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1.
Reference Series in Phytochemistry ; : 573-597, 2022.
Article in English | Scopus | ID: covidwho-1888827

ABSTRACT

Chronic inflammation and oxidative damage have been proven as fundamental factors associated with many systemic diseases, leading to increased morbidity. To deal with this, formulation of new functional foods, dietary polyphenols, and supplements containing multiple natural antioxidants and/or anti-inflammatory agents is required to reduce oxidative stress and inflammatory cascade. Several studies have shown a positive association between increased intake of dietary antioxidants and reduced risk for chronic inflammatory diseases and oxidative stress. This chapter concentrates on the underlying mechanisms of how different groups of dietary antioxidants, like vitamin C, vitamin E, flavonoids, carotenoids, and plant polyphenols, prevent the processes of inflammation and oxidative stress responses. Oxidative stress and inflammation mechanisms are discussed in the light of critical balance of pro- and anti-inflammatory cytokines. Also, roles of dietary antioxidants were discussed as an adjunctive treatment strategy to COVID-19 patients. Given the convincing evidence for protective as well as curative role of dietary antioxidants in inflammatory processes, more detailed understanding on the effects of nutrients on multiple aspects and development of novel anti-inflammatory agents is required to optimize approaches. To improve the bioavailability and targeted delivery of external antioxidants, nonreactive carriers or vehicles are needed to be designed with more precision and accuracy. © 2022, Springer Nature Switzerland AG.

2.
Int J Mol Sci ; 23(11)2022 May 27.
Article in English | MEDLINE | ID: covidwho-1888430

ABSTRACT

Platelets play a variety of roles in vascular biology and are best recognized as primary hemostasis and thrombosis mediators. Platelets have a large number of receptors and secretory molecules that are required for platelet functionality. Upon activation, platelets release multiple substances that have the ability to influence both physiological and pathophysiological processes including inflammation, tissue regeneration and repair, cancer progression, and spreading. The involvement of platelets in the progression and seriousness of a variety of disorders other than thrombosis is still being discovered, especially in the areas of inflammation and the immunological response. This review represents an integrated summary of recent advances on the function of platelets in pathophysiology that connects hemostasis, inflammation, and immunological response in health and disease and suggests that antiplatelet treatment might be used for more than only thrombosis.


Subject(s)
Hemostasis , Thrombosis , Blood Platelets/physiology , Hemostasis/physiology , Humans , Inflammation , Platelet Activation , Platelet Function Tests
3.
International Journal of Hematology-Oncology and Stem Cell Research ; 16(2):117-127, 2022.
Article in English | EMBASE | ID: covidwho-1887375

ABSTRACT

COVID-19 and malignancy can affect the susceptibility of one another. Clinically recovered COVID-19 individuals display immune abnormalities that persist several months after discharge. The lymphopenia-related immunosuppression, functional exhaustion of cytotoxic lymphocytes (such as CD8+ cytotoxic T-cells and natural killer cells), hyperinflammatory responses, oxidative stress, downregulation of interferon response, development of the myeloid-derived suppressor cells, downregulation of tumor suppressor proteins and perhaps reactivation of the latent oncogenic viruses may directly and/or indirectly play a role in the cancer development and recurrence in severe COVID-19 patients. SARS-CoV-2-infected malignant patients may be at higher risk of death of their cancer than SARS-CoV-2-uninfected patients with the same cancers. On the other side, the patients with some types of cancers may be more vulnerable to SARS-CoV-2 infection compared with the non-cancerous individuals, due to their immunocompromised state resulted from malignancy, chemotherapy, and other concomitant abnormalities as well as perhaps greater expression of angiotensin-converting enzyme 2. SARS-CoV-2-infected cancerous patients are unable to produce an effective anti-virus immune response and may exhibit more severe forms of COVID-19. This review described the possible impacts of SARS-CoV-2 infection on cancer development and recurrence, and the potential cancer impacts on COVID-19 development, while the possible interventions are highlighted.

