Question

Covid 19: One of the problems that arises with patients suffering from COVID 19 is due to accumulation of fluid in their lungs. This makes it very difficult to breathe. You have walked into the emergency room and the interns are arguing about osmosis, diffusion and the symptoms of Covid. One of the interns is arguing that there is no link between the sysmptoms of Covid and osmosis and the other is saying yes there is. Since they know you are taking physiology this summer they turn to you ask you for your opinion.

1. Since Covid starts as a respiratory infection, is there a symptom and/or condition that would involve water movement and what would that be? (2 pt)

2. What would cause water to move to cause this condition or symptom? (2 pt)

3.How would our innate immune response contribute to this issue?

Answer 1

Ans :

1.  About 14% of COVID-19 cases are severe, with an infection that affects both lungs. As the swelling gets worse, your lungs fill with fluid and debris.

You might also have more serious pneumonia. The air sacs fill with mucus, fluid, and other cells that are trying to fight the infection. This can make it harder for your body to take in oxygen. You may have trouble breathing or feel short of breath. You may also breathe faster

2.As the air sacs are damaged, there is an influx of liquid which is mostly inflamed cells and protein and this fluid build-up leads to pneumonia. This further impairs the oxygen intake by the lungs and hinders the oxygen exchange. Due to the novelty of the Covid 19 strain, there is no immediate treatment to directly cure pneumonia in Covid 19 patients and are mostly given supportive care.

The infection can damage the walls and linings of the air sacs in your lungs. As your body tries to fight it, your lungs become more inflamed and fill with fluid. This can make it harder for them to swap oxygen and carbon dioxide

3. Innate immune response :

  Cytotoxic T-cells (CTLs) and Natural Killer (NK) cells are required to generate an effective immune response against viruses, functional exhaustion of which enables disease progression. Patients with severe COVID-19 present significantly lower lymphocyte, and higher neutrophil, counts in blood. Specifically, CD8+ lymphocytes and NK cells were significantly reduced in cases of severe infection compared to patients with mild infection and healthy individuals. The NK group 2 member A (NKG2A) receptor transduces inhibitory signalling, suppressing NK cytokine secretion and cytotoxicity. Overexpression of NKG2A has been observed on CD8+ and NK cells of COVID-19 infected patients compared to healthy controls, while NKG2A overexpression also functionally exhausts CD8+ cells and NK cells, resulting in a severely compromised innate immune response. Blocking NKG2A on CD8+ cells and NK cells in cancers modulated tumor growth, restoring CD8+ T and NK cell function. A recently proposed mechanism via which SARS-CoV-2 overrides innate immune response of the host is by over-expressing NKG2A on CD+ T and NK cells, culminating in functional exhaustion of the immune response against the viral pathogen. Monalizumab is an inhibiting antibody against NKG2A which can restore the function of CD8 + T and NK cells in cancers, successfully ceasing tumor progression with no significant side effects in Phase 2 clinical trials. We hypothesize that patients with severe COVID-19 have a severely compromised innate immune response and could be treated via the use of Monalizumab, interferon α, chloroquine, and other antiviral agents.