Case severity is the most inconsistent element of the COVID-19 pandemic. Those with patience for the details have likely grown dissatisfied with the stump narratives on offer, despite admirable efforts on behalf of officials and health systems to brief the public as often as possible.
In the time since SARS-Cov-2 penetrated the US an increasing number of young otherwise healthy Americans have evidenced severe manifestations of the ensuing respiratory disease, while a similar portion remains asymptomatic for the entire duration of infection.
Some of the causal factors will remain unknown for the foreseeable future, as is the case with the critical forms of influenza that impact young demographics every year. By and large, the pathology of any illness survives on a cocktail of circumstance and genetic predispositions.
A series of studies derived from the DNA of patients with aggressive COVID-19 symptoms were linked by the human receptor angiotensin-converting enzyme 2 (ACE2). The most common SARS viruses that affect humans rely on ACE2 for viral entry.
SARS-Cov-2’s trimeric spike protein binds to the receptor before hijacking cells. The more we understand about this critical interaction the better we can develop therapeutics capable of averting it.
A new paper published in The New England Journal of Medicine compellingly suggests that the interaction between SARS viruses and ACE2 might be a correlate of their infectivity. In fact, some physicians have motioned for the discontinuation of ACE inhibitors and angiotensin-receptor blockers (ARBs), both prophylactically and in the hopes of treating COVID-19.
“It is my opinion that [host] genetic differences are a key factor … for susceptibility to severe acute pneumonia,” Alessandra Renieri, a geneticist at the University of Siena in Italy, who is one of the many academicians collecting DNA samples from willing patients who are currently hospitalized with COVID-19, explained in LiveScience.
ACE2 is not the only genetic parallel observed in critically ill patients. Some of the pioneering research operates in the negative spaces.
A preliminary study conducted in China determined physiological similarities that keep some individuals protected against advanced respiratory inflammation caused by SARS-Cov-2.
Thirty-seven percent of surveyed patients had the same blood type. There were 63% more fatalities among type A blood patients than type O patients of the 206 initial COVID-19 deaths that occurred in Wuhan.
“If you are type A, there is no need to panic. It does not mean you will be infected 100%,” researcher Gao Yingdai told the South China Morning Post. “If you are type O, it does not mean you are absolutely safe, either. You still need to wash your hands and follow the guidelines issued by authorities.”
The World Health Organization reports that more than 80% of laboratory-confirmed cases were defined as mild-to-moderate, 14% were severe and 6% could be described as critical.
Medical professionals gauge case severity by oxygen levels in the blood and lung damage that worsens by 50% or more within a 24 to 48-hour window .
Men and smokers are roughly 1.3 times more likely to evidence life-threatening incarnations of COVID-19.
Sufferers of chronic obstructive pulmonary disorder are between two and 11 times more likely to endure severe respiratory symptoms and patients with kidney disease are between two- and 16-fold more likely to evidence the same.
Any preexisting condition that exacerbates inflammation, like hypertension, asthma, and diabetes carries similarly start risk increases.
“These conditions appear to track closely with advancing age,13 which is emerging as the strongest predictor of COVID-19–related death.14 Unfortunately, reports to date have not rigorously accounted for age or other key factors that contribute to health as potential confounders in risk prediction. With other infective illnesses, coexisting conditions such as hypertension have been key prognostic determinants,10 and this also appears to be the case with COVID-19,” The New England Journal of Medicine reports.
RAAS inhibitors, which are often used to treat patients with the aforementioned underlying conditions, might also be playing a huge role in recovery statistics.
Conversely, routinely consuming VItamin C, receiving moderate physical activity, sufficient sleep and staying hydrated have all been linked to mild forms of COVID-19.