The novel coronavirus — termed SARS-CoV-2 — belongs to a family of viruses that target and infect the upper respiratory tract of mammals. At least six types of coronaviruses are known to infect humans that cause common cold. Scientists have reported the existence of coronaviruses in bats and birds dating back to millions of years ago. They believe that the cross-species transmission is more of a recent event.
The current novel coronavirus has two ancestors, SARS-CoV, which caused over 900 deaths in 2002-03 in China and Hong Kong, and MERS-CoV, which affected Saudi Arabia in 2012, causing close to 850 deaths. Both these viruses first originated in bats before crossing over to humans.
Evidence suggests that the transmission of the novel coronavirus had its inception at the end of December 2019 at a seafood and wild animal market of Wuhan in the Hubei province of China. It is believed that the deadly virus originated from bats and transferred into an intermediate host, the precise identity of which still remains uncertain, before infecting humans.
When a virus jumps to a completely new host, unrelated to their old ones, certain evolutionary changes take place. With this evolution, severe dreadful diseases emerge as we have seen in the past with bird flu, where the viruses moved from birds to humans, and in Ebola, where the virus either jumped from infected bats or other primates to humans. Sometimes, these jumps can also mean a dead end for the virus when there aren’t enough hosts available for its spread.
How does the novel coronavirus enter the human cell?
Structure of the novel Coronavirus
The mechanism that allows any virus to jump across species depends on two fundamental factors. First, it needs access to the host cell. It should also be able to recognize and bind to the proteins on the host cells. This then enables the virus to enter the cell and cause infection. Just like how two pieces of a Lego block fit together, all it takes for the virus to bind efficiently is structural complementarity to the proteins on the host cell.
The novel coronavirus, which is about 60 to 140 nanometers in diameter, has a protein envelope with spike-like projections on its surface, giving it a crown shape. We can consider the first Lego piece to be this spike protein, which has sugars attached around its surface. These sugar-linked proteins (also known as glycoproteins) specialise in recognizing binding sites in the host cell. Another component opens up the virus and allows its RNA to penetrate the host cells. The second Lego piece is a protein called the angiotensin converting enzyme 2 (ACE-2) which is present in cells on the surface of our air passage, bronchial tract, lungs, arteries, and even kidneys. This protein is involved in regulating blood pressure. The novel coronavirus enters our bodies through the airways, goes through the bronchial tract and reaches the lungs. This gives them an access to receptor proteins on these cell surfaces. It turns out that the ACE-2 enzyme and the binding site of the spike protein of the virus complement each other. This makes the binding efficient, like two snug fitting Lego pieces. Soon after entering our airways, the virus rapidly invades the lung cells which are involved in producing mucus and in protecting our lungs from bacteria, virus and other dust particles. The virus attacks and kills these cells. The patient’s airways fill up with fluid making it difficult for the person to breathe. This phase lasts about a week.
It’s only in the next phase that the patient’s immune system gets triggered and recognizes the virus as an invader. At this point, the immune cells activate a variety of chemicals known as cytokines. These chemicals accumulate in the lungs, clogging them completely and making it harder for the patient to breathe. Thus, as pneumonia develops in the patient, the lungs are unable to get enough oxygen and start accumulating carbon dioxide.
At this stage, the patient develops a fever. Under normal conditions, when an invader attacks our body, our immune system fights only the infected cells. But, sometimes, when the immune system goes beyond its control, it goes hay-wire and indiscriminately kills all sorts of cells including the healthy cells of the host. This triggers further immune response resulting in the accumulation of more mucus and clogs lungs worsening the pneumonia. The continued lung damage results in respiratory failure and eventually death.
Elderly people and people with medical conditions such as diabetics, cancer, AIDS, high blood pressure, lung disease and smokers are at high risk of developing pneumonia. The most common reason is the decline of immune function with age, which slows down the production of white blood cells (WBC) and has fewer types of WBCs available to fight an infection. When the virus enters the respiratory tract, their immune system does not recognize the new virus as quickly as the younger people. The delayed response enables the virus to make its way to lungs easily and swiftly.
Recent studies suggest that the novel coronavirus can bind much more strongly to human cells than other related coronaviruses. Due to this strong binding, fewer viruses are needed to cause infection when a person inhales coronavirus through their nose or mouth. Studies have also shown that the spike protein in the novel coronavirus is activated by an enzyme called furin, which is mostly found in the human liver, lungs and small intestine. This suggests that the virus can attack these organs and the infected person can have multiple organ failure. This unique activation site, not present in SARS and other coronaviruses, might enable the novel coronavirus to spread efficiently and rapidly between humans. Moreover, the most common cold viruses tend to infect the upper respiratory tract (nose and throat) and SARS infects the lower respiratory tract (lungs). But, the novel coronavirus infects and replicates throughout our airways, which makes it more dangerous.
What does the future hold?
It has been found that viruses that have RNA as their genetic material jump between species more frequently than viruses that have DNA as their genetic material. Since the RNA viruses need new hosts to survive, their infections, while acute, may not be permanent. They last a relatively shorter time compared to DNA viruses such as herpes virus where the infections are often chronic. This gives us hope that being a RNA virus, the novel coronavirus might not be a permanent crisis.
Scientists from different parts of the world have been working towards finding mutations in the SARS-CoV-2 genome, including those from India. This information is vital for vaccine production. It is crucial to know whether the virus is constantly emerging in a new form or if the different variants of the same virus have infected humans worldwide. The researchers would need to collate data from a large population across the globe to find the answer.
For the virus to be successful in spreading the infection widely, it needs a high density of its host that can transmit the virus. This emphasizes the importance of physical distancing to break the propagation-chain of this virus. Thus, until a proper vaccine is available, breaking the chain is the best way to curb the number of infected people.