24 March 2020
Bhubaneswar: The novel coronavirus (COVID-19) has shaken the world to its core and has forced people all over in their homes. Technically speaking it is a packet of genetic material surrounded by a spiky protein shell one-thousandth the width of an eyelash and leads such a zombielike existence that it’s barely considered a living organism. But as soon as it gets into a human airway, the virus hijacks our cells to create millions of more versions of itself.
So how do you kill something that hangs between living and dead?
The evil genius plan of coronavirus, or any virus in general, is to lead a dormant life till it finds a suitable host. In the case of COVID-19, it finds easy purchase in humans without them knowing. Before its first host even develops symptoms, it is already spreading its replicas everywhere, moving onto its next victim. It is powerfully deadly in some but mild enough in others to escape containment. And, for now, we have no way of stopping it.
As researchers race to develop drugs and vaccines for the disease that has already sickened 350,000 and killed more than 15,000 people, and counting, this is a scientific portrait of what they are up against.
This new coronavirus, SARS-CoV-2, adeptly cuts the difference. It dwells in the upper respiratory tract, where it is easily sneezed or coughed onto its next victim. But in some patients, it can lodge itself deep within the lungs, where the disease can kill. That combination gives it the contagiousness of some colds, along with some of the lethality of its close molecular cousin SARS, which caused a 2002-2003 outbreak in Asia.
Another insidious characteristic of this virus: By giving up that bit of lethality, its symptoms emerge less readily than SARS, which means people often pass it to others before they even know they have it.
It is, in other words, just sneaky enough to wreak worldwide havoc.
When viruses encounter a host, they use proteins on their surfaces to unlock and invade their unsuspecting cells. Then they take control of those cells’ own molecular machinery to produce and assemble the materials needed for more viruses. But viruses function through us. With no cellular machinery of their own, they become intertwined with ours. Their proteins are our proteins. Their weaknesses are our weaknesses. Most drugs that might hurt them would hurt us, too.
For this reason, antiviral drugs must be extremely targeted and specific, opine top virologists.
And because viruses evolve so quickly, the few treatments scientists do manage to develop don’t always work for long. This is why scientists must constantly develop new drugs to treat HIV, and why patients take a “cocktail” of antivirals that viruses must mutate multiple times to resist.
But there is a silver lining to this whole scenario. The virus’ RNA is changing over time. Until one day, not so far in the future, it will be just another one of the handful of common cold coronaviruses that circulate every year, giving us cough or sniffle and nothing more.