Updated: Jan 17
Since the end of 2019, when a disease similar to SARS-CoV-1 emerged in Wuhan, China, the scientific community has made it a priority to learn more about the virus which, 8 months later, remains a global pandemic.
On January 11, Yong-Zhen Zhang at Fudan University in Shanghai and his colleagues deposited the genome sequence of a virus isolated from a 41-year-old who had worked at an animal market into a public database, which alerted the world to the existence of a new coronavirus related to SARS-CoV-1. Work by other groups identified the same virus in people with pneumonia. Together, researchers firmly implicated this new coronavirus as the cause of the disease which was initially contracted from bats. On February 11th, the virus was officially named COVID-19.
Early on, important question scientists needed the answer to was “how does the virus infect human cells?” Coronaviruses are decorated with ‘spike’ proteins that interact with specific proteins on the surface of the cells they are infecting. After binding to the cell receptor, the spike has to be cleaved by an enzyme, known as a protease, in the host cell. This activates the spike, which fuses the virus and cell membranes. The SARS-CoV-2 spike binds to the ACE2 receptor at least ten times more tightly than SARS-CoV-1 does and also has a feature that SARS-CoV-1 lacks: a sequence of amino acids that allows it to be recognized and cleaved by an enzyme called furin.
Initial reports of the disease described a severe respiratory illness, mostly affecting the elderly, and similar to that caused by SARS-CoV-1. But in mid-March, we learned that people infected with COVID-19 do not always show symptoms. Data from the cruise ship Diamond Princess revealed that 17.9% of those who tested positive for COVID-19 on the ship had no symptoms after more than 3,700 people had been quarantined aboard the vessel in February when a passenger tested positive.
A study in April attempted to learn more about how the virus is released into the environment. Researchers showed that ‘viral shedding’ seems to peak before or at the same time as symptom onset. That same month in Wuhan, China, researchers looked into the aerodynamics of the viral particles to get more answers about how the virus infects populations. What they found were some areas of the hospitals, staff areas, in particular, had higher concentrations of viral RNA in aerosol-sized droplets. Unfortunately, they could not determine if those droplets were infectious. Meanwhile, according to reports from a US-based research team in April, both SARS-CoV-2 and SARS-CoV-1 were stable and infectious in artificially generated aerosols for up to three hours.
By June, the research community had generated over 80,000 viral sequences of SARS-CoV-2. We have seen symptoms range from mild respiratory infections to those that include gastrointestinal, neurological, renal, cardiovascular, and other complications. The virus’s impact moved beyond older populations and infiltrated younger groups as well. In July, children infected with COVID-19 were reportedly suffering from the multisystem inflammatory syndrome, similar to Kawasaki disease, from a COIVD-19 infection.
We still do not have all the answers, but each discovery brings us closer to an effective treatment or even a vaccine. Among the facts we hope to know soon are how exactly the virus is transmitted between people, the length of time the virus can survive on surfaces, what causes people to experience different complications, and how many asymptomatic people are infected with COVID-19.
Acutis supports our colleagues in infectious disease research and feels privileged contribute to this battle by testing for COVID-19 – and its antibodies – in an effort to detect positive cases and subsequently slow the spread of this disease.