5.
Future Virology ; 17(4):197-199, 2022.
Article in English | EMBASE | ID: covidwho-1887070
6.
Journal of Urology ; 207(SUPPL 5):e1044-e1045, 2022.
Article in English | EMBASE | ID: covidwho-1886529

ABSTRACT

INTRODUCTION AND OBJECTIVE: SARS-CoV-2 can invade different testicular cell types, such as spermatogonia, spermatids, Sertoli, and Leydig cells. We investigated the viral presence inside the sperm of negative PCR infected men up to 3 months after discharge from the hospital. METHODS: This cross-sectional study included 13 of a 26 moderate-to-severe SARS-CoV-2 infected men cohort (mean 34.3 ± 6.5 years;range: 21-50 years old). Patients were enrolled 30 to 90 days after the diagnosis. Semen samples were obtained by masturbation and processed within one hour according to WHO guidelines. All patients were PCR negative for the virus in the ejaculate. Samples were liquefied for 30 min at room temperature in 0.1M phosphate buffer before centrifuging at 500 g for 10 min. The supernatant was removed, and pellets were fixed in 2,5% v/v glutaraldehyde in 0.1M phosphate buffer for 2h at 4°C, post-fixed in 1% OsO4 for 1h at 4°C, stained overnight in 1% aqueous uranyl acetate. Then, the pellets were dehydrated sequentially in 30%, 70%, and 100% ethanol and embedded in epoxy resin. Ultrathin sections (70nm) were obtained in an ultramicrotome, collected on nickel grids, and double-stained by uranyl acetate and lead citrate. Micrographs were obtained with a Jeol JEM 1010 electron microscope (Tokyo, Japan, 80 kV). RESULTS: We identified viruses inside spermatozoa in 9/13 patients up to 90 days after discharge from the hospital. Moreover, in all 13 men, a type of DNA-based extracellular traps, probably in a cfDNAdependent manner, like described in the COVID-19 systemic inflammatory response. FIGURE: High magnification electron micrograph of a spermatozoon with the nucleus (nu) displaying the typical condensed chromatin. The remained cytoplasm contains several viral particles (ranging in diameter from 90 to 110 nm). The inset corresponds to a higher magnification of the boxed area containing two virions, showing the SARS-CoV-2 characteristics: viral envelope (white arrowhead), nucleocapsids (black arrowhead), and spike-like projections (white arrow). CONCLUSIONS: Although SARS-CoV-2 is not found in the infected men's semen, it was intracellularly present in the spermatozoa. The potential implications for assisted conception should be addressed. (Figure Presented).

7.
Journal of Urology ; 207(SUPPL 5):e633, 2022.
Article in English | EMBASE | ID: covidwho-1886521

ABSTRACT

INTRODUCTION AND OBJECTIVE: Angiotensin-converting enzyme II (ACE2) is the main receptor for severe acute respiratory syndrome coronavirus 2 (SARS CoV-2) to enter the host cells. The higher expression of ACE2 receptor in the testis makes it more susceptible to SARS-COV-2 infection. Recent studies have reported orchitis, impaired spermatogenesis, and presence of viruses in semen of affected men. The main objective of this study is to understand the molecular alterations induced by SARS-CoV-2 and signaling pathways dysregulated in testis. METHODS: A data mining approach was employed to identify the RNA sequencing data of human testis infected with SARS-CoV-2. The FASTQ files (PRJNA661970) were retrieved from European Nucleotide Archive (ENA) for both the infected and control groups (noninfected). RNA seq data were further processed and analyzed, using BioJupies to generate a list of differentially expressed genes (DEGs). In addition, downstream analysis was carried out, using ingenuity pathway analysis software (Qiagen, USA) to identify the differentially regulated pathways and unique non-directional gene networks. RESULTS: A total of 17,824 genes were identified in the testis of both SARS CoV-2 infected and control groups, of which 4,131 genes were differentially expressed (2,492 downregulated and 1,639 upregulated) with a fold change cut-off of±2 and P <0.05. Bioinformatic analysis revealed that molecular pathways, such as inflammatory response, reproductive system development and function, and cell-to-cell signaling and interaction, were dysregulated in testes of men infected with SARSCoV- 2. Furthermore, we have also identified enrichment of 37 DEGs in the germ cell-Sertoli cell junction signaling pathway (Table 1). CONCLUSIONS: Our bioinformatic results clearly indicate that homeostasis of germ cell-Sertoli cell junction is disturbed during SARSCoV- 2 infection, which could be a predisposing cause for impaired spermatogenesis. Future studies are warranted to understand the impact of mild, moderate, and severe SARS-CoV-2 infections on germ cell-Sertoli cell junction in both vaccinated and unvaccinated populations that may affect their reproductive performance and fertility.

