COVID-19 pneumonia is a lung infection resulting from the SARS-CoV-2 virus. The immune system’s response to the virus leads to inflammation in the lungs’ tiny air sacs, known as alveoli, causing them to swell and fill with fluid. This accumulation makes it difficult for oxygen to move from the lungs into the bloodstream, leading to breathing difficulties. This type of pneumonia often affects both lungs simultaneously, a condition referred to as bilateral pneumonia.
Initial Viral Phase
The progression to COVID-19 pneumonia begins when the SARS-CoV-2 virus enters the respiratory system and targets the alveolar epithelial cells. The virus gains entry into these cells by binding its spike protein to an ACE2 receptor on the cell surface. These ACE2 receptors are abundant on lung alveolar cells, making them a primary target.
Once attached, the virus hijacks the cell’s machinery, inserting its genetic material and forcing the cell to produce copies of the virus. This replication continues until the host cell dies, releasing new viral particles to infect neighboring cells. The death of these lung cells triggers a localized inflammatory response as the body recognizes the damage.
The Hyperinflammatory Phase
Following the initial viral damage, the body’s immune system mounts a more significant response. While this response is often appropriate, in some patients, the immune reaction becomes dysregulated and excessive, leading to a phase of hyperinflammation. This is driven by the body’s own overactive defense mechanisms, a condition often called a “cytokine storm.”
During a cytokine storm, a massive and uncontrolled release of signaling proteins (cytokines) causes widespread inflammation throughout the lungs. This damages healthy lung tissue far beyond the initial sites of infection.
The intense inflammation damages the walls of the alveoli and the surrounding capillaries, making them more permeable. This allows fluid and immune cells to leak from the bloodstream into the air sacs, impairing the lungs’ ability to transfer oxygen into the blood.
Acute Respiratory Distress Syndrome (ARDS)
The hyperinflammatory phase can lead to a severe medical condition known as Acute Respiratory Distress Syndrome (ARDS). ARDS is a form of respiratory failure where the lungs are so damaged they cannot provide adequate oxygen to the body’s organs. This is a direct consequence of the widespread inflammation and fluid accumulation from the cytokine storm.
The resulting fluid buildup, known as pulmonary edema, prevents the normal exchange of oxygen and carbon dioxide. As a result, oxygen levels in the blood can drop to dangerously low levels, a state called severe hypoxemia.
Patients who develop ARDS experience extreme shortness of breath and require intensive medical care. They often need mechanical ventilation to support their breathing, as a ventilator takes over this work to ensure the body receives enough oxygen.
The Fibrotic and Recovery Phase
For patients who survive the acute stages of COVID-19 pneumonia, the body begins a long process of healing. The immune system controls the inflammation, and excess fluid in the lungs is gradually reabsorbed. However, the repair process for significant lung damage can lead to long-term complications.
In some individuals, healing results in the formation of scar tissue in the lungs, a condition called pulmonary fibrosis. This scarring occurs as the body attempts to repair damaged alveolar walls, and fibroblasts become overactive, laying down excess collagen.
This scar tissue is thicker and stiffer than healthy lung tissue. The presence of fibrosis can permanently alter the lung structure, making the lungs less flexible and impairing the transfer of oxygen. This can lead to persistent breathing difficulties, shortness of breath, and reduced exercise capacity.