Current scientific knowledge about the coronavirus causing a global COVID-19 pandemic is like a television screen with missing pixels to Mayo Clinic’s Dr. Gregory Poland.
Trouble is, as the picture fills in, scientists and public health leaders are discovering misconceptions that may have misguided the world’s initial response to this virus, named SARS-CoV-2.
It’s more infectious than SARS-CoV-1, which spread globally in 2002-2003 but fizzled out after only causing eight confirmed U.S. cases. It’s more destructive at a cellular level than garden-variety coronaviruses that cause common colds. And yet, it’s still just one of many viruses engaged in ceaseless quests to find hosts in which to spread.
“The good news is that it is impossible to get infected with this virus if you don’t breathe it in or introduce it to your body with your hands,” said Poland, director of Mayo’s Vaccine Research Group. “There’s nothing exotic about this virus. It’s just a different virus, so if you take the actual precautions [such as hand washing and covering coughs], there’s no way to get infected.”
“Therein lies the hard part,” he said, “because human behavior is irrational.”
Leading theories based on the genetic composition of SARS-CoV-2 is that it originated in bats and passed through an animal host that passed it along to humans this winter. The first SARS was passed from bats to humans via civet cats that were sold in markets in China, and that may be the case with the new virus as well — though it has genetic features that suggest it might have passed through pangolin anteaters.
Close up, the COVID-19 virus looks like a dog’s chew toy — a ball with protruding crown-like spikes (hence the name corona, which in Latin means crown.) The spikes help the virus bind to cells via their ACE-2 receptors, enzymes on the cell surfaces that have a role in regulating blood pressure.
Adding to the virus’ efficiency is the fact that its new, so nobody has immunity to it.
“There has been an evolution from SARS in the COVID-19 virus so that it binds much more tightly and effectively” to those receptors, said Dr. Ashley Haase, head of the University of Minnesota’s Department of Microbiology and Immunology.
A consequence of the virus attacking ACE-2 receptors is that they no longer regulate a hormone called angiotensin II, which then causes lungs to constrict and fluid to build up. Many infected patients struggle to breathe and, in severe cases, need ventilators to maintain adequate airflow.
Initial reports out of China suggested that 80% of cases produced only mild symptoms, but that anywhere from 1% to 3.4% of cases were fatal and that the elderly and people with other health problems were at greatest risk. Tracking of the first U.S. cases also found a rising death rate with age.
Some patients defy the odds. Minnesota’s first hospitalized case was a person in the 30s age range who has been in critical condition.
Genetics might play a factor in the severity of illness — a theory advanced by the deaths of a mother and three adult children in a New Jersey family. Other doctors found that patients with severe illness spent extended time with other infected patients and developed higher viral loads.
“The ones that have been the most severe cases have tended to be within that zone of close contact while someone is symptomatic for an extended period of time,” said Dr. Clayton Cowl, Mayo’s chair of preventive medicine.
One study raised concerns about people who take ACE inhibitor drugs for diabetes, which seem to result in a buildup of ACE-2 enzymes and more targets for the virus.
The COVID-19 virus is complex and has a “novel proofreading capacity” to prevent harmful mutations that could choke its replication, said Dr. Frank Rhame, a virologist with Allina Health in Minneapolis.
One positive: the complexity of this virus presents opportunities for drugs to “gum up” its replicating process. Studies underway with an experimental drug, remdesivir, target a key enzyme for the virus.
One concern: the virus spreads more easily than initially thought. People with SARS were most infectious after five days and the onset of telltale symptoms. The COVID-19 virus, by comparison, sets up shop early in the throat and nasal cavities, even before symptoms have emerged.
“By the time a patient has symptoms, you’re already behind the epidemiologic curve,” Haase said, “because that person has had contact and passed it to other folks.”
The COVID-19 virus was found in studies to last up to 24 hours on cardboard and for days on metal surfaces, though only in pristine lab conditions. Traces of the virus also were found on the Grand Princess long after people disembarked from the cruise ship, which had been quarantined for days due to COVID-19 cases on board.
Even so, hand-to-mouth contact probably isn’t the dominant cause of this outbreak, said Michael Osterholm, director of the U’s Center for Infectious Disease Research and Policy. Many cases are due to patients coughing or sneezing droplets that land on others, but Osterholm said there is now adequate proof that it hangs in the air and presents risks that way as well.
“We’ve never had one that was like this virus in terms of how it transmits and how it causes disease,” he said.
The state health department is aware of the potential for airborne transmission, but is considering that risk more in the context of hospital rooms and making sure that health care workers in close contact with patients are protected, said Kris Ehresmann, infectious disease director for the Minnesota Department of Health.
This coronavirus clearly isn’t the measles, though, she said. Measles can spread through the air so easily that health officials in 1991 found that it traveled from an infected person on the field at the Metrodome during a Special Olympics event to fans in the upper deck.
Viruses are measured by R-naught values, or the number of people who will catch them from other infected people. The value for measles is as high as 18. COVID-19’s value is 2 to 3, comparable to pandemic strains of influenza.
Ehresmann said new information about the virus has changed how her department does investigations to quarantine close contacts of people with the infection. At first, state epidemiologists searched for contacts of infected people who had already developed symptoms. Now they also ask infected people about contacts in the 24 hours before symptom onset.
Some of the pioneering work on how viruses spread, even in the absence of coughing or sneezing, was done at the U in the 1950s, Rhame said. Volunteers stuck their heads inside boxes and talked. Sensors measured how far particles traveled.
“A lot of stuff comes out of our mouths when we’re just talking,” Rhame said, although “it doesn’t go much farther than 2 meters.”
One hope is that the COVID-19 virus is similar to common coronaviruses that tend to dissipate in warm, humid climates. Even the SARS outbreak declined in warmer months, but Osterholm said he believes that was coincidental and noted that the MERS coronavirus persists in the heat of the Gulf region.
“It had nothing to do with the seasons,” he said.
Health officials said they believe the best protection is the ongoing series of social distancing strategies to separate people so they don’t transmit the virus to others so quickly.
So-called “bend the curve” strategies, to stretch out the onset of cases over time so that hospitals aren’t overwhelmed, come in part from analysis of the 1918 Spanish flu. Hardest-hit cities at that time, such as Philadelphia, resisted social distancing.
“This distancing business is a war of attrition,” Rhame said. “It’s a war of tiny effects by a large concerted effort over a long time that will bring that R-naught value down. That’s desperately needed.”
Jeremy Olson • 612-673-7744 • @stribjo