Given how rapidly our understanding of COVID-19 is changing, we’ve made an update to our original conversation about the impact of this virus, its transmission and treatment protocols. Stay tuned and check back often for the latest!
As a healthcare marketing firm working with companies promoting pharmaceutical therapies, our staff often reviews clinical studies to better understand the meaning of this research in terms of patient health outcomes and risks. At no time has this been more valuable—on a personal level— than it is right now during the pandemic. Yet the lack of proven clinical evidence and clinical trials means that even those of us who work in healthcare are often trying to project and predict the potential impact of this virus with largely anecdotal reports.
However, there is still some exciting, emerging COVID-19 research going on right now, and new reports and studies are being initiated and examined every day. Given the vast amount of information being disseminated, we’ve tried to summarize what we feel are some of the most interesting areas of study, theory and research for you here. Below are some of the early insights and data points we’ve collected amidst this rapidly-changing crisis. They represent just a few key areas that are important for anyone in healthcare to follow.
Risk factors, illness progression and how the virus takes hold.
We do have some understanding of how this virus attacks our cells and impacts our organs and body, thanks to research on similar illnesses like SARS, as well as our knowledge from studying other types of flus and coronaviruses. And we also know a lot about the risk factors that seem to predispose people to more serious illness.
And in fact, to understand the risks and comorbidities that can lead to more severe illness or even death in those infected, it helps to understand how COVID-19 replicates itself and how that impacts the body. The novel coronavirus latches on to a common receptor—ACE2—found in human lungs and the small intestine as well as in other organs like the kidneys and heart. (These organs are frequently damaged in more serious COVID-19 cases leading to issues like heart attacks and kidney disease.) ACE2 receptors are a part of the sympathetic nervous system, and their job is to bind to the ACE2 hormone as part of the body’s overall response to stress. The ACE2 hormone helps constrict blood vessels, which then raise our blood pressure.
In fact, some research has shown that high blood pressure is one of the most risk factors for the progression of the virus, so that’s certainly something that researchers and clinicians will be examining closely. This relationship between the ACE2 receptors, blood pressure and certain comorbidities may give us a clue about what’s really going on in some patients with severe illness. For example, people with diabetes and high blood pressure often take drugs called ACE inhibitors. These drugs actually make our bodies create more ACE2 receptors. Some scientists are looking at whether this is why people with these conditions have more severe cases of COVID-19. However, this is just a theory and it’s important to note that US heart groups have issued guidance telling patients NOT to discontinue these drugs.
Additionally, it’s useful to note that inhaling nicotine has an impact on ACE2 receptors in the lungs, which is also being studied right now. This is especially important in light of the vaping epidemic in young Americans, as it’s expected that vaping has the same impact on these receptors as smoking regular cigarettes. Interestingly, some studies have noted that smokers are actually under-represented in COVID-19 cases, especially in China. However, smokers who were infected had more severe disease progression. (With all of the other risk factors associated with smoking and vaping, now may end up being a good time to encourage people to quit the habit regardless!)
We also understand a lot about the course the illness takes from recent COVID-19 research. For most people (approximately 80 percent), the virus will not take hold aggressively in the lungs and they will not experience the more serious form of infection. Calling this illness “mild” may be a misnomer, as many individuals still feel like they have a serious case of the flu. They will likely experience the most common symptoms—fever, cough, body aches and shortness of breath—for some time. (A few interesting studies are showing that even with the mildest form of the illness, the loss of a sense of taste or smell may be one of the most common symptoms.) It can still take days, or even weeks, to recover from COVID-19, but these individuals won’t require oxygen supplementation, or even worse, ventilator support, which has been associated with poor outcomes in certain patients.
For those that do progress to more serious illness, this typically happens in the second week, after experiencing milder symptoms along with more concerning ones like significant trouble breathing. Many clinicians tell COVID-19 patients who are isolating at home that keeping an eye out for this particular symptom, and that testing their oxygen levels with a pulse oximeter daily is a great way to ensure that they don’t need hospitalization. Some people decompensate very quickly once they reach this point. Because by now, acute pneumonia has taken hold, making it more difficult for their body to get oxygen to cells, all while the immune system is trying to mount a strong defense to attack the virus which leads to something called a cytokine storm. This is actually an over-reaction by the immune system which can lead to organ shutdown, sepsis and even death.
Promising new therapies emerge
However, there are some exciting therapies being used to help “calm the storm” that seems to happen during week two in patients with severe illness. The best news is that these are affordable and readily-available medications—all part of the steroid family of drugs—that have already been used and tested in patients for decades. (While clinicians initially had concerns that steroids could actually worsen COVID-19 symptoms, recent evidence shows that they have a significant impact on reducing mortality and the need for mechanical ventilation.)
Another important piece of the clinical puzzle is the fact that doctors have realized most patients should not be put on ventilators—or their use should be delayed as long as possible—because they are associated with negative outcomes. Instead, other forms of oxygen, through nasal cannulas and BPAP machines—are actually preferable given their efficacy and safety. The simple act of proning patients, or putting them on their stomach instead of their back, has also been shown to be an easy, effective way to help improve oxygen exchange in the lungs.
Yet an additional clue to the more severe illness caused by COVID-19 actually lies outside of the lungs, and instead involves the patient’s blood vessels. Thromboembolic events (related to blood clots) have frequently been documented in COVID-19 patients, even those without severe disease. This has led to heart attacks and strokes in some individuals, even those who have not been hospitalized for serious illness. As a result, many doctors are now prescribing anti-coagulants, or blood thinners, to patients, especially those at risk for blood clots.
Other interesting, but less proven therapies of note, are based on various studies about certain vitamins, minerals and enzymes in terms of their immune-modulating effects, including vitamin D, zinc and an antioxidant and potential lung function precursor called N-Acetyl-L-Cysteine. In the case of vitamin D, researchers have long wondered if the low levels of vitamin D most people have in the winter may predispose them to colds and flu. Interestingly, Italy, which has been particularly hard-hit by the virus, does not generally fortify its food supply—like milk and other dairy—with vitamin D.
Zinc has been shown to reduce respiratory illness in some studies. WHO acknowledges that zinc-deficient children are at increased risk of respiratory tract infections including those affecting the acute lower respiratory tract. Again, these are not proven treatments for COVID-19, but may be useful sources of study for boosting immune function. Much more evidence is needed before anyone knows whether these will be useful in preventing infection or duration/severity of illness.
Stay tuned for more data.
In summary, the COVID-19 landscape is rapidly evolving and just trying to keep pace with the sheer amount of theories, clinical studies and trials can be overwhelming. We hope that our summary helped separate at least some of the current theory from evidence, and we’ll keep you apprised of new data points from COVID-19 research as they emerge!