8.
Journal of Urology ; 207(SUPPL 5):e415, 2022.
Article in English | EMBASE | ID: covidwho-1886501

ABSTRACT

INTRODUCTION AND OBJECTIVE: Neurodegenerative diseases, such as multiple sclerosis (MS), often lead to the development of neurogenic lower urinary tract symptoms (LUTS). We previously characterized neurogenic bladder dysfunction in a mouse model of MS induced by a coronavirus, mouse hepatitis virus (MHV). The objective of this study was to identify genes and pathways linking neuroinflammation in the central nervous system with urinary bladder dysfunction to enhance our understanding of the mechanisms underlying LUTS in demyelinating diseases. METHODS: Adult C57BL/6 male mice (N=12) received either an intracranial injection of MHV (6,000 PFU) or sterile saline (control). The lumbosacral (L6-S2) spinal cord (SC) segments and urinary bladders were collected during acute infection stage (week 1) and at the first peak of demyelination (week 4) after inoculation with the virus. Total RNA was isolated and analyzed using Nanostring nCounter Neuroinflammation panel. The expression levels of 770 genes associated with neuroinflammation were assessed and compared between the specimens. RESULTS: Transcriptome analysis of SC specimens confirmed a significantly increased expression of 132 genes in MHV mice (tens to hundreds fold change) involved in the regulation of astrocyte, microglia and oligodendrocyte functions, neuroinflammation and immune responses. Out of 132 genes up-regulated in the SC, only 2 genes (siglec1, 46-fold in the SC, 2.6-fold at 1 week and 1.8-fold at 4 weeks in the bladder;and zbp1, 568-fold in the SC, 2.8-fold at 1 week and 2.2-fold at 4 weeks in the bladder) were up-regulated in the urinary bladders of MHV-infected mice. Additionally, two genes were significantly up-regulated (ttr, 2.2-fold at 1week and 1.7-fold at 4 weeks;and ms4a4a, 2.3-fold at 1week and 1.6-fold at 4 weeks), and two were down-regulated (asb2, -1.8-fold at 1 week and -1.6-fold at 4 weeks, and myct1, -1.7-fold at 1week and -1.6-fold at 4 weeks) exclusively in the urinary bladders of MHV mice. CONCLUSIONS: Two genes, siglec1 (encodes type 1 transmembrane protein, expressed in microglia and macrophages, promotes neuroinflammation) and zbp1 (encodes a Z-DNA binding protein, plays role in the innate immune response) link the development of neuroinflammation in the central nervous system with neurogenic changes in the urinary bladders of MHV-infected mice. Further research is needed to establish a functional relationship between expression of these genes and neurogenic LUTS.

