The researchers discovered that people who succumbed to Covid-19 had 10 times the virus in their lower airways when compared to severely ill patients who survived.
Coronavirus build-up in the lungs might have led to the steep mortality rates during the pandemic, according to a new study. The results, however, contrast with earlier suspicions that simultaneous infections, including bacterial pneumonia or overreaction of the immune defence system, played a major role in the increased risk of death, the NYU Grossman School of Medicine said in a release.
The study was led by researchers from the NYU Grossman School of Medicine and has been published in Nature Microbiology.
The researchers discovered that people who succumbed to Covid-19 had, on an average, 10 times the virus in their lower airways when compared to severely ill patients who survived. The investigators, however, did not find any evidence to implicate a secondary bacterial infection as the cause of death. The researchers cautioned that this might have been possible due to the frequent antibiotics course administered to critically ill patients.
Dr. Imran Sulaiman, the lead author of the study, said their findings suggest the failure of the body to cope with the immense number of virus in the lungs was mainly responsible for deaths caused by Covid-19 during the pandemic.
The researchers had designed the study to clarify the role played by viral load, secondary infections, and immune cell populations in Covid-19 mortality. Dr. Sulaiman further said that the investigation provided the most detailed survey yet of the lower airway environment in patients infected by the coronavirus.
The researchers collected fungal and bacterial samples from the lungs of 589 women and men hospitalised at NYU Langone. All these patients needed ventilation. The study analysed the amount of virus in the lower airways for a subset of 142 patients who also required bronchoscopy to clear the air passages.
The study found that the deceased had, on an average, 50 per cent lower production of an immune chemical that targets the virus when compared with the patients who survived.