New cell atlas of COVID lungs reveals why SARS-CoV-2 is deadly and different


Sumary of New cell atlas of COVID lungs reveals why SARS-CoV-2 is deadly and different:

  • A new study is drawing the most detailed picture yet of SARS-CoV-2 infection in the lung, revealing mechanisms that result in lethal COVID-19, and may explain long-term complications and show how COVID-19 differs from other infectious diseases..
  • Led by researchers at Columbia University Vagelos College of Physicians and Surgeons and Herbert Irving Comprehensive Cancer Center, the study found that in patients who died of the infection, COVID-19 unleashed a detrimental trifecta of runaway inflammation, direct destruction and impaired regeneration of lung cells involved in gas exchange, and accelerated lung scarring..
  • Though the study looked at lungs from patients who had died of the disease, it provides solid leads as to why survivors of severe COVID may experience long-term respiratory complications due to lung scarring..
  • In particular, targeting cells responsible for pulmonary fibrosis early on could possibly prevent or ameliorate long-term complications in survivors of severe COVID-19,”.
  • The new study is unique from other investigations in that it directly examines lung tissue (rather than sputum or bronchial washes) using single-cell molecular profiling that can identify each cell in a tissue sample and record each cell’s activity, resulting in an atlas of cells in COVID lung..
  • “A normal lung will have many of the same cells we find in COVID, but in different proportions and different activation states,”.
  • “In order to understand how COVID-19 is different compared to both control lungs and other forms of infectious pneumonias, we needed to look at thousands of cells, one by one.”.
  • In collaboration with investigators at Cornell University, the researchers also compared their findings to lungs of patients with other respiratory illnesses..
  • Compared to normal lungs, lungs from the COVID patients were filled with immune cells called macrophages, the study found..
  • Typically during an infection, these cells chew up pathogens but also regulate the intensity of inflammation, which also helps in the fight..
  • “In COVID-19, we see expansion and uncontrolled activation of macrophages, including alveolar macrophages and monocyte-derived macrophages,”.
  • This results in a vicious cycle where more immune cells come in causing even more inflammation, which ultimately damages the lung tissue.”.
  • In a typical infection, a virus damages lung cells, the immune system clears the pathogen and the debris, and the lung regenerates..
  • But in COVID, the new study found that not only does SARS-CoV-2 virus destroy alveolar epithelial cells important for gas exchange, the ensuing inflammation also impairs the ability of the remaining cells to regenerate the damaged lung..
  • Though the lung still contains cells that can do the repairs, inflammation permanently traps these cells in an intermediate cell state and leaves them unable to complete the last steps of differentiation needed for replacement of mature lung epithelium..
  • This suggests that in addition to reducing inflammation, targeting IL-1beta may help take the brakes off cells required for lung repair.”.
  • The researchers also found a large number of specific fibroblast cells, called pathological fibroblasts, that create rapid scarring in COVID-19 lungs…

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