9.
Human Gene ; 33, 2022.
Article in English | EMBASE | ID: covidwho-1885810

ABSTRACT

Aims: The aim of this study was to extract the signaling mediators or biological pathways that link covid-19 to other diseases such as type 1 diabetes mellitus (T1DM). Methods: Microarray data of covid-19 (GSE164805) was extracted from Gene Expression Omnibus (GEO) and analyses were performed by R package and GEO2R. Functional enrichment analysis was done to extract enriched molecular pathways (MP), biological process (BP) and molecular function (MF). Then commonly up- and down-regulated genes in covid-19 and T1DM were extracted by comparing deferentially expressed genes (DEGs) of GSE164805 and GSE9006. Results: Down-regulated DEGs in the severely progressing covid-19 patients (SPCP) had a link to T1DM. Major histocompatibility system (MHC) class II, gamma interferon (IFNγ), and IL-1B were enriched in extracted pathway that leads to T1DM. In addition, comparing extracted DEGs from GSE164805 and GSE9006 indicated that MTUS1, EGR1 and EGR3 are the genes that are up-regulated in both SPCP and T1DM. Conclusion: The findings of this study indicate that coincidence of SARS-COV-2 infection and T1DM may increase the severity of both diseases. Although covid-19 reduced the T cell mediated immune response, but increased mediators of T-cell signaling pathway such as IL-1 in both diseases. This could potentiate the inflammation response and worsens the severity of covid-19 cytokine storm or increase the resistance to insulin.

10.
Pediatric Blood and Cancer ; 69(SUPPL 2):S210, 2022.
Article in English | EMBASE | ID: covidwho-1885436

ABSTRACT

Background: Incidental diagnosis of malignancy during unrelated illness is challenging, both for diagnostic clarity and therapeutic decision-making. There are reported cases of incidental discovery of Wilms tumor (WT) in the setting of trauma, but there are none reported in the setting of acute inflammatory illness, such as Multisystem Inflammatory Syndrome in Children (MIS-C), and thus no guidance regarding timing of definitive therapy. Objectives: We describe a patient with MIS-C and incidentally diagnosed WT in order to inform the management of future patients with simultaneously diagnosed malignancy and acute inflammatory illness. Design/Method: Information was obtained by retrospective review of the electronic health record. Results: A healthy 5-year-old female presented with six days of fever, cervical lymphadenopathy, urinary symptoms, and rash. Labs showed acute kidney injury, prompting imaging that revealed a left-sided renal mass, most likely a WT. The constellation of signs and symptoms was initially suggestive of obstructive uropathy resulting in urinary tract infection. However, subsequent development of conjunctivitis and oral mucosal changes, positive SARS-CoV-2 nucleocapsid antibodies, rising inflammatory markers, and mild-moderate coronary artery dilation on echocardiogram, made MIS-C the most fitting diagnosis. The patient rapidly improved after initiation of aspirin, methylprednisolone, and intravenous immunoglobulin. Cross-sectional imaging showed no metastatic disease or local tumor invasion. A multidisciplinary team of pediatric subspecialists discussed appropriate timing for upfront resection and decided to defer surgery for at least two weeks while inflammation resolved. Unfortunately, the patient continued to have ongoing inflammation requiring a prolonged steroid course, and surgery was ultimately deferred until one month following diagnosis. Surgery was uncomplicated and pathology demonstrated stage II favorable histology WT. Chemotherapy began on post-operative day 9. Conclusion: The lack of published cases of malignancy incidentally discovered during acute illness, coupled with the rapidly rising rate of pediatric cases of COVID-19 and MIS-C, present a challenge for clinicians who must treat the concurrent conditions. This report highlights the complexities of managing a WT for which upfront resection is standard in the United States. Surgery is typically performed quickly due to the fast-growing nature and risk of rupture. Reports of paraneoplastic inflammatory syndromes (non-WT) suggest that tumor resection in the setting of acute inflammation is safe, but pediatric data remains scarce. This patient's multidisciplinary team chose to delay tumor resection given the potential morbidity of major surgery in the setting of a raging inflammatory state. The patient had a favorable clinical outcome both in terms of her MIS-C and WT.

