Everyone is affected by the Covid-19 pandemic. For us in Malaysia, large gatherings for wedding are out. Mosque attendance is limited by number. Masks are required to enter premises.
We noted an interesting article written by Robert Lee Hortz and Natasha Khan about deadly facts of Covid-19 virus on September 8th, 2020, in Wall Street Journal online.
They likened the Covid-19 virus as a killer with a crowbar, breaking and entering human cells with impunity. It hitchhikes across continents carried on coughs and unclean hands, driven by its own necessity to survive. Cheap and modern travels make it easy for Covid-19 virus to spread to frequent fliers.
Initially, it was believed that the virus lives in horseshoe bats, which habour hundreds of different kinds of coronavirus. Then it moves to a new animal species (human). A professor at the University of Hong King, Yuen Kwok Yung, who studied SARS outbreak in 20023, showed that 39 per cent of Chinese horseshoe bats could be harbouring SARS-related coronaviruses.
He noted that bats’ cells can survive surges in metabolism that their hearts can go from 10 beats a minute during hibernation to 1,000 beats a minute in flight. It is thought their constitution makes them ideally suited to be reservoir where a virus can stay, biding its time before jumping to another host species, an event known as a spillover.
Even with a spillover, a virus that jumps to a new species doesn’t always spread. Some like avian flu, an influenza originally in birds that can infect humans, largely stops with the new host and don’t move from human to human. According to the article, there are more viruses than stars in the known universe. Trillions upon trillions of virus float in the air and ride the clouds. Scientists at the University of British Columbia, Canada, estimate that 800 million viruses rain onto every square metre of our planet every day. A coronavirus itself is so small that 500 of them could fit within the diameter of a human hair.
Many scientists can’t decide whether a virus is actually alive in any conventional sense. Viruses lead a kind of borrowed life, chemists say. They are a sub-microscopic essence of the need to reproduce that by nature is at cross-purposes with humankind.
“Viruses don’t think. They don’t have desires, “ said Columbia University virologist Angela Rasmussen.
In the absence of desire, they have purpose: to spread, multiply and survive.
There are at least 320,000 different viruses that infect mammals. About 219 species are known to be able to infect humans. The article noted that 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 isn’t the first virus to have its impact broadened by travels. Smallpox, which killed 300 million people or more in the 20th century alone, first traversed the world by sailing ships 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, which is sealed in 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 cell’s reproductive machinery.
Without that maneuver, the coronavirus is impotent. It could never reproduce and churn out the millions of new virus cells in a spreading infection. When it kills, it is almost out of carelessness. Its own survival depends on sparing its victims as vehicles for its propagation.
While estimates vary, SARS-CoV-2 appears to kill about 0.6 per cent of the people it infects—six times that of a typical flue. 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 of 9.6 per cent, while MERS, which stands for Middle East respiratory syndrome, which was reported in 2012, has an even higher case fatality rate of 34 per cent.
The current coronavirus causes serious symptoms in many of its victims. The effects are severe in approximately 20 per cent of the people it afflicts, according to David Hui, a respiratory expert of the Chinese University of Hong Kong. Investigators 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 cell open with a molecular structure called a spike protein that it uses like a crowbar to force entry.
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 generally higher among men than women.
Once inside a human cell, the new coronavirus has a rare ability to silence alarms that would normally alert the immune system to mobilize antibodies and virus-killing cells, according to microbiologists at the Ichan School of Medicine at Mount Sinai, New York, USA.
Doctors who first encountered it diagnosed it as a respiratory virus. They looked for symptoms of fever, coughs and shortages of breadth. But Covid-19 virus 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 an outbreak, it sent people to the hospital with delirium, blackouts, brain inflammation or strokes.
The virus has infected millions of people who never got sick or were only mildly ill, which allowed it to reproduce while its victims spread it in ever-widening social circles.
The virus’s own internal chemistry alone wasn’t enough to account for so much variations of symptoms, severity and deaths.
Variations of contributing causes
There are many possible contributing causes: old age, gender, underlying chronic diseases such as diabetes, lack of healthcare and poor diet. Investigators also turned their attention to gene variations that make some uniquely vulnerable.
“The immune system in people is as diverse as beauty, height, intelligence and any other human feature, “ said molecular immunologist Michel Nussenzweig at Rockefeller University in New York, US. “Not everybody is the same in their ability to fight infection.”
At Rockefeller and New York Genome Center, scientists are comparing the entire genomes of those most severely affected by the virus to those who experience only mild symptoms—and then to the coronavirus itself.
These scientists extract the virus from the nose swab mucus collected from the people it infected and, through high-speed genome sequencers, reduce it to biochemical code for analysis. Some are samples drawn from people who suffered no more than a fever and a cough. Others come from autopsies.
The bad news is that the virus is evolving
The four bases of virus RNA are written in an alphabet composed of nucleotide chemicals: adenine (A), cytosine (C), guanine (G) and uracil (U). In its rush to make new copies of itself, the virus is prone to random errors.
“The virus changes on a fairly clockwork basis, “ said computational biologist Michael Zody at the genome centre. “ Every two weeks or so, it seems that the virus picks up a new mutation.”
That adds up about 25 random changes a year, much less than the seasonal flu, which has a mutation rate of almost 50 mutations a year. Most of the changes in the coronavirus don’t make any difference now. In time, it is possible that some might make it easier to transmit from person to person or become deadlier.
Recently, researchers led by biologist Bette Korber at Alamos National Laboratory in New Mexico, US, identified a small change in the 30,000 chemical characters of the coronavirus. In a section of the code that affects its spike protein, a single “A” had turned to “G”. That version has become more common in almost every country, compared with the original version that first arose in Wuhan, China. It may have outcompeted the original strain, but may not be making patients any sicker, scientists said.
That is the only good news.
The article quoted Emma Hodcroft at the University of Basel, Switzerland. “Any of these mutations could functionally make the virus different. But this virus is young and we haven’t seen any evidence of this happening yet. It’s only been in humans a few months, and it’s doing very well.”
The coronavirus pandemic will be with us for a long time. Innovators from drug developers, medical equipment engineers, test kit biochemists, architects and telecommunication companies need to come out with novel solutions to combat this new coronavirus, and new ones that could emerge in the future.