Less than a year after being discovered, the coronavirus has worked its way across the globe, infecting nearly 28-million and killing nearly 900,000 people worldwide. In March of this year, the virus was declared a pandemic and many countries (including South Africa) retreated into a lockdown, in an attempt to minimise its spread. Although scientists know a lot more about Covid-19, and have been working hard at finding a way to contain and treat it, the virus that shut down the world remains mysterious. Recently, a Hong Kong man was reinfected by the virus, despite having contracting it months earlier. As the virus slowly mutates and continues to infect individuals around the world, scientists and medical experts are facing a far smarter opponent than previously thought. – Jarryd Neves
âReally diabolicalâ: inside the coronavirus that outsmarted science
By Robert Lee Hotz and Natasha Khan
The new coronavirus is a killer with a crowbar, breaking and entering human cells with impunity. It hitchhikes across continents carried on coughs and careless hands, driven by its own urgent necessity to survive.
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It has a gregarious side that makes it hard to resist. It loves a party. The persistent social climber claims its victims around the world by riding on moments of the most innocent of human interactionsâa shared laugh, a conversation, an embrace. And it is a liar. SARS-CoV-2, which causes Covid-19, often misleads the bodyâs immune systems.
Taken on its own terms, SARS-CoV-2 is the infectious disease success of the past 100 years.
Almost unmatched in the annals of emerging human contagions, it has parlayed a few chance infections into a pandemic of around 27-million confirmed cases so far.
Doctors long expected the advent of such a virus, but even so, the shrewdness of the coronavirus caught many by surprise, and goes a long way to explaining how the world has struggled to contain it ever since.
âWe underestimated it,â said Peter Piot, the head of the London School of Hygiene & Tropical Medicine and a co-discoverer of Ebola, who fell victim to the coronavirus himself in March.
Modern travel made it easy for the new coronavirus to spread to frequent fliers. It slipped unnoticed aboard a cruise ship in Japan and into Zumba classes in South Korea. It infected mourners at a funeral in suburban New York, a choir in Skagit County, Wash., and students on spring break in Florida.
Initially, it was widely believed the virus made its home in bats, which harbour hundreds of different kinds of coronaviruses. But it ventured into new species.
In Hong Kong, Yuen Kwok-yung had been waiting more than a decade for a virus like this to surface.
Batsâ cells can survive surges in metabolismâtheir hearts can go from 10 beats a minute during hibernation to 1,000 beats in flight. It is thought their constitution makes them ideally suited to be a reservoir where a virus can stay, biding its time before jumping to another host species, an event known as a spillover.
At the end of December, Dr Yuen, who has been known to show off his photo collection of bats in caves, was beginning to suspect his fears were realized after hearing about a mystery pneumonia afflicting patients around 600 miles away in Wuhan. He warned Hong Kong officials that something was coming, helping spur the cityâs response.
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After Chinese officials posted the gene sequence of the new coronavirus to share with scientists around the world on January 12th, he and others grew increasingly sure where the killer came from. It was so similar to known bat SARS-related coronaviruses, it must have once been one of them, Dr Yuen said.
Even with spillover, a virus that jumps to a new species doesnât always spread. Some, like avian flu, an influenza originally in birds that can infect humans, largely stop with the new host and donât move from human to human.
But around the same time at the HKU-Shenzhen hospital, where Dr Yuen also heads the microbiology and infectious-disease department, six family members had returned to the southern Chinese city after a visit to Wuhan. They began to feel unwell. The virus had got to them, from the oldest family member, who eventually died, to a 10-year old boy.
The cluster suggested the virus had a dangerous trait, Dr Yuen said: It was spreading between humans.
He shared his findings with experts from the Chinese Center for Disease Control and Prevention, adding to a growing body of evidence that led China to confirm to the world that the virus was leaping from person to person.
Even in those early days, said Dr Yuen, âI suspected that this virus may spread widely throughout the world like the 1918 Spanish flu.â
A borrowed life
All told, there are more viruses than stars in the known universe. Trillions upon trillions of viruses float in the air and ride on the clouds. Scientists at the University of British Columbia estimate that 800-million viruses rain onto every square metre of the planet every day. A coronavirus itself is so small that 500 of them could fit within the diameter of a human hair.
