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Coronavirus: This is why COVID-19 becomes a deadly disease

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A recent study, published in the journal Nature Microbiology and led by the researchers from NYU Grossman School of Medicine, sheds light on factors that increase the risk of death in critically ill people with COVID-19 infection, concluding that the risk is increased by the concentration of the virus in a specific organ of the body

The findings revealed that persons who died from COVID-19 had 10 times the amount of virus, or viral load, in their lower airways as seriously ill patients who survived their disease. Meanwhile, the investigators found no evidence linking the deaths to subsequent bacterial infection, though they noted that this could be related to the repeated course of antibiotics given to severely ill patients.

“Our findings suggest that the body’s failure to cope with the large numbers of virus infecting the lungs is largely responsible for COVID-19 deaths in the pandemic,” says study lead author Imran Sulaiman.

He points out that current CDC guidelines do not advocate for the use of antivirals like remdesivir in critically ill patients on mechanical ventilation. However, according to Sulaiman, the findings of the NYU Langone study imply that these drugs may still be useful in treating these patients.

Despite previous fears that the virus would cause the immune system to attack the body’s own lung tissue, resulting in lethal levels of inflammation, the researchers discovered no indication that this was a substantial contributor to COVID-19 mortality in the group tested. Indeed, according to Sulaiman, the strength of the immune response appeared to be proportional to the amount of virus in the lungs.

According to Sulaiman, the new study was meant to elucidate the significance of secondary infections, viral load, and immune cell types in COVID-19 mortality. According to him, the study presents the most comprehensive evaluation of the lower airway environment in coronavirus patients.

For their study, the researchers collected bacterial and fungal samples from the lungs of 589 men and women who were hospitalized at NYU Langone facilities in Manhattan and Long Island. Mechanical ventilation was required in all cases. The researchers evaluated the amount of virus within the lower airways of 142 individuals who also had a bronchoscopy operation to clear their air passages and identified the microorganisms present by analyzing small portions of the germs’ genetic code. The researchers also looked at the types of immune cells and chemicals found in the lower airways.

The study discovered that individuals who died had 50 percent reduced production of a type of immune molecule that targets the coronavirus compared to COVID-19 patients who survived the disease. These tailored proteins are part of the body’s adaptive immune system, a group of cells and molecules that “remember” newly met invading bacteria, making the body better prepared for future exposure.

“These results suggest that a problem with the adaptive immune system is preventing it from effectively combating the coronavirus,” says study senior author Leopoldo Segal, MD.

“If we can identify the source of this issue, we may be able to find an effective treatment that works by bolstering the body’s own defenses,” says Segal, an associate professor in the Department of Medicine at NYU Langone.

He emphasizes that the researchers only looked at coronavirus patients who survived their first two weeks in the hospital. According to him, bacterial infections or autoimmune reactions may play a larger role in COVID-19 mortality that occurs earlier.

According to Segal, the next step for the research team is to monitor how the microbial community and immune response in the lungs of coronavirus patients change over time.

Image Credit: Getty

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