12.
Pharmacol Ther ; 238: 108173, 2022 Mar 18.
Article in English | MEDLINE | ID: covidwho-1886025

ABSTRACT

Refined from pools of random sequence oligonucleotides, nucleic acid aptamers have been found to bind an almost limitless array of targets, including clinically-relevant proteins. Comparable to their antibody counterparts, aptamers display significant advantages over protein-based therapeutics in part due to their flexibility in chemical modifications, small size, and scalability. Despite the perceived benefits, and amidst the growth of an increasing number of clinically approved nucleic acid-based therapeutics, orthodox biologics remain dominant. Research over the last three decades has identified several aptamers that contain the potential to reshape the medicinal field as both diagnostic tools and treatments. Herein, we provide a tailored overview of promising developments in therapeutic nucleic acid-based aptamers in the treatment of infection and inflammation and their proposed future applications.

13.
Med Drug Discov ; : 100136, 2022 Jun 13.
Article in English | MEDLINE | ID: covidwho-1885989

ABSTRACT

The emergence of new SARS-CoV-2 variants continues to pose an enormous public health concern. SARS-CoV-2 infection disrupted host immune response accounting for cytokine storm has been linked to multiorgan failure and mortality in a significant portion of positive cases. Abruptly activated macrophages have been identified as the key pathogenic determinant of cytokine storm in COVID-19. Besides, reactive microglia have been known to discharge a surplus amount of proinflammatory factors leading to neuropathogenic events in SARS-CoV-2 infected brains. Considering the fact, depletion of activated macrophages and microglia could be proposed to eradicate the life-threatening cytokine storm in COVID-19. Clodronate, a non-nitrogenous bisphosphonate drug has been identified as a potent macrophage and microglial depleting drug. While recent advancement in the field of liposome encapsulation technology offers most promising biological tool for drug delivery, liposome encapsulated clodronate has been reported to effectively target and induce prominent phagocytic cell death in activated macrophages and microglia compared to free clodronate molecules. Thus, in this review article we emphasize that depletion of activated macrophages and microglial cells by administration of liposome encapsulated clodronate can be a potential therapeutic strategy to diminish the pathogenic cytokine storm and alleviate multiorgan failure in COVID-19. Moreover, recently developed COVID-19 vaccines appear to render the chronic activation of macrophages accounting for immunological dysregulation in some cases. Therefore, the use of liposome encapsulated clodronate can also be extended to the clinical management of unforeseen immunogenic reactions resulting from activated macrophages associated adverse effects of COVID-19 vaccines.

14.
Life Sci ; 304: 120703, 2022 Jun 11.
Article in English | MEDLINE | ID: covidwho-1885980

ABSTRACT

AIMS: Biologically active molecules cytokines and growth factors (GFs) are critical regulators of tissue injury/repair and emerge as key players in COVID-19 pathophysiology. However, specific disease stage of GFs dysregulation and, whether these GFs have associations with thromboembolism and tissue injury/repair in COVID-19 remain vague. MAIN METHODS: GF profiling in hospitalized moderate (non-ICU) and critically ill (ICU) COVID-19 patients was performed through legendPlex assay. KEY FINDINGS: Investigation revealed profound elevation of VEGF, PDGFs, EGF, TGF-α, FGF-basic, and erythropoietin (EPO) in moderate cases and decline or trend of decline with disease advancement. We found strong positive correlations of plasma VEGF, PDGFs, and EPO with endothelial dysfunction markers P-selectin and sCD40L. Interestingly, the HGF and G-CSF were upregulated at the moderate stage and remained elevated at the severe stage of COVID-19. Moreover, strong negative correlations of PDGFs (r2 = 0.238, P = 0.006), EPO (r2 = 0.18, P = 0.01) and EGF (r2 = 0.172, P = 0.02) and positive correlation of angiopoietin-2 (r2 = 0.267, P = 0.003) with D-dimer, a marker of thromboembolism, was observed. Further, plasma PDGFs (r2 = 0.199, P = 0.01), EPO (r2 = 0.115, P = 0.02), and EGF (r2 = 0.108, P = 0.07) exhibited negative correlations with tissue injury marker, myoglobin. SIGNIFICANCE: Taken together, unlike cytokines, most of the assessed GFs were upregulated at the moderate stage of COVID-19. The induction of GFs likely occurs due to endothelial dysfunction and may counter the adverse effects of cytokine storms which is reflected by inverse correlations of PDGFs, EPO, and EGF with thromboembolism and tissue injury markers. The findings suggest that the assessed GFs play differential roles in the pathogenesis of COVID-19.

