of the human respiratory tract – can be infected by both the viruses.

However, recent studies have shown that the SARS-CoV-2 spike protein binds more strongly to the human ACE2 protein than the SARS-CoV spike protein. Additionally, the new virus’s spike also has a target site for another human protein called furin, which is made in nearly all cells of the body. This furin-dependent activation is another property absent in the old SARS virus.

These two features together set the SARS-CoV-2 virus apart, and are important reasons why it spreads so effectively.

But in spite of all that we know today about coronaviruses, some questions are still hard to answer, such as what course the current pandemic will take and if there will be future outbreaks of the same virus. Since coronaviruses have animal hosts, the possibility of a newer, deadlier version in the future is always on the horizon.

Immunity to the disease is another thing we need to understand better. For example,  will the disease become weaker and fade out or will it accumulate enough mutations to survive and recur every winter, like its distant cousin influenza? Time will tell.

For now, we do what we can based on what we know.

Arun Panchapakesan is a molecular biologist working in the HIV-AIDS laboratory at the Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru.

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