Biology Professor Bineyam Taye explains
As the COVID-19 pandemic began to spread in the United States, students in Assistant Professor of Biology Bineyam Taye’s epidemiology courses were privy to a practical application of their studies. They used a matrix to decide how they would advise policy makers to invest in preparedness for epidemics, such as calculating case fatality rate (the proportion of people who die from COVID-19 among individuals diagnosed with the virus over a period of time). They also helped to determine an outlook for the virus, examining its basic reproduction number — the amount of cases expected on average in a homogeneous population as a result of infection by a single case.
Step inside Taye’s spring virtual classroom and learn his understanding of the novel coronavirus’s epidemiology:
Until you have a full natural history of a disease, there aren’t many answers.
At this point, Taye says, there are more unknowns about COVID-19 than there are absolutes. “Researchers don’t fully elucidate the mechanism of how the virus is transmitted and has persisted in the external environment. Anyone is at risk.”
We’ll know more once there’s a documented natural history — defined as the “progression of the disease without any intervention,” Taye says.
In some ways, COVID-19 is similar to other diseases. We can learn from them.
COVID-19 has a 79% genetic similarity to the SARS virus, Taye says. “Both of them jump from animal to human, and both have similar kinds of clinical presentations, [such as] flu-like symptoms. The biggest difference between SARS and coronavirus is, [with] coronavirus, people can transmit the disease while they are asymptomatic. But in SARS, people spread the virus when they are critically ill or symptomatic. So, it was simple to identify sick people and contain the SARS epidemic.
“One of the biggest mistakes policy makers can learn from the SARS epidemic is that there was an effort to develop a vaccine, but it was stopped because we controlled SARS,” Taye says. “That vaccine could have been used now or could serve as a good starting point to develop a vaccine for the coronavirus.”
This isn’t the worst pandemic we’ve seen. It’s just the worst in our lifetime.
“Spanish flu is the worst pandemic on record. Between 50–100 million people worldwide died. The case fatality rate is also very high for Spanish flu.” The major difference with COVID-19 is that the spread may be higher because travel is more accessible.
Long term, we will develop immunity through infection or a vaccine.
Students in Taye’s course studied population attributable fraction, the proportional reduction in population disease or mortality that would occur if exposure to a risk factor, like COVID-19, were reduced by an alternative ideal exposure scenario, such as social distancing and using face masks. But those are short-term solutions to a long-term problem.
“A lot of people are infected because COVID-19 is a novel virus and no one is immune. But after time, when the majority of people are infected, we will develop antibodies. Then the chance of reinfection is expected to be low, [as long as] there is no mutation — meaning no new strain. However, emerging evidence is not in full favor of community-level immunity (herd immunity) resulting from previous infection.”
The only game changer would be developing immunity via vaccine, Taye adds. It might be similar to the flu vaccine — a slightly different formulation administered each season because new strains pop up through mutation. To prevent a rebound of the coronavirus pandemic, the population needs a vaccine.