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The Quad: Breaking down the science behind COVID-19 virus, looking into how it functions

(Emily Dembinski/Daily Bruin)

By Samantha Dorfan

April 29, 2020 4:12 p.m.

The virus that has poked holes in the entire global infrastructure for the past few months is physically far smaller than the period at the end of this sentence.

That something so minuscule can act as one of the biggest threats currently imaginable to humanity is a testament to the ironically complex nature of viruses, which, without properly understanding, can make this disease even more baffling than it already is. Here, we break down the basics of COVID-19 to try to make sense of the way it infiltrates the body.

A coronavirus is defined as a single-stranded RNA virus that typically leads to an upper respiratory infection. Severe acute respiratory syndrome coronavirus 2, or SARS-CoV-2, which was first reported in December in Wuhan, China, is of the same family of virus as the Middle East respiratory syndrome, the severe acute respiratory syndrome and even the common cold. Humans commonly fall ill at the hands of complications like bronchitis and pneumonia from less severe coronaviruses, and are able to recover.

Hong Zhou, a professor in the Department of Microbiology, Immunology and Molecular Genetics as well as the director of the Electron Imaging Center for NanoMachines, explained how other coronaviruses function differently than the latest one.

“The other coronaviruses are usually seasonal,” Zhou said. “We don’t talk about them because they don’t cause problems for humans.”

The same cannot be said about the most recent coronavirus cousin. The thing that sets it apart is that human immune systems have no idea what to do with it.

Scientists often describe this phenomenon by referring to the virus as “novel.” Given SARS-CoV-2 originated in animals, it is a pathogen that is not just unfamiliar to anyone’s body but that is unbeknownst to the entirety of mankind, according to the Mayo Clinic.

It is believed that COVID-19 may have originated in a wet market in Wuhan, China, which was home to animals sold for consumption. Animals provide a vehicle for the virus to spread and it can exist within them without humans ever knowing. Moreover, an environment like a wet market can be conducive to the spread of viruses since many different species share a small space where bodily fluids can drop from one cage to another and eventually to human handlers.

 

[Related: Campus Queries: For how long does the novel coronavirus remain infectious on different surfaces?]

The microcosmic wet market ecosystem example goes to show the ease at which such viruses can spread among animals as well as people. However, when it comes to transmission, not all viruses are created equal. The 2019 coronavirus is extremely contagious in comparison to its predecessors: while all coronaviruses can spread through touch, it has become clear that COVID-19 may have a little bit more to it.

For starters, it’s important to note that viruses are entirely dependent on the cells they infect. These nonviral cells contain their own code for the government of healthy cellular mechanisms. Viruses, however, do not care about the health of the cells they infect. They invade, bringing with them their own instruction manual, and proceed to usurp cellular resources in order to make more of themselves. In comparison to the thousands of genes contained within healthy human cells, viruses bring with them two to 10 genes – a gross oversimplification of what’s required for health.

Picture a well-oiled democratic society with a complex system of checks and balances to keep everything running smoothly. Suddenly this society is overpowered by a ruler from another land who throws away the nuanced system and has the single goal of utilizing the resources of the city to help his people reproduce.

In their quest to hijack the human cell, viruses must first bind to it by means of some structure or protein. All coronaviruses use what is called a “spike protein,” but the proteins present in SARS-CoV-2 bind a lot more tightly. Then, the protein is activated by an enzyme called furin that is present in various human organs, essentially allowing the virus to attack the body from multiple different entry points causing potential failure in multiple different organs. Studies have shown the furin activation site discovered in SARS-CoV-2 is different than that of other coronaviruses, which likely influences the body’s violent reaction to it.

These are mechanisms that give COVID-19 a certain competitive edge against other coronaviruses. All viruses, however, attack with a certain brutality that is built into their very machinery and part of their danger comes with the mutations that arise every so often.

“Just like anything in nature, viruses have to figure out a way to exist,” Zhou said. “To gain existence, the virus must adapt to the environment.”

[Related: UCLA announces aim to offer remote instruction option for fall quarter]

Timothy Brewer, a professor of epidemiology in the Fielding School of Public Health, explained that many of the mutations that occur may be silent, thereby leaving a virus unchanged in a meaningful way.

“And so the question is, will there be some meaningful mutation that either makes the virus more or less deadly, or more easy or less easy to transmit?” he said. “That certainly is possible, but we haven’t seen any real evidence for that yet.”

As a result of the complicated nature of viral mechanisms, there is still no cure to target COVID-19. Scientists around the world are testing different contestants, but according to Brewer, the treatment plan will depend on the frequency of mutation.

“We’ll have to see if it is more like influenza, (where) the mutation rate really isn’t that important for treatment, and we can use one medicine, or if it is more like HIV, where we might need to use combinations of medicines because it’s mutating so rapidly,” he said.

The timeline of such treatments for COVID-19 is still ambiguous. Zhou made clear that neither a treatment nor a vaccine will appear overnight. The polio vaccine, for example, was first widely used more than 60 years after the first epidemic began in the United States in 1894.

“There is a process you have to follow for safety and efficacy,” Zhou said. “Many times it will not be successful and you have to repeat the process again.”

As we await the approval of something more permanent, the best way to combat the tiny virus that has brought society to a standstill may just be to stop its spread by staying at home and washing our hands. Understanding how viral operations work is the first step in figuring out how to overcome them and get back to life as we know it.

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