15.
Inflammation ; 2022 Jun 08.
Article in English | MEDLINE | ID: covidwho-1885472

ABSTRACT

The SARS-CoV-2 instigated "cytokine storm" elicited upon infection is known to majorly cause lung injury and even mortality in severe cases. Early clinical prognosis to alleviate the exaggerated release of inflammatory cytokines is thus looked upon. Considering the recent attention and advantages of saliva as a clinical specimen, i.e. ease and painlessness of collection, which does not require trained staff and could allow self-sampling, the present study attempts to explore saliva for detection of IL-6, TNF-α and IL-10 which constitute major inflammatory genes that are elevated in COVID-19 using RT-PCR. Blood specimens of the same patients were also parallelly assessed to compare and validate the inflammatory marker expression. A total of 64 COVID-19 subjects who met the inclusion criteria were enrolled in this pilot study. Paired samples of blood and saliva from each patient were collected as per standard sampling protocols. RNA from all specimens were extracted using Qiagen RNA Blood Mini Kit and subjected to RT-PCR. IL-6, TNF-α and IL-10 expression were assessed in Ct (cycle threshold) values. It was observed that all 64 (100%) patients expressed IL-6 gene and TNF-α gene, whereas only 7 (5.19%) patients expressed IL-10 in both blood and saliva samples. The mean Ct values of IL-6 gene expressed in blood and saliva were 26.68 ± 2.26 and 28.53 ± 3.11 respectively. Similarly, the mean Ct values of TNF-α gene expressed in blood and saliva were 27.98 ± 2.45 and 28.92 ± 3.70 respectively. The observed mean Ct values of IL-10 gene expressed in blood and saliva were 31.26 ± 3.96 and 30.11 ± 4.12 respectively. Accordingly, the results indicate that inflammatory genes IL-6, TNF-α and IL-10 were detectable in both patient saliva as well as in blood. Moreover, mean Ct values of IL-6, TNF-α and IL-10 in both samples were found to be comparable. This finding thus suggests the possible use of saliva as an alternative specimen to blood for monitoring inflammation in COVID-19 patients.

16.
J Tissue Eng Regen Med ; 2022 Jun 11.
Article in English | MEDLINE | ID: covidwho-1885455

ABSTRACT

Acute cardiac injuries occur in 20%-25% of hospitalized COVID-19 patients. Herein, we demonstrate that human cardiac organoids (hCOs) are a viable platform to model the cardiac injuries caused by COVID-19 hyperinflammation. As IL-1ß is an upstream cytokine and a core COVID-19 signature cytokine, it was used to stimulate hCOs to induce the release of a milieu of proinflammatory cytokines that mirror the profile of COVID-19 cytokine storm. The IL-1ß treated hCOs recapitulated transcriptomic, structural, and functional signatures of COVID-19 hearts. The comparison of IL-1ß treated hCOs with cardiac tissue from COVID-19 autopsies illustrated the critical roles of hyper-inflammation in COVID-19 cardiac insults and indicated the cardioprotective effects of endothelium. The IL-1ß treated hCOs thus provide a defined and robust model to assess the efficacy and potential side effects of immunomodulatory drugs, as well as the reversibility of COVID-19 cardiac injuries at baseline and simulated exercise conditions.