Many scientists canât decide whether a virus is actually alive in any conventional sense. All viruses lead a kind of borrowed life, chemists say. They are a submicroscopic essence of the need to reproduce that by nature is at cross-purposes with humankind.
âViruses donât think. They donât have desires,â said Columbia University virologist Angela Rasmussen.
In the absence of desire, they have purpose: to spread, multiply and survive.
At least 320,000 different viruses infect mammals. There are 219 virus species that are known to be able to infect humans. One researcher found more than a hundred different viruses living inside human lungs. At least six other types of coronavirus are known to infect humans. Several cause the common cold.
SARS-CoV-2 isnât the first virus to have its impact broadened by travel. Smallpox, which killed 300-million people or more in the 20th century alone, first traversed the world by sailing with the Vikings a thousand years ago, new research into the history of epidemics suggests.
The coronavirus belongs to a category of viruses that work by transmitting chemical code, called RNA, sealed inside a protective protein envelope. RNA is a nucleic acid present in all living cells that usually acts as a messenger to relay genetic instructions in DNA, telling the cells what to do. Once the virus gets inside a host cell, it seizes the cellâs reproductive machinery.
Without that manoeuvre, the coronavirus is impotent. It could never reproduce and churn out the millions of new coronavirus cells in a spreading infection. When it kills, it is almost out of carelessness. Its own survival depends on sparing its victims to continue as vehicles for its propagation.
While estimates vary widely, SARS-CoV-2 appears to kill about 0.6% of the people it infectsâabout six times that of a typical flu. By comparison, two other human coronaviruses are far more lethal but harder to contract. SARS-CoV, the original SARS in the 2003 outbreak, has a case fatality rate of 9.6%, while MERS, which stands for Middle East respiratory syndrome, which was first reported in 2012, has an even higher case fatality rate of 34%.
But the current coronavirus causes serious symptoms in many of its victims. As David Hui, a respiratory disease expert at the Chinese University of Hong Kong, said, it is âmild, until it decides to become nasty.â He said the effects were severe in approximately 20% of the people it afflicts.
Investigators quickly realized that SARS-CoV-2 usually seeks out type II lung cells in the people it hijacks. These coat membranes lining the nose, throat and sinuses, and deep into the lungs. The coronavirus pries the cells open with a molecular structure called a spike protein that it uses like a crowbar to force entry.
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In images that scientists made to study it, the round virus bristles with spikes. The spike protein locks onto a receptor called the angiotensin-converting enzyme 2, or ACE-2, which typically regulates a protein that increases blood pressure and inflammation. The receptors seem to be more numerous among older people and higher generally among men than women.
Researchers at the Francis Crick Institute in London used a technique called cryo-electron microscopy to compare this structure to the spike protein of a bat coronavirus most like that of SARS-CoV-2. They saw subtle differences in the spike of SARS-CoV-2 that make it able to bind about 1,000 times more tightly to a human cell than the bat virus, the scientists said.
Once inside a human cell, the new coronavirus has a rare ability to silence alarms that would normally alert the immune system to mobilise antibodies and virus-killing cells, according to microbiologists at the Icahn School of Medicine at Mount Sinai, New York. To do so, it makes special proteins that interfere with the cellâs surveillance system, scientists at the University of Minnesota reported in May.
Bewildering complications
Doctors who first encountered it diagnosed it as a respiratory virus. They looked for symptoms of fever, cough and shortness of breath. But Covid-19 triggered bewildering complications.
People complained of nausea or diarrhea. Some had arrhythmias or even heart attacks. Some suffered kidney damage or liver failure. Some lost their sense of smell or taste. Other patients turned up at clinics with blood clots or swollen purple bumps on their toes.
In most countries where the virus triggered outbreaks, it sent people to the hospital with delirium, blackouts, brain inflammation or strokes, researchers at the UKâs Liverpool University reported in The Lancet Neurology in July.
In a separate review, researchers at Columbia University Vagelos College of Physicians and Surgeons found that up to a third of those infected had neurological symptoms.
By coming into contact with this virus, âyou wouldnât know what kind of effect a meeting with it would have: Maybe you will be unscathed, but maybe you would die,â said the University of Oxfordâs Sarah Gilbert, whose team is developing a vaccine against the virus that is in late-stage human trials.