Coronavirus testing also tracks infectious rates, lethality, differential infectivity, identifies carriers and allows us to project more accurate outcomes
In any health situation, especially a pandemic crisis, we must have effective education about emergence and rapid expansion of a mutant virus such as SARS-CoV-2.
In December 2019, the emergence of a novel strain of betacoronavirus, that is now referred to as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 or 2019-nCoV), led to a global outbreak of CoronaVirus Disease 2019 (COVID-19). COVID-19 is a viral upper respiratory tract infection that can cause a wide range of symptoms anywhere from common cold or flu-like symptoms, to acute respiratory distress syndrome (ARDS); similar to symptoms caused by a coronavirus strain previously identified in 2003 as SARS-CoV (severe acute respiratory syndrome coronavirus).
New virus to the immune system
Clearly, our immune system is seeing SARS CoV-2 as a new virus; a situation that reminds us about how jolting mutant viruses can be to our immune system. However, this is hardly the first time we have been confronted with something like this because in reality we have seen mutant virus epidemics and pandemics occur on a regular basis.
A few significant viral pandemics were: the 1918 flu killing 20-30 million, in 1956-57 the Asian flu killed over a million, in 1968 the Hong Kong flu was estimated at 1-2 million deaths, the 2009 swine flu H1N1 that infected 61 million and ended up killing 12,000 Americans, and in the wake of HIV/AIDS in 2018, we still lost 700,000 lives globally.
Perhaps, like with any significant challenge we rise, and as such, we are learning to identify key clinical factors, coronavirus testing techniques and therapeutic relatedness between SARS-CoV-2 and the earlier SARS-CoV.
Data and trends
Epidemiology begins with elucidating SARS-CoV-2 as it travels around the globe, differentially infecting populations. While keeping in mind that practicing quarantine and social distancing is always the first defense, understanding how to manage SARS-CoV-2 with immune system adjuvants and lifestyle interventions prepares us for future outbreaks.
During this pandemic it’s necessary we acknowledge that the data being presented on any given day is just a snapshot, however, trends have begun to emerge. Scientists and clinicians have been absolutely amazing, providing real-time data regarding SARS-CoV-2 worldwide. A number of real-time publications are now available giving us an unprecedented look at this virus, its behavior and health impact.
Research is beginning to give us some insights on the biological mechanisms for viral binding and replication of SARS-CoV-2 as well as its impact on targeted human cells. Understanding the life cycle infectivity, viral load of severe acute respiratory syndrome and the immune system response of SARS-CoV-2, will lead to improved clinical knowledge and outcomes. Perhaps the most interesting acquired information will be the science I hope to present about how natural phytochemicals, virome interactions, microbiome interactions and nutrition, all shape our amazing relationship between our immune responses and emerging viral challenges. Although, new findings indicate that the clinical spectrum of COVID-19 can be very heterogeneous, underlying conditions and age are distinct virulence influencers and the following educational information reflects current research and real-time clinical publications. It is paramount all decisions regarding COVID-19 patients must be made by trained health care practitioners.
What does SARS-CoV-2 tell us about our health?
SARS-CoV-2 may exploit our autoimmune issues through inflammatory mechanisms. After spending considerable time in the literature some interesting correlations exist, although, for discussion here, I would like to mention age as a risk factor separately from the underlying conditions and comorbidities like heart disease, diabetes, pulmonary disease and obesity.
Age risk factors are listed in table 1, where you might notice that the fatality rates related to age groups, are uniquely telling. In contrast to many viral infections that put younger populations at risk, SARS-CoV-2 appears to be quite different in that its greatest impact appears to be on the older populations. Nevertheless, it is important to note that since the total number of COVID-19 cases remains unknown, the fatality rates are skewed. It is expected that we will have a more accurate picture as more statistical information comes in. A higher priority is our understanding of the underlying immunological risk factors.
*The CDC has a broad estimated fatality risk range of 0.25%–3.0% for COVID-19, while saying that “lower estimates might be closest to the true value.”
The need for more coronavirus testing
First, this means more coronavirus testing because COVID-19 can look a lot like other illnesses or remain asymptomatic. Coronavirus testing also tracks infectious rates, lethality, differential infectivity, identifies carriers and allows us to project more accurate outcomes. Perhaps most importantly, coronavirus testing identifies those people who need to be isolated.
Clinical reviews of mild cases were found to have an early viral clearance, with 90% of these patients repeatedly testing negative by day 10 post-onset. In contrast, all severe cases still tested positive at or beyond day 10 post-onset. This means the viral load of severe cases was around 60 times higher than that of mild cases, suggesting that critically ill people are not clearing the viral load.
