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COVID-19
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
While the main target of COVID-19 is the upper respiratory tract with the resultant fever, dry cough, fatigue, and dyspnea, recent evidence has emerged that the endothelial system is the key to many of the more detrimental symptoms.9 The virus enters the alveolar epithelial cells via the ACE-2 receptor and disrupts the cells causing intense inflammation with damage to the significant vascular element of the lungs.9 One of the severe consequences of this unchecked process is a “cytokine storm” resulting in a propagating hyper-inflammatory process that causes extensive ongoing tissue damage.10 A second process that has been identified as a “bradykinin storm” may be equally or more significant.11 The cytokine storm creates extensive damage, while the bradykinin storm induces extensive vascular leakage which allows the virus to get into the circulation and extends the damage throughout the circulatory tree resulting in a series of unusual consequences: blood clots, heart attacks, and strokes (especially in individuals under 50 years of age).12
Immuno-Pathologic Basis of COVID-19 and the Management of Mild and Moderate Cases
Published in Srijan Goswami, Chiranjeeb Dey, COVID-19 and SARS-CoV-2, 2022
Debdeep Dasgupta, Srijan Goswami, Chiranjeeb Dey
The levels of IL-2, IL-7, IL-10, GSCF, IP-10, MCP1, MIP1a, and TNF-α in the blood of severely ill COVID-19 patients were also elevated. In short, the aberrant release of multiple cytokines appears to trigger a cytokine storm that produces immunopathogenic damage to tissues and organs, even while the immune response seeks to suppress and eradicate the virus (Wiersinga et al., 2020). Thus, it can be mentioned that the cytokine storm involves an immune response that causes collateral damage that may be greater than the immediate benefit of the immune response. Figure 7.5 and Table 7.1 represent specific organs involved and respective signs and symptoms of a systemic cytokine storm. Further studies should be done to find out the detailed pathogenesis of COVID-19 and cytokine storms (Wiersinga et al., 2020; Price et al., 2020; Dutta et al., 2020; Fajgenbaum and June, 2020; WHO, 2020a; Yuki et al., 2020; Kumar and Al Khodor, 2020; Parasher, 2021; Cevik et al., 2020; Abbas et al., 2016; Oliveira et al, 2020).
Convalescent Plasma and Antibody Therapy in COVID-19
Published in Debmalya Barh, Kenneth Lundstrom, COVID-19, 2022
Didem Rıfkı, Eymen Ü. Kılıç, Şükrü Tüzmen
SARS-CoV-2 is defined as the etiological agent that caused the COVID-19 pandemic at the end of 2019. Considering its dramatic consequences on people’s health, economics, daily life, education, and politics, scientists all over the world have been working hard to understand the physiopathology of this disease in order to develop efficient treatment strategies. Immunomodulation has gained importance as a potential therapeutic strategy for this disorder, as the main battle of care is the cytokine storm. Specific and nonspecific immunotherapies, such as convalescent plasma (CP) and specific immunoglobulins, are being investigated for the treatment of extreme COVID-19 disease, but no conclusive proof of their efficacy has yet been found, with the exception of the approval of Regeneron’s monoclonal antibody (mAb) cocktails. CP therapy is focused on the concept of using antibodies produced from naturally recovered individuals to prevent and cure COVID-19. It has also decreased viral antigen levels, improved blood oxygen saturation, and increased lymphocyte ratio [1]. CP treatment, which involves transfer of antibodies to the recipient, provides both antiviral and immunomodulatory activities through anti-inflammatory cytokines and antibodies [1].
RSV induced rhabdomyolysis: a case report
Published in Acta Clinica Belgica, 2023
Stijn Arnaert, Thomas Malfait, Astrid Deruyck, Farah Desoete, Maria Nersisjan, Inge Matthijs, Bart Maes
Another possible underlying mechanism could be a maladaptive cytokine release in response to a viral infection. A cytokine storm is a systemic, excessive and uncontrolled inflammation determined by elevated circulating cytokine levels, an acute systemic inflammatory response and secondary organ dysfunction [9]. Interferon-y, interleukin 1,6 and 18, TNF are thought to be the most important proinflammatory cytokines in this immunopathologic process [9]. Downstream signal transduction is mediated by JAK-STAT or MAP pathway. (Figure 2) This causes cell migration (Th1-cells, NK-cells …), production of acute phase proteins, fever and increased protein catabolism [10]. Muscle wasting is observed in healthy animals exposed to proinflammatory cytokines due to an increase in ubiquitine expression and proteasome enzyme activity. Unfortunately, the precise mechanism by which inflammation modulates protein turnover is not yet described [10].
Varicella Zoster Viral Retinitis following Chimeric Antigenic Response T-cell Therapy for B-cell Lymphoma
Published in Ocular Immunology and Inflammation, 2022
Waleed K. Alsarhani, Ahmed M. Abu El-Asrar
The reason why the patient developed ocular and skin viral infection may be related to lymphocyte depletion due to the premedication chemotherapy that patients usually receive prior to CAR T-cell therapy. Another possible factor that may have increased the risk of VZV reactivation is hypogammaglonulinema related to B-cell aplasia.5 Hypogammaglobulinemia was shown to raise the risk of systemic viral infections.4 Neutropenia, another risk factor for infection, has been described in 94% following CAR T-cell infusion.6 The primary malignancy along with anti-tumor regimens certainly played a role in weakening the immune system and exposing the patient to infections. A recent study showed that the induced cytokine storm to be the most important risk factor for systemic infections.3 In fact, CRS may be confused with systemic infections since they share similar symptoms and signs.7 Indeed, we believe that the mechanism of the infection in our patient is multifactorial.
Association of TNF-α G-308 a Promoter Polymorphism with the Course and Outcome of COVID-19 Patients
Published in Immunological Investigations, 2022
Ahmed Saleh, Ahmed Sultan, Mohamed A Elashry, Ahmed Farag, Metwaly Ibrahim Mortada, Mayada A Ghannam, Ahmed M Saed, Elsayed Ghoneem
As soon as viral antigens are recognized by the immune system, they are presented by the antigen presenting cells both to the CD8-positive cytotoxic T and natural killer cells in the context of major tissue histocompatibility (MHC) antigens as usual. This activates both the innate and adaptive immunity, causing the production of large amounts of chemokines and proinflammatory cytokines. In some patients, this activation becomes so massive that leads to the development of cytokine storm. This results in thrombotic tendency and multi-organ failure and eventually causes death (Li et al. 2020). Previous studies conducted on SARS and the Middle East respiratory syndrome (MERS) induced by different strains of coronavirus, focused on the so-called cytokine storm, showed high release of proinflammatory cytokines such as interleukin-6 (IL-6), TNF-α), IL-8, IL-12 and, IL-1β as well as interferon gamma inducible protein (Lau et al. 2013). In COVID-19-associated ARDS (CARDS), elevated plasma levels of cytokines including IL-6 have been demonstrated and usually correlated with the severity of the clinical course (Huang et al. 2020). IL-6 may play a key role in the inflammatory storm, which underlies the COVID-19 pathogenesis (Huang et al. 2020). Although, higher levels of IL-6 were associated with the need for mechanical ventilation owing to a more severe disease, preliminary data on CARDS patients treated with tocilizumab, favorable outcomes were observed (Liu et al. 2020; Rojas-Marte et al. 2020).