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Clinical diagnosis

Case 193

3. Viral pneumonia


【Progress】
 Polymerase chain reaction (PCR) test using nasal fluid revealed positive following day. He was admitted in the designated hospital the local health center introduced.

【Discussion】
 In human, there are two types for immune system to protect our body from attacks of harmful microbes of virus, bacteria and parasites. Namely, we can survive under innate immunity and acquired (or adaptive) immunity (1, 2). The first line of defense in respiratory tract is mucus, cilia, surfactant, alveolar macrophages, neutrophils and lymphocytes (including B cell, T cell, natural killer cell). Cilia covers bronchial tree and moves with beats to excrete foreign bodies. Mucus includes Ig A and lysozyme to counter microbes. Macrophages, neutrophils and natural killer cells engulfed harmful micro-organisms and macrophages also infected phagocytes. Further, B cell and T cell play a role to produce interferon. When the first line defense cannot overcome the invasion of microbes, the second line defense works. The second line defense indicates more accumulation of neutrophils, lymphocytes, monocytes, basophils and eosinophils from whole blood and/or bone marrow. These cells are collected by cytokine and chemokine from the cells in charge of the first line defense. Cytokine indicates signaling protein for cell to cell communication and chemokine is a kind of cytokine, for infected cell to cell.
 The third line defense, called adaptive immunity begins to work associated with the second line defense. Lymphocytes of T cell and B cell recognize antigen and produce antibody (Ig G, Ig M, Ig E, Ig D). It requires time, immediately after to several days to respond to microbes depending on virgin infection or past-experienced infection and depending on the kind of microbes.
 When the first line to the third line defense are unable to overcome, the final line defense begins to work. This is not only to attack to pathogen but also to make adverse effect on host. Addition to various chemotactic factors of tumor necrosis factor and interleukins produced by lymphocytes, various protease produced by macrophages and leukocytes causes destruction alveolar walls, leading to acute respiratory distress syndrome (ARDS).
 Clinical cases of Influenza virus infection are categorized into three types; resistant host, elimination of pathogen; tolerant host, reduction in tissue damage: susceptible host, failure to clear the pathogen or tolerant-immune-mediated damage (3). Resistant host indicates no symptoms, implying the first line defense works. Tolerant host indicates respiratory symptoms, implying the first to third line defense works. Susceptible host indicate ARDS, implying the final battle between virus and host.
 Influenza virus has an envelope and single-stranded RNA with spikes of haemagglutinin (HA) and neuraminidase (NA) which are antigenic and targets to produce antibody. Influenza virus invades from oral cavity and/or nasal cavity. The flu patients experience temporal loss of taste and small in 3 to 22% (3-5). The mechanism is not well understood. Influenza can infect and hide nasal cells, tongue cells and their nerve cells.
 The risk factors worsening symptoms after influenza infection are high aged, immune-compromised, and smoking. Cigarettes smoke lowers potency of first line immune function by disordering bronchial epithelial cells, macrophages, leukocytes and lymphocytes and activates resident cells and recruit cells, leading to release inflammatory chemotactic factors, oxygen radicles and proteases.
 Vaccine might be an ideal treatment for influenza. Vaccine for four types of influenza virus (A/H1N1, A/H3N2, B/Yamagata, B/Victoria) is mixed. Each antigen is produced by culturing influenza virus in eggs, taking out viable virus and processing to eliminate fat-soluble component. It is called non-activation vaccine. It takes several days to product antibody which is effective to respond viral infection for several months. Effective rate is 30 to 70% (6 - 9). The ratio is relatively low but vaccination is reported to play a imperative role to prevent from worsening the stage so as to become a susceptible host even if infected.

【Summary】
 We present a middle-aged male with corona virus infection. He was transported to the designated hospital for infectious disease. He suffered from persistent cough and chest CT showed viral pneumonia, indicating to be a tolerant host. He recovered relatively soon. It is borne in mind that there are four defense lines for virus infection attack in the respiratory tract human. The first defense line is cilia, mucin, surfactant, macrophages, dendritic cells, and natural killer cells. They try to wash away virus or phagocyte virus. The second defense line is B cell, T cell, eosinophils, basophils and neutrophils. These cells most come from whole blood and bone marrow immediately after the message called cytokine from T cell, and aide the first line cells. B cells secrete IgA, granular cells phagocyte virus and T cell get information of virus antigen. The third defense line is that production of antibody (Ig G) by T cells based on antigens using virus component. The fourth defense line is the final action of immune system for virus attack. This line triggers when the first to third line falls into non-effective. Cytokine smoke arises, tumor necrosis factors and interleukin from lymphocytes, and protease from macrophages & leukocytes, secrete, inducing acute respiratory distress syndrome (ARDS). High age and cigarette smoke weaken and tear first line defense, implying easily to fall into ARDS.


【References】
1.Chen X, et al. Host Immune Response to Influenza A Virus Infection. Front Immunol. 2018; 9: 320.
2.Akiko Iwasaki, et al. Innate immunity to influenza virus infection. Nat Rev Immunol. 2014; 14(5): 315–328.
3.Mehta H, et al. Cigarette smoking and innate immunity. Inflamm. res. 57 (2008) 497–503
4.Edwards D, et al. Immunological effects of tobacco smoking in "healthy" smokers. COPD. 2009 Feb;6(1):48-58
5.Godoy P, et al. Smoking may increase the risk of influenza hospitalization and reduce influenza vaccine effectiveness in the elderly. Eur J Public Health. 2018 Feb 1;28(1):150-155.
6.Vaccines against influenza WHO position paper - November 2012.”. Wkly Epidemiol Rec 87 (46): 461-76.
7.Jefferson, T et al. Vaccines for preventing influenza in healthy children. Cochrane Database of Systematic Reviews: 2018, CD004879.
8.Jefferson, T et al. Vaccines for preventing influenza in the elderly. 2010 The Cochrane database of systematic reviews (2): 2010 CD004876.
9.Manzoli L et al. Effectiveness and harms of seasonal and pandemic influenza vaccines in children, adults and elderly: a critical review and re-analysis of 15 meta-analyses. Hum Vaccin Immunother 2012; 8 (7): 851-62.

2020.6.10



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