COVID Q&A: Answering Your Questions
It has officially been six months since communities around the world went into quarantine to avoid contracting and spreading the novel coronavirus. While there’s still plenty of unanswered questions and undiscovered science around the virus that’s forced us to adapt to a “new normal,” scientists and doctors around the world, including LSU researchers and alumni, have already gained a better understanding as to the impacts the coronavirus can have.
In the College of Science, answering questions is the challenge we all pursue. So we asked you for some of your questions, which we collected and posed to a few LSU College of Science researchers in the Department of Biological Sciences and an LSU alumnus working on the frontlines in New York City, one of the country’s earliest epicenters.
Dr. Tad Dallas is an assistant professor of ecology, who uses laboratory microcosms and field data together with quantitative modeling and machine learning approaches to address a diverse set of questions in population, community and disease ecology.
Hollie Hale-Donze is an instructor of biological sciences, as well as rector of the Science Residential College. Hale-Donze has almost 20 years of research experience in immunology and infectious diseases and has frequently taught courses on immunology and microbial pathogens at LSU.
Finally, Dr. Stephen Andrew “Andy” McCullough is a cardiologist and an assistant professor of Clinical Medicine in the Department of Medicine in the Division of Cardiology at Weill Cornell Medicine and New York Presbyterian Hospital in New York. McCullough graduated from LSU in 2008 with a bachelor’s degree in biological sciences, with minors in chemistry and music.
Q: How do masks protect us given the pore size is much larger than a typical virus?
Hale-Donze: Cloth face masks with multiple layers can reduce transmission of the viruses from an individual who is unaware they are infected—also known as asymptomatic. When we sneeze, cough or even talk, we generate different size respiratory droplets that are propelled outwards of 6 ft or more. Those droplets can contain viruses. If an infected person wears a cloth face mask, many of the largest drops are trapped in the mask resulting in reducing the number of aerosolized particles in the air and the distance they travel. Combining this with social distancing helps prevent the number of virus particles reaching an uninfected individual.
Recent data published in the Journal of General Internal Medicine is suggesting there are benefits of wearing a mask for the uninfected individual too. Researchers from the University of California San Francisco and John Hopkins University suggest that by wearing a mask, we can reduce the amount of virus particles we inhale which may result in milder symptoms. They conclude, “This theory of viral inoculum and mild or asymptomatic disease with SARS-CoV-2 in light of population-level masking shows the benefits of mask-wearing for the individual (as well as others) as a pillar of COVID-19 pandemic control.”
While no mask can prevent 100 percent of virus transmission because the viral particles are smaller than the gaps in the cloth, the combination of universal mask wearing, and social distancing can significantly reduce viral transmission and disease. Until a vaccine or drug is developed, this is the best way of controlling the spread of this virus.
Reference: Masks Do More than Protect Others during COVID-19: Reducing the Inoculum of SARS-CoV
Q: What’s the difference between the coronavirus and COVID-19? Or are they interchangeable?
Dallas: Coronavirus is a general term for an entire family of viruses, including SARS—which emerged in 2002—and MERS, which has caused a number of smaller outbreaks starting around 2012. COVID-19 is the name of the disease itself, with disease defined here as the manifestation of the negative effects of the pathogen, which is SARS-COV2 (severe acute respiratory syndrome coronavirus 2).
Q: We have a new flu vaccine every year with a new strain. Why is it so hard to get a coronavirus vaccine?
Hale-Donze: The short simple answer—because it is a novel coronavirus. In general, most vaccines take around 10 years to develop, from identifying which viral antigen (a molecule that elicits an adaptive immune response) to target, to pre-clinical trials where candidate vaccines are studied in cell cultures and then in animal models. The final phases are clinical trials. This research is done in phases from small groups to more large numbers as the vaccine is tested. Each phase is very controlled and must follow a protocol. Each phase addresses one specific question: phase 1 is often safety and dosage; phase 2: efficacy and side effects; phase 3 is usually the critical phase where the numbers are sufficient to demonstrate whether or not a product offers a treatment benefit to a specific population and show side effects across a more diverse study group; phase 4 occurs post FDA approval to monitor drugs. Some of the pre-clinical trial study requirements were waived in order to begin clinical trials. There are several vaccine candidates in phase 3 testing.
For the record, Influenza was first isolated in 1933 and the first flu vaccine was actually administered in 1940. Over the course of the last 80 years, the vaccine has evolved and through epidemiology, we have gotten to a point that we know which strains of influenza are more likely to be seen in a given season, so the vaccine contains several targets for different strains that get rotated in and out of the lineup, so to speak. The fastest vaccine ever developed was for mumps, and it took four years.
