Strange New World: Dr. Crystal Ellis Sheds Light on the Virology and Origin of SARS-CoV-2
In a Zoom lecture series entitled “Revisioning the New Normal,” MCPHS faculty members are bringing their expertise to bear on the basic biology, public health response, and societal implications of COVID-19.
In a relatively short time, COVID-19 has managed to upturn much of daily life. Since emerging in the United States in early spring of 2020, the virus has killed hundreds of thousands of people, infected millions more, and brought entire countries to a standstill as their populations isolate to slow the spread of the disease. But how much do you know about the SARS-CoV-2 virus itself?
In a Zoom lecture series entitled “Revisioning the New Normal,” MCPHS faculty members are bringing their expertise to bear on the basic biology, public health response, and societal implications of COVID-19. “We thought it would be a great learning opportunity to bring faculty in to have these discussions,” said Devan Hawkins, Instructor of Public Health in the School of Arts and Sciences as he introduced the first speaker, Crystal Ellis, PhD, MS, Assistant Professor of Biology, to a virtual audience on June 16. Dr. Ellis, a microbiologist whose research has focused primarily on another deadly infectious disease—cholera—began her talk by explaining some of the factors that set SARS-CoV-2 apart.
“SARS-CoV-2 is a coronavirus, which is a family of viruses that include some very mild diseases, like the common cold, and some very severe ones, like pneumonia,” Ellis explained. “Most people are harmlessly infected with coronaviruses at some point in their lives.” The particular danger of SARS-CoV-2 only became clear after the disease emerged in the Chinese province of Wuhan in early 2020; over the next three months, the disease spread rapidly to nearly every country and territory of the globe, and the WHO officially declared COVID-19 (the disease caused by SARS-CoV-2) a pandemic. While the actual numbers of fatalities and new infections are constantly shifting and subject to change depending on testing availability and reliability, the pandemic’s toll has been astonishing. “Regardless of how you calculate the number of fatalities,” Ellis said, “the COVID-19 outbreak is worse than several other outbreaks (including cholera and SARS) that have occurred over last ten years. Cholera kills about 200,000 people annually; COVID has already killed about twice that number of people in half that time.”
Why is SARS-CoV-2 so deadly? Ellis enumerated several key factors: “First, we are an immunologically naïve population,” she explained. “We have little to no natural immunity, and no exposure to related strains or vaccines, as we have with the flu. Therefore, everyone is potentially infectable. Second, SARS-CoV-2 spreads very quickly in casual contact, through respiratory droplets (the little droplets that exit your nose and mouth when you breathe, talk, or sneeze).” Ellis went on to explain that the size and weight of respiratory droplets make masks a particularly useful strategy to help curb the spread of COVID-19. “It’s much harder to get [the virus] from a surface than we previously thought.”
But COVID-19’s truly dangerous potential comes when you consider two key elements: the R0 value, or reproductive number, and the mortality rate. The R0 value is the number of other people to whom each infected person is likely to spread a disease. “The flu has an R0 value of about 1.5,” reported Ellis. “COVID-19 has a value of between 3 and 4.” In addition to spreading quickly, COVID-19 has a particularly lethal bent: in the US alone, the disease has a mortality rate of around 5%, compared to the flu’s 0.1%. This staggering mortality rate is all due to, as Ellis puts it, “a bit of RNA wrapped in a tiny bit of protein.” Like most viruses, SARS-CoV-2 is comprised of a protein exterior with a nucleic acid interior; in a trait shared by some, but not all viruses, the protein and nucleic acid center of SARS-CoV-2 are wrapped in a lipid “envelope,” which helps shield the virus from recognition by the host’s immune system. “Some viruses also have spikes,” Ellis explained. “These spikes are made of carbohydrates and proteins that stick out along the outside of the virus and enable it to infect specific sites on a host, with varying degrees of connective strength. Spikes, more than the interior of the virus, mutate often and are subject to heavy natural selection. This is why you can be subject to one strain of the flu, develop antibodies, and recover, but then be subject to the flu again the next year.”
Coronaviruses are named after their particularly distinctive spike pattern, with proteins arranged in groups of three that resemble tiny crowns. Those spikes allow SARS-CoV-2 to bind to a host’s spleen, intestines, and lung epithelial cells. It is in those lung epithelial cells that COVID-19 wreaks the most havoc, leading to the bilateral pneumonia that is the disease’s trademark.
As Ellis explained, drug researchers have focused multiple efforts on developing compounds that interrupt the virus’s attachment cycle; however, in the interim before an effective vaccine or treatment is developed, there are other ways humans can take advantage of SARS-CoV-2’s vulnerabilities. “Knowing more about the virus’s structure taught us that handwashing and alcohol disinfectants would be useful in breaking up the lipid envelope,” said Ellis. “Not all viruses are like that! For instance, norovirus, which causes the familiar 24-hour stomach bug, don’t have an envelope, so hand sanitizer won’t kill it. But with SARS-CoV-2, sanitizer works pretty well to prevent the spread, along with soap and water and face coverings.”
However, as researchers race to battle the disease, many mysteries remain. “One SARS-CoV-2 genome sequenced from the Wuhan outbreak has been extensively studied: it contains info for 29 predictive proteins. We don’t know what they all do. Some help to make copies of the virus; some to suppress immune responses,” Ellis said. “Knowing more about the genome also helps with developing drugs and confirming the disease’s origin.”
Unraveling the virus’s genome will also help dispel some of the persistent myths that have surrounded COVID-19. Ellis noted that comparative genomics have quite thoroughly debunked the notion that the virus was somehow engineered or made in a lab. “SARS-CoV-2 is very closely related to the SARS-CoV virus in bats, and there would be no reason to choose a genome from a bat disease that doesn’t already have a track record of jumping to humans,” Ellis explained. “Additionally, computational predictions for binding of the SARS-CoV-2 virus are very poor: yet more evidence that the virus is not engineered. Someone trying to create a virus would predict that this virus would bind to human cells very poorly, but in fact, it does.”
Ellis’s talk, though it gestured to the vast amounts we still don’t know about the tiny virus that has overturned our world, left the MCPHS community with a better grasp on the knowledge scientists and researchers have gleaned.