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COVID-19 pathogenesis and host immune response
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Surbhi Bihani, Shalini Aggarwal, Arup Acharjee
The first-line defense of a host against pathogen attack is the innate immune system. Mounting evidence suggests that a disproportionate innate immune response is primarily responsible for the genesis of SARS-CoV-2 infections (Z. Zhou et al. 2020; Blanco-Melo et al. 2020; Hadjadj et al. 2020). A balanced cytokine response accounts for the major first line defense against viruses and is imperative for an effective antiviral response. Heightened release of pro-inflammatory cytokines, also called a cytokine storm, is a common reaction to respiratory viral infections leading to an acute inflammatory state that begins at the infection site and can spread to other parts of the body through systemic circulation. A repercussion of cytokine storm is acute lung injury (ALI) characterized by loss of endothelial and epithelial integrity and excessive transepithelial migration of inflammatory neutrophils (Tisoncik et al. 2012), which is also a principal clinical characteristic of severe COVID-19 patients (L. Li et al. 2020; Ciabattini et al. 2020). Serological profile and bronchoalveolar lavage fluid (BALF) of clinical COVID-19 patients has revealed significantly increased levels of cytokines like IL-6, CCL8, CXCL8 (IL-8), CXCL9, CXCL16, IL-1RA, CCL2, and CXCL2 (Blanco-Melo et al. 2020; Z. Zhou et al. 2020; Liao et al. 2020). These cytokines have varied roles in inflammation and immune reactions that bring about the virus-associated pathophysiology. The cellular landscape of BALF from severe and critical cases of COVID-19 has revealed a higher number of neutrophils and macrophages as compared to moderate cases, and evidence suggests that extensive infiltration of inflammatory immune cells contributes to lung damage and mortality (Barnes et al. 2020; Liao et al. 2020; Merad and Martin 2020). The cytokine storm can also result in multiple organ damage leading to various clinical manifestations and worsening the existing clinical condition in the infected patient. For example, islet cells get damaged due to the cytokine storm, which might accelerate the development of diabetic conditions, and the severe condition is engendered in the case of diabetic patients (Hayden 2020). Hence, comorbidities play a vital role in the conversion of the COVID-19 non-severe cases to severe cases.
Blood biochemical parameters for assessment of COVID-19 in diabetic and non-diabetic subjects: a cross-sectional study
Published in International Journal of Environmental Health Research, 2022
Syeda Umme Fahmida Malik, Parveen Afroz Chowdhury, Al Hakim, Mohammad Shahidul Islam, Md Jahangir Alam, Abul Kalam Azad
Ferritin is an important factor of immune dysregulation, especially under extreme hyperferritinemia, via direct immune-suppressive and pro-inflammatory effects which leads to the cytokine storm (Abbaspour et al. 2014). The fatal outcomes of COVID-19 are accompanied with cytokine storm syndrome upon which the disease severity depends (Zhou et al. 2020a). In the present study, it was found that the ferritin level increased significantly in COVID-19 positive patients in comparison with the negative individuals (Table 2). Ferritin, known as an infection marker and associated with the immune and inflammatory response, is increased during viral and/or bacterial infections (Lalueza et al. 2020). The increased level of ferritin observed in 86 (87.76%) of COVID-19 patients [males 51 (59.30%), females 35 (40.70%)] indicated that serum ferritin might be a potential biomarker for progression and severity assessment of COVID-19. Some other studies also reported that elevated levels of ferritin might be associated with a composite poor outcome (Huang et al. 2020; Vargas-Vargas and Cortés-Rojo 2020).
Repurposing pharmaceutical excipients as an antiviral agent against SARS-CoV-2
Published in Journal of Biomaterials Science, Polymer Edition, 2022
Manisha Malani, Prerana Salunke, Shraddha Kulkarni, Gaurav K. Jain, Afsana Sheikh, Prashant Kesharwani, Jayabalan Nirmal
Replication of viruses requires essential enzymes like RNA-dependent RNA polymerase and several proteases [51,52]. SARS-CoV-2 is known to majorly infect the oral cavity cells and respiratory tract, causing life-threatening respiratory and cardiac failure by exaggerating the release of cytokine [53]. Overexpression of various pro-inflammatory cytokines leads to cytokine storm syndrome like conditions causing systemic inflammation [54]. Hence the disease and mortality due to COVID-19 infection is mostly because of exaggerated immune system rather by virus itself. Thereby two important targets to inhibit viral infection could be a) to prevent its entry into the host cell by inhibiting membrane fusion of host and virus envelope or disrupting its lipid membrane and b) to inhibit its replication by inactivating its enzymes.
COVID-19: a pandemic challenging healthcare systems
Published in IISE Transactions on Healthcare Systems Engineering, 2021
Lidong Wang, Cheryl Ann Alexander
According to the National Institute of Health (NIH) Office of Infectious Diseases, there are a few definitive treatment regimens for use with COVID-19 patients dependent upon their progress along the pathogenicity of the disease. And while the NIH and Federal Drug Administration (FDA) have come to an agreement on what therapies should be used for what pathway the patient is in, the FDA has agreed on several Emergency Use Authorizations (EUAs) to treat COVID-19. While drugs that have the special EAUs are being used depending upon the clinical progression of the patient’s disease, there are still other diseases in clinical trials, etc. According to scientists at the NIH, there are two main processes along the pathogenesis of COVID-19 (COVID-19 Treatment Guidelines Panel, 2021). Early in the disease, COVID-19 is driven by SARS-CoV-2 viral particles within the cells of the human host. However, later during COVID-19, symptoms are typically caused by an exaggerated inflammatory/immune response, which causes tissue damage, fluid in the lungs, activation of the clotting cascade causing microthrombi, and other similar symptoms caused by release of cytokines. Scholars have named this stage as the “Cytokine Storm”, where the disease is primarily driven by the activation of many various cytokines causing an acute and severe inflammatory response (Aid et al., 2020). Based on this evaluation of the two stages of COVID-19, antivirals and convalescent plasma therapies would be more effective during the initial stage of COVID-19, while immunosuppressive or anti-inflammatory drugs would be most effective during the second stage of COVID-19 (COVID-19 Treatment Guidelines Panel, 2021).