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Know the Enemy! Understanding the Coronavirus

By Shlomo Maital

   Let’s try to understand this coronavirus enemy better, with the help of experts. (from the Washington Post, by Sarah Kaplan, William Wan and Joel Achenbach). Sorry, this blog is long, 1,500 words.

How long have viruses evolved? Are they actually ‘alive’?

“Viruses have spent billions of years perfecting the art of surviving without living — a frighteningly effective strategy that makes them a potent threat in today’s world. That’s especially true of the deadly new coronavirus that has brought global society to a screeching halt. It’s little more than a packet of genetic material surrounded by a spiky protein shell one-thousandth the width of an eyelash, and it 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 more versions of itself.

OK, so coronavirus is not alive …but how come it is so darn SMART?!

“There is a certain evil genius to how this coronavirus pathogen works: 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.

How to respiratory viruses like coronavirus make us ill?

“Respiratory viruses tend to infect and replicate in two places: In the nose and throat, where they are highly contagious, or lower in the lungs, where they spread less easily but are much more deadly.   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 those of 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.

So, we have to hand it to COVID-19 – it’s pretty darned smart. Even without a brain. All, through millions of years of evolution.

“Viruses much like this one have been responsible for many of the most destructive outbreaks of the past 100 years: the flus of 1918, 1957 and 1968; and SARS, MERS and Ebola. Like the coronavirus, all these diseases are zoonotic — they jumped from an animal population into humans. And all are caused by viruses that encode their genetic material in RNA. That’s no coincidence, scientists say. The zombielike existence of RNA viruses makes them easy to catch and hard to kill.   Outside a host, viruses are dormant. They have none of the traditional trappings of life: metabolism, motion, the ability to reproduce.     And they can last this way for quite a long time. Recent laboratory research showed that, although SARS-CoV-2 typically degrades in minutes or a few hours outside a host, some particles can remain viable — potentially infectious — on cardboard for up to 24 hours and on plastic and stainless steel for up to three days. In 2014, a virus frozen in permafrost for 30,000 years that scientists retrieved was able to infect an amoeba after being revived in the lab.     When viruses encounter a host, they use proteins on their surfaces to unlock and invade its unsuspecting cells. Then they take control of those cells’ molecular machinery to produce and assemble the materials needed for more viruses.

How does coronavirus “proofread” errors, as it multiplies within the human body?

“Let’s say dengue has a tool belt with only one hammer,” said Vineet Menachery, a virologist at the University of Texas Medical Branch. This coronavirus has three different hammers, each for a different situation.   Among those tools is a proofreading protein, which allows coronaviruses to fix some errors that happen during the replication process. They can still mutate faster than bacteria but are less likely to produce offspring so riddled with detrimental mutations that they can’t survive.   Meanwhile, the ability to change helps the germ adapt to new environments, whether it’s a camel’s gut or the airway of a human unknowingly granting it entry with an inadvertent scratch of her nose.

Where did coronavirus come from?

“Scientists believe that the SARS virus originated as a bat virus that reached humans via civet cats sold in animal markets. This current virus, which can also be traced to bats, is thought to have had an intermediate host, possibly an endangered scaly anteater called a pangolin.   “I think nature has been telling us over the course of 20 years that, ‘Hey, coronaviruses that start out in bats can cause pandemics in humans. Such viruses usually simply cause colds and were not considered as important as other viral pathogens, he said. think of them as being like influenza, as long-term threats,’” said Jeffery Taubenberger, virologist with the National Institute of Allergy and Infectious Diseases.   Funding for research on coronaviruses increased after the SARS outbreak, but in recent years that funding has dried up.

Why is it proving so hard to come up with ‘weapons’ to fight coronavirus?

