As COVID-19 continues to ravage throughout the world, more and more research and studies are being conducted to understand how severe the virus’ impact is, and why it’s severity continues to vary across infected patients.
While it’s noted that many infected COVID patients fall extremely ill facing symptoms like fever, chills, loss of smell, and sometimes fatal respiratory issues, there are other patients that contract the virus and experience minimal symptoms. But how can a virus that’s made its way around the world as a devastating pandemic taking a record-breaking amount of lives, impact people differently?
Epidemiology research has found there are two factors that can potentially cause a difference in the virus’ level of severity, aside from factors such as underlying health conditions and age. By conducting a GWAS (genome-wide association study), scientists and researchers have successfully collected data based on gene variants in two regions during peak times (Spain and Italy). The study collected, genotyped, and analyzed samples from a number of individuals, breaking them down into control groups (samples without the virus) and patients groups that have tested positive for the virus:
Italy:
835 COVID patients
1255 control participants
Spain:
775 COVID patients
950 control participants
Ultimately, the study resulted in the discovery of two gene variants that appear to be directly associated with the virus’ severity level; specifically focusing on the potential for respiratory failure following contracting the virus. The findings suggested that two main genomic regions related to a higher risk of respiratory failure are identified within the patient’s blood type and specific human chromosomes. The study found that patients with type A blood were at a higher risk of respiratory failure than patients with type O blood. Stating that the odds for patients with blood type A to be hospitalized for respiratory failure were close to 1.5 times the odds for patients with other blood types. While patients with blood type O held a more protective effect and about two-thirds the odds of ending up hospitalized than other blood types.
The other genomic region that the GWAS identified involved human chromosome 3p21.31and several genes within (SLC6A20, LZTFL1, CCR9, FYCO1, CXCR6, and XCR1). It’s highlighted within the study notes that while a causative gene cannot be drawn reliably from the current data, the SLC6A20 specifically encodes a transporter that interacts with the angiotensin-converting enzyme 2 (ACE2), the cellular receptor that COVID-19 needs to enter host cells. Thus increasing the odds of being hospitalized with respiratory failure from COVID-19 to 1.77 times higher in patients with the variants on chromosome 3 than those without. According to Andre Franke, a geneticist at Christian-Albrechts-University of Kiel and co-author of the study, the gene cluster on chromosome 3 has an even higher effect size than that of the ABO genomic region, “but we cannot say at the moment which of the many candidate genes is most important. All of them are very attractive in this region”
It’s important to note that these findings are still quite open-ended, and do not determine a prediction of whose case will be more severe. However, it does lead to a plausible place to begin making these determinations.