Bacteria and viruses have existed for a very long time. Since viruses require a host to reproduce, they have been destroying bacteria for millions of years. Some of those bacteria later developed into mitochondria as a result of their cooperative adaptation to life in eukaryotic cells (cells that have a nucleus containing chromosomes).
In the end, mitochondria developed into the centers of power for all human cells.
Let’s fast-forward to the emergence of new coronaviruses like COVID-19 and SARS-CoV-2. Roughly 5% of SARS-CoV-2 patients experience respiratory failure (low blood oxygen) necessitating hospitalization. Nearly 46,000 of the infected patients in Canada, or 1.1% of all cases, have died.
It is a throwback to the early battle between viruses and bacteria, more specifically between this novel virus and the bacteria’s evolutionary offspring, our mitochondria. This is the tale of how a team assembled during the pandemic recognized the mechanism by which these viruses were causing lung damage and lowering oxygen levels in patients.
Following MERS-CoV in 2012 and SARS-CoV in 2003, SARS-CoV-2 is the third new coronavirus to produce human outbreaks in the twenty-first century. To get ready for the next pandemic, we need to comprehend how coronaviruses damage the lungs more thoroughly.
*How COVID-19 affects lungs
Patients with severe COVID-19 pneumonia frequently have abnormally low oxygen levels when they get to the hospital. They differ from patients with other kinds of pneumonia in two peculiar ways:
First, they suffer widespread injury to their lower airway (the alveoli, which is where oxygen is taken up).
Second, they shunt blood to unventilated areas of the lung, which is called ventilation-perfusion mismatch. This means blood is going to parts of the lung where it won’t get sufficiently oxygenated.
by: Miss Cherry May Timbol – Independent Reporter
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