Clinical diagnosis
Case 250
【Discussion】
Viral infection is the battle between viral potency and immune system. Virus come into vital cells for their surviving and proliferating. As the first immune defense, mucin, IgA, and cilia defend the attack from virus. In this stage, virus in air or fluids attempt to attach or invade to respiratory cells, indicating not yet to be infected, even if PCR test or antigen test is positive. When the immune system is tough, virus enter the weak site, taste and/or smell nerve ends. Further, virus reach to pulmonary alveolus, macrophages phagocyte virus. When viral potency surpasses the first immune system such as more numbers of virus or more talent of each virus, infection to respiratory cells is established. Cough and fever imply successful infection of virus to respiratory cells. Macrophages phagocytes virus and secrete cytokine, IL-6 which signals to stimulate fever pivotal center of hypothalamus (1). Cytokines from macrophages or dendritic cells stimulate monocytes and lymphocytes to cope with viral infection. Of lymphocytes, killer cells phagocytes virus, helper T cells make signal to B cells to create antibody, and to memory T cells for to memorize its antigen. First, IgM, lymphocytes, monocytes move and get together on the fore front line at the capillaries surrounding alveolus. Several days after, IgG, B cells, plasm cells also gather as the supporting troops (2).
Virus can proliferate when it invades to respiratory cells with appropriate receptor (ACE2, angiotensin converting enzyme 2). Once virus invades respiratory cells, alveolar type 1 cells, alveolar type 2 cells for viral proliferation, virus can also invade to immune cells, although, in this situation, virus cannot replicate in immune cells (2). Infected respiratory cells and infected immune cells secrete cytokine to make messages to monocytes and neutrophils to phagocyte themselves, so called cytokine storm. Monocytes and macrophages are already exhausted for long-term battle with virus. Neutrophils are preserved and phagocyte infected lymphocytes and migrate into alveolar cells not only to phagocyte virus, infected alveolar cells and infected lymphocytes but also to induce permeability of vessels causing to fill edematous fluids in alveolar space. As a result, apoptosis and phagocytosis of lymphocytes reduce number of lymphocytes, indicating less production of antibody. Elevation of KL6 indicates damages of alveolar type II cells, elevation of LDH indicates cell damages, elevation of D dimer indicates thrombus formation caused by extracellular trapping by macrophages and neutrophils (3-7).
In our case, the count of lymphocytes was getting decreased with the bottom of 214/mm3, least five days before he passed away.
In conclusion, the decrease of lymphocytes counts implies more potency of virus against immune response, indicating to cause acute respiratory distress syndrome in a clinical state and a radiological finding, diffuse alveolar cell damages in pathology, leading poor prognosis.
【Summary】
We presented a seventy seven-year-old male suffering from COVID-19. His symptoms worsened as the gradual decrease of lymphocytes counts. The least lymphocyte count was 214/mm3, five days before he passed away. It is borne in mind that in viral infection, the decrease of lymphocytes count indicates virus infects lymphocytes and neutrophils phagocyte infected lymphocytes, implying less production of antibody. Entering of neutrocytes into alveolus also causes permeability of capillaries, inducing fluids filling in, leading consolidation on chest CT and blockade of O2-CO2 exchange. Namely, the decrease of lymphocytes implies that the more potency of virus surpass against weak immune response.
【References】
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2021.11.22