Not All Cases Are Made Equal: A Closer Look to the Disparities Caused by COVID-19

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Issue 15, Volume 110

By Jenny Liu 

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COVID-19 is the disease caused by SARS-CoV-2, a type of coronavirus named for the crown-like spikes on the surface of the virus. We’ve seen other coronavirus outbreaks such as SARS and MERS in previous years, and since those epidemics, certain patterns have been discovered that allow us to gain a deeper level of insight into the causes of the novel coronavirus. As the virus progresses and more research is performed on the pathogen, scientists have revealed that the cause of the shockingly high number of deaths should not be solely attributed to the fact that people of greater age and those who have preexisting health conditions are more likely to develop COVID-19. That’s surface level. There’s more behind the scenes regarding the rising number of deaths.

To shed some light on the situation, we can examine the virus from two perspectives: the biological and the sociocultural.

The biological perspective analyzes the inner workings of our body systems in relation to the virus. New findings have led scientists to think that some immune systems are stronger than others when combating COVID-19.

One gene sequencing project by consumer genomics company 23andMe is using its database of millions of customers to search for clues that may shed light on how one’s genetic makeup may affect the immune response to COVID-19. Their research has found that certain people are more susceptible to COVID-19 due to the presence of the angiotensin-converting enzyme 2 (ACE2) receptor, a protein that is present in a variety of different tissues in the chest area, including both the upper and lower respiratory tract as well as heart tissue. Genetic and behavioral differences can account for increased ACE2 expression; for instance, it has been demonstrated that increased ACE2 expression occurs in smokers. Some people also demonstrate less gene activity for ACE2 receptor sites, meaning that the cells would have fewer receptors for the virus to attach itself to and therefore are less likely to contract a severe case of COVID-19.

A novel approach to inhibit ACE2 expression would use drugs categorized as angiotensin receptor blockers such as losartan, valsartan, and telmisartan. They block angiotensin II, a type of hormone, from binding to the ACE2 receptor sites to the muscles on blood vessels, thus preventing COVID-19 from spreading through the body. While this seems promising, it’s important to mention that the evidence isn’t fully conclusive, and 23andMe’s project is just one of many gene sequencing projects that are happening in order to find solutions to combat this novel coronavirus.

Furthermore, another disparity occurs not in the makeup of the immune system but in the immune system’s response. In the early stages of the coronavirus, antiviral medications and antibiotics can be helpful. However, in the later stages, our immune system can begin to auto-destruct; the coronavirus can spread around the body for weeks before the immune system registers the amount of danger it’s in. Once the body comprehends the danger it is in, usually a few weeks after the initial infection, it kicks into a hyperactive state.

This is when the body crashes.

The release of cytokine storms, an overwhelming inflammatory response, pushes the body into critical conditions. Cytokine is a molecule the body releases to activate inflammation and eradicate a virus, but in excess, it can kill the host or cause permanent organ damage.

Therefore, doctors are put in a dilemma; you treat only the virus, and the body still won’t be able to fully register the amount of danger it’s in, causing an overly active and potentially detrimental immune response later on. You treat only the storm, and, in essence, you’re attacking the patient’s own immune system. Either way, the body’s still in grave danger. A balance must be maintained.

The thing is, some people survive these storms and some don’t.

It might have to do with the types of preexisting health conditions people have. According to Benjamin Lebwohl, the director of research at Columbia University’s Celiac Disease Center, people with preexisting immune conditions such as celiac and inflammatory bowel disease may be at higher risk. It is a crucial distinction that allows us to make better treatment methods moving forward. This discovery also means that there needs to be a better way of attacking cytokine storms.

Because cytokine storms release interleukins, or proteins produced to regulate immune system responses such as inflammation, we can use interleukin inhibitors to slow down the inflammatory response. As a result, it may prove to be less of a threat to a person’s health. Drugs inhibiting interleukins such as tocilizumab and ruxolitinib are now being further investigated via a clinical trial and have fared well with patients. However, this treatment is expensive (upwards of $18 thousand a year). These drugs also belong to a class known as “biologics,” meaning that they are derived from living organisms through means of biotechnology, making them difficult to obtain. The medicinal reserves would not last long if they were to be used to treat people on a large scale.