Q: Why is herd immunity important?
Dallas: Herd immunity is the threshold at which a wholly susceptible population can be vaccinated (or become infected and temporarily immune to reinfection) to drive the basic reproduction number (R0) below 1, meaning the epidemic would presumably die out.
R0 is defined as the number of infections produced by a single infected individual entering a wholly susceptible population. R0 and herd immunity are useful for epidemiological modeling, and somewhat in vaccination efforts, but should not be used in mitigation efforts, as herd immunity thresholds tend to be incredibly high (e.g., something like polio has a R0 of around 5 on the conservative end, meaning 80% of the population would need to be vaccinated to attain herd immunity). Add in the complexities of differential social contacts (e.g., service workers interact with many people), potential superspreaders (those that infect many due to being asymptomatic and/or having higher viral loads), and age structure in infection (age influences tendency to become infected and transmit through differential social contacts, immune function, etc.), and herd immunity should not be a thing we really discuss as a mitigation strategy.
Q: Why do children fare better while carrying more virus and adults could be near fatally ill with less virus in their systems?
McCullough: We don't know don't exactly know why adults get acute respiratory distress syndrome from the virus. It's being studied. There are thoughts about it. Does it directly affect the lungs? Is it the immune system causing acute respiratory distress? Is that a direct effect of the virus? We don't scientifically know the answer to that. We do know that children and young adults four weeks after recovery from their infection can develop something called multi-system inflammatory syndrome, which is where the immune system goes haywire and wreaks havoc on most of the organ systems in the body. And that happens between three to four weeks after their initial infection with coronavirus. We don't know what percentage of people get that, but we know that just because children have minimal symptoms doesn't mean that they're going to be free of bad outcomes from the virus. And those outcomes include heart failure, kidney failure, and death.
Q: (Pt. 1) How do researchers develop models to estimate the spread and severity of disease? (Pt. 2) Why do we need to have models?
Dallas: Researchers develop models based on simplifying assumptions about how the disease spreads in a population, and can vary from simple models which track susceptible, infected, and recovered individuals as groups (called the SIR model), to complex models which follow each individual in a population and incorporate variation in age structure, social contacts, infectivity, infectious period, and many other relevant epidemiological parameters. The models are incredibly useful for estimating the potential spread of the pathogen, with clear implications to planning the response warranted to help the healthcare system deal with the burden of disease. It is important to note that these models aren't simply for mitigation of infectious disease. They are incredibly useful for vaccination program design, and to understand the theory of how epidemics spread. So apart from the obvious social good of epidemiological models, which are too often ignored by policymakers, there is a fundamental good of understanding spreading processes in complex systems.
Q: How do you determine who should be admitted to the hospital versus who should weather the infection at home?
McCullough: That's a different question based on the timeline that you asked it. In March, you could not get admitted to the hospital unless you were basically dying in New York.
Now, you basically look at a person and you ask questions as to whether or not you think that that person is able to sufficiently care for themselves at home. That's your first, “Can you eat, drink, shower, take care of yourself?” If the answer to that question is “no,” then you need other people to take care of you. So you get admitted to the hospital.
Then the next question is, “Do you have any abnormalities of a group of numbers that are called vital signs—pulse, blood pressure, and the concentration or saturation of oxygen—and if there are any abnormalities of those numbers, you will be admitted to the hospital. And then after that, you asked the question, “Okay, all of the vital signs are normal. Is there any evidence of something called end organ damage? Does the person have kidney failure? Is their heart involved? Do they have a normal EKG?” If there are any signs of other organs being affected, then you would admit them to the hospital. That's how you get admitted. You can't take care of yourself. You have abnormal vital signs, or some other organ is involved that’s unexpected.
Q: A lot of symptoms that are considered to be coronavirus symptoms, like tiredness, shortness of breath, congestion, are also pregnancy symptoms. Should anyone who is pregnant be that much more aware of what they are feeling?
McCullough: In our Cornell experience—and our OB-GYNs published this—, we found in our labor and delivery unit many people who were either at the onset of labor or in false labor, who were Coronavirus-positive in March because there’s so much symptom overlap. Patients thought they were in labor, but they actually just had COVID.
If there is ever a reason to get tested for coronavirus, you should take the opportunity to get tested. Because, one, you’ll learn if you don’t have it. Or two, if you do have it, you’ll know to isolate and to let others who have been around you that you’ve tested positive.