“Most antimicrobials work by interfering with the functions of the germs they target. For example, penicillin blocks a molecule used by bacteria to build their cell walls. The drug works against thousands of kinds of bacteria, but because human cells don’t use that protein, we can ingest it without being harmed. 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, said Stanford virologist Karla Kirkegaard. They tend to target proteins produced by the virus (using our cellular machinery) as part of its replication process. These proteins are unique to their viruses. This means the drugs that fight one disease generally don’t work across multiple ones.   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.

“Modern medicine is constantly needing to catch up to new emerging viruses,” Kirkegaard said.   SARS-CoV-2 emerges from the surface of cells cultured in a lab. (National Institutes of Health/AFP). SARS-CoV-2 is particularly enigmatic. Though its behavior is different from that of its cousin SARS, there are no obvious differences in the viruses’ spiky protein “keys” that allow them to invade host cells.   Understanding these proteins could be critical to developing a vaccine, said Alessandro Sette, head of the center for infectious disease at the La Jolla Institute for Immunology. Previous research has shown that the spike proteins on SARS are what trigger the immune system’s protective response. In a paper published this month, Sette found the same is true of SARS-CoV-2.

“This gives scientists reason for optimism, according to Sette. It affirms researchers’ hunch that the spike protein is a good target for vaccines. If people are inoculated with a version of that protein, it could teach their immune system to recognize the virus and allow them to respond to the invader more quickly.

“It also says the novel coronavirus is not that novel,” Sette said.

And if SARS-CoV-2 is not so different from its older cousin SARS, then the virus is probably not evolving very fast, giving scientists developing vaccines time to catch up.

“In the meantime, Kirkegaard said, the best weapons we have against the coronavirus are public health measures, such as testing and social distancing, and our own immune systems.”

Man oh man – this baby is a formidable enemy. And it’s not even alive. Maybe we all-powerful all-knowing human beings should be in future a little more modest about who we are and what we can do.

Dealing with the Trump Presidency: a Survival Guide for 4 to 8 Years

By Shlomo Maital


OK, so counting four years from Jan. 20, or possibly eight – how do we survive?

Mark Blyth, a political science professor at Brown University, has some sage advice, published in the Washington Post.

   The basic problem: In democracy, we vote for what we want. And increasingly, Blyth notes, we are simply NOT getting it.

“Unsurprisingly, people are beginning to realize that they are no longer getting what they vote for. Instead, they are being asked to pay more and more for what they already receive through taxes, taken from stagnant or declining incomes, which also must service their debts. In such a world it’s great to be a creditor and lousy to be a debtor. The problem for democracy is that most people are debtors. In such a creditor-friendly world, however, democracy is reduced knowing that the menu of policy will never vary. Trump’s win in the Midwest, British voters deciding to leave the European Union, Italy’s referendum and Greece’s revolt against its creditors are all connected in this way.”

     In short: Most of us owe money. A few OWN money. The system has been rigged in their favor. And it may stay that way under Trump, the billionaire.

     So how do we respond? Blyth observes:

     “At the end of the day, when you no longer get what you vote for and when the role of voting is reduced to affirming the status quo, voters will vote for the most undemocratic of options if that is all that is “off the menu.” That’s democracy in action in a world devoid of choice. When you can’t get what you want and most people do not benefit from the economic outcomes of government, it’s also what makes democracy unstable.”

       Americans voted “off the menu” (a minority of them, true) because that was the only choice ‘off the menu’.   And it has made democracy unstable, and is doing so all over the Western democracies.

       We’ll survive this. Take a deep breath. Take a long view.  Watch how the brilliant, wise American Constitution protects its citizens from scoundrels. At some point, centrist politicians will begin to understand that voters want real change, want to unrig the system to help debtors not creditors, and want actions, not promises. It may take a few more ringing defeats, like Trump, Brexit, and Italy to wake these politicians up.

       For four years, or eight years, Americans must say clearly what they want, and vote that ticket in every election. Mid-term elections are only two years away.   How will Trump supporters vote, when they feel they are again, not getting what they want?

Blog entries written by Prof. Shlomo Maital

Shlomo Maital