Yet another surprising disparity rests on the basis of sex: men seem more likely to develop severe symptoms and die from COVID-19 than their female counterparts. Sixty-two percent of Italy’s 25,452 deaths were men as of May 1. And 56 percent of Spain’s 25,613 deaths were men as of May 5. New York, the place with the highest number of COVID-19 related deaths in the United States, has 19,415 deaths, with 54 percent of them being men as of May 4. This has caused scientists to hypothesize that the immune systems of men and women are wired differently, with women’s immune systems able to mount a stronger immune response.

According to Sabra Klein, a virologist at the Johns Hopkins University Bloomberg School of Public Health, the strength of the female immune system may be evaluated by observing the innate and adaptive immune systems. The innate immune system, the first line of defense against a virus, has a component called the Toll-like receptor 7. The receptor is found on the X chromosome and can quickly detect pathogens. Because women have two X chromosomes and men only have one, the greater number of receptors per cell allows more proteins and antibodies to be produced. The adaptive immune system, which is more specialized, is then activated if the innate immune response is insufficient to control infection, and it destroys invading pathogens.

Estrogen, the female sex hormone, also plays a role in strengthening the immune response by regulating some of the genes associated with B cell production, which are responsible for making antibodies.

Ultimately, the strength of the immune system—arguably the most important component of our fight against the severe pandemic—rests on non-biological factors as well. Even though its foundation is genetic, people’s chances of survival can be toppled by pervasive sociocultural factors that ultimately work against racial and ethnic minority groups.

According to the Centers for Disease Control and Prevention (CDC), African-Americans account for 72 percent of all COVID-19 deaths in Chicago, even though they are only one-third of the city’s population. In Louisiana, blacks represent 70 percent of the dead but only 33 percent of the population. In Michigan, blacks comprise 40 percent of the fatalities but are only 15 percent of the population. These startling statistics are examples of how the death rates are several times higher among racial minorities and people of low socioeconomic status.

Income inequality is a leading cause of the rising number of deaths and infected cases among racial and ethnic minority groups. In the U.S., people from minority groups generally have less access to resources, which often leads to poorer health. Minority groups’ struggles with economic instability have only been exacerbated by the COVID-19 pandemic. With many racial and ethnic minorities working minimum-wage jobs, the massive layoffs as a result of the health crisis have hurt many families. Developmental economist Imraan Valodia at the University of Witwatersrand, Johannesburg, predicts the lockdown will lead to a 45 percent loss of income for the poorest 10 percent of households.

Another sociocultural factor affecting one’s likelihood of being infected is environmental injustice; high numbers of ethnic-minority households in North America live in poorer neighborhoods with poor infrastructure and degrading environmental quality. An environmental report with data collected over a 20-year period concluded that more than half of the people who live within 1.86 miles of toxic waste facilities, lands, and incinerators in the U.S. are people of color. These facilities contribute to air pollution and safety issues. A case study of the Bronx, New York, found that individuals who lived close to waste facilities were 66 percent more likely to be hospitalized for asthma. Air quality is a risk factor for bad respiratory health, which has been known to worsen symptoms of COVID-19.

Precarious housing is yet another factor of the rising number of deaths and infected cases among racial and ethnic minority groups, as many homeless people are less able to observe social distancing. The ones who find themselves in a shelter might not be as better off, as shelters are rapidly filling up with people and thus facilitating the spread of disease.

This global health crisis, although a saddening event, truly teaches us a lesson about the preparation we need to take (or didn’t take) in order to combat it. It doesn’t bring to light new issues, only issues magnified and exacerbated. It calls to attention the discrepancies in our human biology—how something as minuscule as a protein can prove to determine life or death for a person. Additionally, the pandemic serves as a warning for how the inequity in income, healthcare, and environmental injustice can prove devastating for racial and ethnic minority groups. Instead of focusing solely on the preexisting health conditions, we need to do something to help the minority groups through this. It is within our capabilities to erase the inequality that continues to fuel the pandemic, and we must act upon it before more lives are lost.