Analysis of the critically ill cases of COVID-19 has been startling and has led researchers to identify comorbidities, (see Table 2), related to critically infected COVID-19 patients.
Professor Micheal Osterholm, director of the Center for Infectious Disease Research and Policy (CIDRAP), predicted the obesity risk factor before SARS-CoV-2 had reached the United States. His hypothesis was based on the similar inflammatory physiology of obesity to smokers, who were a high-risk group in China. In fact, research on critically ill patients in Kirkland, Wash., have identified the highest risk characteristics including: pulmonary disease, diabetes, kidney disease and obesity among other immune-related chronic issues.
Inflammation’s role related to risk
By digging deeper into the mechanism of the infective cycle of SARS-CoV-2, a relationship begins to emerge between chronic inflammation and autoimmune conditions that helps explain how they create a greater risk in humans. Conceptually, comorbid conditions like obesity and diabetes increase risk because immune system function and dysfunction is significantly impacted by insulin response, glucose metabolism, inflammation and lipid metabolism. Therefore, people with these conditions often have compromised innate and acquired immunity, placing them directly on the path for developing serious COVID-19 symptoms. Currently, the CDC lists people with severe obesity, defined as a BMI of at least 40 kg/m2, and diabetes as being at high risk for developing severe illness from COVID-19.
A case study in China showed that from the beginning of the outbreak through Feb. 11, 2020 via coronavirus testing, the death rate among patients with COVID-19 who had diabetes was 7.3% compared to 0.9% for those without it. Conversely, better controlling diabetes, obesity, and heart disease, or otherwise reversing these chronic inflammatory-autoimmune conditions, reimagines how we can decrease SARS-CoV-2 risk in uninfected people.
Moreover, other comorbid data may be explained by the fact that people with obesity often have sleep apnea and other lung abnormalities that can result in hypoxia even before any infection occurs. This leaves an already exasperated lung at risk for further injury if infected with SARS-CoV-2. Saskia Smits et.al. published research on SARS-CoV, which showed that an increase in differential expression of genes, associated with inflammation, could lead to a deficiency in control of viral replication. In turn, this led to prolonged proinflammatory responses, potentially leading to poor outcome clinically. Reflecting on the etiology of risk factors among the critically ill COVID-19 patients, there are comorbid conditions that have been the focus of alternative clinical practice for years. There are significant bodies of research, clinical indications and education regarding the environmental, emotional, nutritional, phytochemical and microbiome impacts on achieving healthy immune and metabolic functions. Therefore, as cornerstones of our alternative model, these datasets represent an important opportunity we cannot and should not overlook now and for future viral interactions.
Shayne Morris, PhD, MBA, CNS, is a biochemist and molecular biologist specializing in beneficial interactions between our bodies systems including the complex microbiota and the use of therapeutic herbal ingredients. Morris’s manufacturing and corporate experience and business education, complement the ever-important clinical research and development at Systemic Formulas. He has pioneered multiple new product designs, patents, and most importantly introduced the concept of “herbalomics” and the “Nutri-Biome.”
1.Arentz, Matt, Eric Yim, Lindy Klaff, Sharukh Lokhandwala, Francis X. Riedo, Maria Chong, and Melissa Lee. “Characteristics and Outcomes of 21 Critically Ill Patients with COVID-19 in Washington State.” Jama (2020).
2. Bialek, Stephanie, Ellen Boundy, Virginia Bowen, Nancy Chow, Amanda Cohn, Nicole Dowling, Sascha Ellington, et al. “Severe Outcomes among Patients with Coronavirus Disease 2019 (COVID-19) – United States, February 12-March 16, 2020.” MMWR. Morbidity and Mortality Weekly Report 69, no. 12 (2020): 343-346.
4. Harold Bays, MD, chief science officer of the obesity medical association and the medical director and president of Louisville Metabolic and Atherosclerosis Research Center
5. Smits, Saskia, Anna Lang, Judith Brand, Lonneke Leijten, Wilfred IJcken, René Eijkemans, Geert Amerongen, et al. “Exacerbated Innate Host Response to SARS-CoV in Aged Non-Human Primates.” PLoS Pathogens 6, no. 2 (2010): e1000756.
6. Wu, Yuntao. “Compensation of ACE2 Function for Possible Clinical Management of 2019-nCoV-Induced Acute Lung Injury.” Virologica Sinica (2020).