17.
J Med Virol ; 2022 Jun 10.
Article in English | MEDLINE | ID: covidwho-1885415

ABSTRACT

The field of immunometabolism investigates and describes the effects of metabolic rewiring in immune cells throughout activation and the fates of these cells. Recently, it has been appreciated that immunometabolism plays an essential role in the progression of viral infections, cancer, and autoimmune diseases. Regarding COVID-19, the aberrant immune response underlying the progression of diseases establishes two major respiratory pathologies, including acute respiratory distress syndrome (ARDS) or pneumonia-induced acute lung injury (ALI). Both innate and adaptive immunity (T cell-based) were impaired in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Current findings have deciphered that macrophages (innate immune cells) are involved in the inflammatory response seen in COVID-19. It has been demonstrated that immune system cells can change metabolic reprogramming in some conditions, including autoimmune diseases, cancer, and infectious disease, including COVID-19. The growing findings on metabolic reprogramming in COVID-19 allow an exploration of metabolites with immunomodulatory properties as future therapies to combat this hyperinflammatory response. The elucidation of the exact role and mechanism underlying this metabolic reprograming in immune cells could help apply more precise approaches to initial diagnosis, prognosis, and in-hospital therapy. This report discusses the latest findings from COVID-19 on host metabolic reprogramming and immunometabolic responses.

18.
Revue Medicale Suisse ; 17(726):334-337, 2021.
Article in French | EMBASE | ID: covidwho-1885057

ABSTRACT

Children appeared to be initially spared by the SARS-CoV-2 pandemic, however, in spring 2020, a new clinical entity was described related to the SARS-CoV-2 infection and named multisystem inflammatory syndrome in children (MIS-C) or pediatric inflammatory multisystem syndrome (PIMS). The gravity of this inflammatory syndrome, the time interval between infection and MIS-C, the response to the various immunomodulatory treatments are all suggestive of an immunologic reaction rather than a virus-mediatred phenomenon. The pathophysiological mechanisms and possible risk factors for MIS-C have not been elucidated. In this article, we summarize what is known to date about the immune response to SARS-CoV-2 in children and about the immune response to SARSCoV-2 in children and about the MIS-C.

19.
Immunologiya ; 43(2):217-223, 2022.
Article in English | EMBASE | ID: covidwho-1884972

ABSTRACT

This review provides information about the role of the immune system in the development of multisystem inflammatory syndrome in children ( MIS - C ) associated with a new coronavirus infection ( COVID -19). The main clinical criteria for establishing the diagnosis are presented, the clinical picture and characteristics of biomarkers in MIS - C are described.. The main reason for the development of multisystem inflammatory syndrome, most researchers consider the activation of theimmune system with the development of a hyperergic inflammatory reaction. At the same time, the heterogeneity of MIS-C underlies various hypotheses of its development. The role of predisposing factors in the development of various variants of the immune response in MIS-C remains to be established, research is ongoing.

20.
Organic Communications ; : 15, 2022.
Article in English | English Web of Science | ID: covidwho-1884921

ABSTRACT

The first incidence of corona virus was reported in China in December of 2019, and the virus quickly spread over the world, eventually being designated a pandemic in March of 2020. It has had a disastrous impact on the global healthcare system. Virus has claimed the lives of 5,298,933 people through December 2021. As a result of the pandemic, there was a boost of research into diagnostic and therapeutic methods to infection. Gradually, the world has discovered new vaccine candidates and medicinal repurposing strategies that have a significant influence on mortality, by which there has been a drop-in death rates over the world since July, 2021. Many patients, particularly those who have been hospitalized due to a viral infection, experience complications beyond discharge that have a significant influence on their lives. Post COVID-19 complications are problems that last longer than 3-4 weeks following a viral infection. There is currently no specific treatment accessible for post COVID-19 problems because whatever medications are available or repurposed are limited to disease prophylaxis and therapeutics. As a result, we're looking for a remedy employing natural substances using the In-Silico technique (molecular docking) and recent research from reputable journals. Allicin, Berberine, Epigallocatechin, Rosmarinic acid and Withaferin-A were docked against ACE (PDB ID: 1O8A), IL-6 (PDB ID: 1ALU), NADPH Oxidase (PDB ID: 2CDU) and TNF-alpha (PDB ID: 2AZ5) using Autodock.

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