Battling a microscopic enemy: What we’ve learned about SARS-CoV-2

It’s been just six months since the first case of COVID-19, the disease caused by the novel coronavirus SARS-CoV-2, was documented in China. In that time, the microscopic organism has infected over 1.3 million people around the world and brought the globe’s largest economies to the brink of recession.

As the disease COVID-19, which was officially declared a pandemic by the World Health Organization on March 11, spread across the world, scientists have scrambled to learn as much as they can about the new virus in hopes of developing vaccines and bring the outbreak under control.

NM Political Report spoke with Dr. Douglas Perkins, Director of the UNM Center for Global Health and professor in the Division of Infectious Diseases, and Dr. Gregory Mertz, professor in the Division of Infectious Diseases at UNM, on what we’ve learned so far on the novel coronavirus that has caused what will likely be remembered as one of the largest and most dangerous public health threats the human race has seen in the 21st Century.

The ‘cytokine storm’

The SARS-CoV-2 virus is a respiratory pathogen that enters the body through the respiratory tract and can cause, in some cases, a viral pneumonia.

“In the most severe cases, that can progress to a common pathway, acute respiratory distress syndrome,” also known as ARDS, Mertz said. ARDS refers to a scenario in which fluid builds up in the small air sacs, called alveoli, that line the lungs and deliver oxygen to the bloodstream.

Typically, ARDS is the result of injury to the lung, which can be caused by something like a major chest injury, or sepsis, which occurs when an infection causes the body to overreact. In the case of COVID-19, the fluid build up is a result of the individual’s own immune system responding to the virus. 

“One of the things that happen is there’s a cytokine storm,” said Perkins. A cytokine storm is essentially an immune system response getting out of hand.

“One’s immune system responds to the virus, and that immunological response causes damages to different tissues within the body, including the lungs,” Perkins said. “And it seems as if it also causes some damage to the heart as well.”

Link between comorbidities still unknown

Reports from doctors and hospital workers on the frontlines of the pandemic — now being substantiated by peer-reviewed research — indicates that certain segments of the population are at a higher risk of suffering severely from the disease. Individuals with underlying chronic illness, for example, appear to be at a higher risk of experiencing severe illness with COVID-19.

But the relationship between the virus and those underlying conditions, called comorbidities, is still largely unknown. Mertz posited that the risk factors associated with underlying chronic illness may just be a correlation.

“Those other conditions are increased in prevalence with people of older age,” Mertz said. “We know that people who are older lose some of their ability to respond to new infections as compared to people who are younger. We know that the ability to produce antibodies and to teach immune cells how to fight infection decline with age. Part of it could be that having those other underlying conditions is associated with age.”

Some chronic illnesses, such as diabetes, are known to increase the risk of infection in individuals. So it’s not unusual that individuals with diabetes are at a higher risk of developing a severe case of COVID-19, Perkins said.

“Oftentimes, when there are underlying comorbidities — and it depends upon the comorbidities — but individuals are less capable sometimes of mounting efficient immune responses. In the context of COVID-19, there are immunological [issues] that are probably pre-existing, and then get exacerbated in the context of having this SARS-CoV-2,” Perkins said.

“One good example, that hasn’t been discussed so much but is an extremely important population, is individuals that are on dialysis. There’s an exceedingly higher risk of contracting and getting the disease COVID-19 in individuals undergoing dialysis,” Perkins said, referring to a study conducted by researchers from Wuhan, China.

But the link between the severity of the infection and other chronic illnesses, like hypertension or acute kidney injury, are not yet understood. 

“Some of the other underlying conditions, like heart disease and high blood pressure, the mechanism may not be as clear. Suffice it to say, there’s a lot of discussion regarding what possible mechanisms might be at play,” Mertz said. “I don’t think we understand the mechanisms yet. There’s no clear understanding of why having high blood pressure would put you at risk for higher seriousness of disease.”

Men appear more likely to die with COVID-19, but why?

Another mystery for researchers to suss out about the virus is why men seem to be at a higher risk of developing ARDS and dying with COVID-19 than women. The trend was first noticed in China, where data indicated 2.8 percent of men who contracted COVID-19 died, while only 1.7 percent of women who contracted the disease died.

Smoking was proposed early as a possible explanation for the discrepancy in outcomes between men and women who contracted COVID-19 in China. Mertz acknowledged that smoking would likely increase an individual’s risk of suffering severe illness from the virus.

“It certainly would make sense, since it would be linked to chronic lung disease, and the cilia in the lungs that are important in brushing stuff out of the lungs, they have decreased function in smokers. There are all sorts of reasons to think that would be the case,” Mertz said.

But both Mertz and Perkins were skeptical that smoking alone could explain the difference in fatality rate. That’s partly because data from Italy and South Korea echo the trend found in China: men with COVID-19 are more likely to die than women. Italian researchers found the death rate to be 7.2 percent for men and 4.1 percent for women; while researchers in South Korea found that, despite more women contracting COVID-19 than men, men accounted for over half of the reported deaths associated with the disease. 

“From the standpoint of what we know about genetics, there are important differences in susceptibility to infections between men and women, because a number of important immune response genes are sometimes associated with the X chromosome,” Perkins said. 

Asymptomatic carriers are unique to SARS-CoV-2

The SARS-CoV-2 virus is related to the coronaviruses that caused the SARS pandemic in 2002-2003 in Asia, and the MERS epidemic in 2012 in the Middle East. Both of those viruses had higher fatality rates than COVID-19, and also had lower infection rates, meaning those viruses didn’t spread as quickly through a population as COVID-19 does, but more people who contracted those diseases died.

A study published in Nature might have an explanation for why COVID-19 has spread across the world so quickly. Authors of that study suggest that the SARS-CoV-2 virus first takes up residence in the throat of an individual. There, the virus can replicate and spread through an infected individual’s breath, before producing any of the telltale symptoms of a COVID-19 infection in the lungs.

There’s also evidence indicating that some individuals might carry the virus without ever experiencing symptoms, or only experiencing very mild symptoms, before recovering. That wasn’t the case with SARS or MERS.

“That’s one of the reasons that we see such a broad scale of this epidemic. It becomes very difficult to quarantine individuals and do contact tracing when one doesn’t know that they’re sick,” Perkins said. “I think the big factor with COVID-19 versus SARS, and also MERS, is that those particular viruses did not appear to have high rates of asymptomatic individuals that were both carrying the disease and transmitting the disease. That appears to be a unique feature about COVID-19, it’s ability to, in some individuals, not elicit clinical signs and symptoms of disease, but yet they’re actively carrying virus around, shedding that virus,and inadvertently infecting other individuals.”

Mertz added that it’s too soon to understand the significance of that unique trait of the SARS-CoV-2 virus, but it’s something researchers will need to look at in the future.

“It’s something we’re all interested in learning about. [But] in the midst of a pandemic like this, you can imagine the kind of research studies you would need to characterize the immune response is people who are asymptomatic or have very mild disease, in comparison to people who with severe disease, it may not be the top priority as you’re trying to respond to the crisis,” Mertz said. “Certainly those issues need to be carefully addressed in research.”