SARS-CoV2 gains entry via a receptor called ACE2.
The virus moves down your respiratory tract. That’s the airway that includes your mouth, nose, throat, and lungs.
Your lower airways have more ACE2 receptors than the rest of your respiratory tract. So COVID-19 is more likely to go deeper than viruses like the common cold
In the lung, the ACE2 receptor sits on top of lung cells called pneumocytes. These have an important role in producing surfactant — a compound that coats the air sacs (alveoli), thus helping maintain enough surface tension to keep the sacs open for the exchange of oxygen and carbon dioxide.
As soon as the body recognizes a foreign protein, it mounts the first response. One part of the body’s immune response — the lymphocytes — begin to produce the first defense IgM-type antibodies and then the longer-term specific neutralizing antibodies (the IgG type).
IgG/IgM serological tests detect human antibodies (proteins belonging to the immunoglobulin class) which are known to be much more stable than viral RNA.
Unlike RT-qPCR, serological tests can detect past infection because virus-specific antibodies (unlike viral RNA) can persist in the blood for several weeks/ months after the onset of symptoms.
*Check clinical significance of an IgM/IgG Serological Test Result in the figure at the end.
In pneumonia, the lungs become filled with fluid and inflamed, leading to breathing difficulties.
For some people, breathing problems can become severe enough to require treatment at the hospital with oxygen or even a ventilator.
Pneumonia that COVID-19 causes tend to take hold in both lungs. Air sacs in the lungs fill with fluid, limiting their ability to take in oxygen and causing shortness of breath, cough, and other symptoms.
While most people recover from pneumonia without any lasting lung damage, pneumonia associated with COVID-19 may be severe. Even after the disease has passed, lung injury may result in breathing difficulties that might take months to improve and completely recover.
The ground-glass and/or consolidative opacities are usually bilateral, peripheral, and basal in distribution
As COVID-19 pneumonia progresses, more of the air sacs become filled with fluid leaking from the tiny blood vessels in the lungs. Eventually, shortness of breath sets in and can lead to acute respiratory distress syndrome (ARDS), a form of lung failure. Patients with ARDS are often unable to breathe on their own and may require ventilator support to help circulate oxygen in the body.
Whether it occurs at home or the hospital, ARDS can be fatal. People who survive ARDS and recover from COVID-19 may have lasting pulmonary scarring.
In severe acute respiratory distress syndrome (ARDS), the inflammation stage gives way to the fibrosis stage. Fibrin clots form in the alveoli, and fibrin-platelet microthrombi (small blood clots) appear the small blood vessels in the lung that are responsible for gas exchange with the alveoli.
Cytokines are chemical mediators that white blood cells such as macrophages release, and they can engulf infected cells. These cytokines — which have names such as IL1, IL6, and TNFα — have actions that include dilating the vessel walls and making them more permeable. In extreme circumstances, this can lead to a collapse of the cardiovascular system.
Cavitation can also occur in areas of airspace disease.
Degree of hypoxemia:
200 mm Hg < PaO2 /FiO2 ≤ 300 mm Hg with PEEP or CPAP ≥ 5 cm H2 O (mild ARDS);
100 mm Hg < PaO2 /FiO2 ≤ 200 mm Hg with PEEP ≥ 5 cm H2 O (moderate ARDS);
PaO2 /FiO2 ≤ 100 mm Hg with PEEP ≥ 5 cm H2 O
(Severe ARDS). When PaO2 is not available, SpO2 /FiO2 ratio <= 315 suggests ARDS.