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Detection Assays and Techniques Against COVID-19
Published in Hanadi Talal Ahmedah, Muhammad Riaz, Sagheer Ahmed, Marius Alexandru Moga, The Covid-19 Pandemic, 2023
Shahzad Sharif, Maham Saeed, Javed Hussain Shah, Sajjad Hussain, Ahmad Adnan, Hanadi Talal Ahmedah, Muhammad Riaz
SARS-CoV2 also called Severe Acute Respiratory Syndrome Corona-virus-2 has become the main source of this infectious pandemic [8]. SARS-CoV-2 recently joins the family of Corona and the genus Betacoronavirus as compared to MERS-CoV and SARS-CoV. Having their CORONA-like resemblance, these viruses are named so. Corona has been derived from the Latin word known as CROWN. Coronavirus-induced Acute Respiratory Distress Syndrome (ARDS) is almost similar to Cytokine Storm Syndrome, causing fluid extravasation and a leap of pulmonary inflammation resulting in breathing collapse. Breathing hindrance, cardiac issues or ARDS may be the main causes. Secondary bacterial infection causes sepsis followed by death due to COVID-19 (Figure 4.1) [9].
Role of Artificial Intelligence in the Era of COVID-19 to Improve Hospital Management
Published in Adarsh Garg, D. P. Goyal, Global Healthcare Disasters, 2023
Lot of challenges have to be faced by the hospitals to control this pandemic situation, by inpatients, and by the ICU patients (Yang et al., 2020; Arentz et al., 2020; Cao et al., 2020), such as slow testing, no systematic detection of COVID-19, less number of ICU beds, need highly expert intensive care physicians who can do fast analysis and respond to recently developed disease, increase multiple organ failure, and cytokine storm syndrome (CSS) caused of sudden exacerbations and death. The role artificial intelligence (AI) will play in a dynamic atmosphere needs to be an innovative effort, otherwise the process of patient care and clinical decision making would be noneffective. This model is to assess the role of AI in the management of inpatients and critically ill patients in ICU with COVID-19. AI-based model would improve the critical care of the COVID-19 patients and will also save the lives of patients.
Neurological manifestations of COVID-19: a systematic review and detailed comprehension
Published in International Journal of Neuroscience, 2023
Zeina Hassan Ousseiran, Youssef Fares, Wafaa Takash Chamoun
Chronic neuro-inflammation and cytokine storm syndrome are associated with disease severity and can have long-term devastating effects on the brain function and structure. Although the exact cellular and molecular mechanisms are poorly understood, they can underlie the pathogenesis mechanisms and the clinical features of different demyelinating and neurodegenerative disorders such as Parkinson disease, Alzheimer disease and multiple sclerosis [100]. Furthermore, Parkinsonism is strongly associated with neurotropic viruses. This association originated from the Spanish flu in 1918 that evoked an increase in the number of Parkinsonian cases in the long term [88]. This had drawn the attention to the possibility of occurrence of a Parkinsonism wave in the near future suggesting that SARS-CoV-2 could affect neuronal brain populations including the brainstem, the diencephalon and other brain regions.
Immune response to COVID-19 infection: a double-edged sword
Published in Immunological Medicine, 2021
The uncontrolled release of cytokines, also called ‘Cytokine storm syndrome’ is plausibly the major factor underlying COVID-19 immuno-pathogenicity [49]. This storm was at the origin of tissues damages, hyper inflammation [50] and even mortality cases [19]. It was triggered by a hyper activation of immune cells, which led to a boom of cytokines release [51]. The over expression of Induced Protein-10, hepatocyte growth factor, monokine-induced gamma IFN, monocyte chemotactic protein-3 and macrophage inflammatory protein 1 alpha were highly associated with the disease severity classes [52]. Interestingly, the upregulation of IL-6 got a special attention in COVID-19 pathogenicity since it plays a major role in recruiting neutrophils to lungs [53] and consequently inducing hyper inflammation, neutrophilia and NETosis. In addition, Mazzoni et al. [54] showed that IL-6 was responsible for impaired cytotoxicity properties of immune cells in severe cases of COVID-19. However, IL-6 level in COVID-19 stays lower than in cytokine release syndrome (CRS) [53,55]. Surprisingly, infected patients displayed reduced levels of anti-viral effectors especially interferon types I and III cytokines [56] and eosinophils [57,58]. This decline in anti-antiviral agents would certainly weaken the innate immune reaction and facilitate viral replication.
The triad: respiratory microbiome – virus – immune response in the pathophysiology of pulmonary viral infections
Published in Expert Review of Respiratory Medicine, 2021
Bárbara N. Porto, Theo J. Moraes
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was initially a pneumonia outbreak in China and then quickly became a pandemic, affecting more than 4 million people worldwide, with more than 300,000 deaths by May 2020 [143,144]. Epidemiological data indicate that SARS-CoV-2 transmits human-to-human through respiratory droplets from coughs and sneezes, with the host being able to shed the virus while asymptomatic [145–147]. Whereas most COVID-19 patients are adults over 18 years, confirmed cases among children have been reported [148,149]. Mortality is higher among seniors over 65 years old and those with preexisting medical conditions [150]. COVID-19 symptoms resemble that of influenza infection, ranging from mild upper respiratory tract symptoms, including fever, fatigue and dry cough, to severe lower respiratory tract symptoms though some features such as anosmia have also been reported with COVID-19. In patients with severe COVID-19, respiratory distress syndrome may develop and promptly progress to respiratory failure due to the exaggerated acute lung injury [143]. In some cases, severe COVID-19 patients have been reported to present a cytokine storm syndrome, which seems to underlie multi-organ failure [151].