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1.
Gene Reports ; : 101509, 2022.
Article in English | ScienceDirect | ID: covidwho-1620685

ABSTRACT

Objective Vitamin D is believed to affect the functionality of the immune system for the prevention of coronavirus disease. To investigate the role of this vitamin against the Coronavirus, this study analyzed the serum levels of vitamin D, the transcription pattern of inflammatory cytokines, and the frequency of total lymphocytes, TCD4+, TCD8+, and NK cells in 50 COVID-19-affected subjects in comparison to 50 healthy participants. Materials and methods This study diagnosed and evaluated 100 patients. Frequency of lymphocytes was determined using flow cytometry. Cytokine expression levels were measured using Real-Time PCR. Serum levels of vitamin D and cytokines levels in cultured cell supernatant were measured by ELISA. Results Patients with COVID-19 exhibited decreased serum levels of vitamin D versus the healthy participants (p = 0.0024). The total number of lymphocytes, TCD4+, TCD8+, and NK cells was significantly reduced in patients with COVID-19 (p < 0.0001). Considerable upregulation of IL-12, IFN-γ, and TNF-α was seen in COVID-19 patients compared to the control group, whereas IFN-α was downregulated in COVID-19 patients. ELISA results also had increased levels of IL-12, TNF-α, and IFN-γ (p = 0.0014, 0.0012, and p < 0.0001, respectively), and decreased level of IFN-α (p = 0.0021) in patients with COVID-19 compared to the control group. Conclusion These findings suggest a probable association among vitamin D concentrations, immune system function, and risk of COVID-19 infection. As a result, it is recommended that vitamin D be considered as a candidate for handling and controlling COVID-19 because of its ability to target the cytokine storm and its antiviral effects.

2.
Int Immunopharmacol ; 100: 108108, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1401541

ABSTRACT

The possibility of human reinfection with SARS-CoV-2, the coronavirus responsible for COVID-19, has not previously been thoroughly investigated. Although it is generally believed that virus-specific antibodies protect against COVID-19 pathogenesis, their duration of function and temporal activity remain unknown. Contrary to media reports that people retain protective antibody responses for a few months, science does not exclude reinfection and disease relapse shortly after initiating all immune responses during the primary onset of COVID-19. Despite production of antiviral antibodies, activated CD4+/CD8+ lymphocytes, and long-lived memory B cells, susceptibility to reinfection in humans for extended periods cannot be precluded due to repeated exposures to coronavirus or potential reactivation of the virus due to incomplete virus clearance. However, the mechanism of reinfection remains unknown. The biological characteristics of SARS-CoV-2, such as emergence of multiple mutations in the virus RNA molecules, transmissibility, rates of infection, reactivation and reinfection, can all affect the trajectory of the virus spread. Innate and adaptive immune response variables, differences in underlying diseases, and comorbidities, particularly in high risk individuals, can influence the dynamics of the virus infection. In this article, immune parameters and viral mutations pertaining to reinfection and disease relapse are reviewed and scientific gaps are discussed.


Subject(s)
COVID-19/immunology , Mutation , Reinfection/immunology , SARS-CoV-2/genetics , Antibodies, Neutralizing/blood , Antibodies, Viral/blood , COVID-19/virology , COVID-19 Vaccines/immunology , Cytokine Release Syndrome/etiology , Humans , Recurrence , Reinfection/virology , SARS-CoV-2/immunology
3.
Adv Pharm Bull ; 11(3): 395-396, 2021 May.
Article in English | MEDLINE | ID: covidwho-1289418
4.
Int Immunopharmacol ; 91: 107331, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1065225

ABSTRACT

The present review provides an overview of recent advances regarding the function of Th17 cells and their produced cytokines in the progression of viral diseases. Viral infections alone do not lead to virus-induced malignancies, as both genetic and host safety factors are also involved in the occurrence of malignancies. Acquired immune responses, through the differentiation of Th17 cells, form the novel components of the Th17 cell pathway when reacting with viral infections all the way from the beginning to its final stages. As a result, instead of inducing the right immune responses, these events lead to the suppression of the immune system. In fact, the responses from Th17 cells during persistent viral infections causes chronic inflammation through the production of IL-17 and other cytokines which provide a favorable environment for tumor growth and its development. Additionally, during the past decade, these cells have been understood to be involved in tumor progression and metastasis. However, further research is required to understand Th17 cells' immune mechanisms in the vast variety of viral diseases. This review aims to determine the roles and effects of the immune system, especially Th17 cells, in the progression of viral diseases; which can be highly beneficial for the diagnosis and treatment of these infections.


Subject(s)
Cell Transformation, Viral , Neoplasms/virology , Th17 Cells/virology , Tumor Virus Infections/virology , Viruses/pathogenicity , Animals , Host-Pathogen Interactions , Humans , Neoplasms/immunology , Neoplasms/metabolism , Th17 Cells/immunology , Th17 Cells/metabolism , Tumor Microenvironment , Tumor Virus Infections/immunology , Tumor Virus Infections/metabolism , Viruses/immunology
5.
Life Sci ; 270: 119124, 2021 Apr 01.
Article in English | MEDLINE | ID: covidwho-1051825

ABSTRACT

The outbreak of SARS-CoV-2 in Wuhan of China in December 2019 and its worldwide spread has turned into the COVID-19 pandemic. Respiratory disorders, lymphopenia, cytokine cascades, and the immune responses provoked by this virus play a major and fundamental role in the severity of the symptoms and the immunogenicity which it causes. Owing to the decrease in the inflammatory responses' regulation in the immune system and the sudden increase in the secretion of cytokines, it seems that an investigation of inhibitory immune checkpoints can influence theories regarding this disease's treatment methods. Acquired cell-mediated immune defense's T-cells have a key major contribution in clearing viral infections thus reducing the severity of COVID-19's symptoms. The most important diagnostic feature in individuals with COVID-19 is lymphocyte depletion, most importantly, T-cells. Due to the induction of interferon-γ (INF-γ) production by neutrophils and monocytes, which are abundantly present in the peripheral blood of the individuals with COVID-19, the expression of inhibitory immune checkpoints including, PD-1 (programmed death), PD-L1 and CTLA4 on the T-cells' surface is enhanced. The purpose of this review is to discuss the functions of these checkpoints and their effects on the dysfunction and exhaustion of T-cells, making them almost ineffective in individuals with COVID-19, especially in the cases with extreme symptoms.


Subject(s)
B7-H1 Antigen/metabolism , COVID-19/immunology , CTLA-4 Antigen/metabolism , Programmed Cell Death 1 Receptor/metabolism , SARS-CoV-2/physiology , T-Lymphocytes/immunology , COVID-19/metabolism , Humans , Monocytes/immunology
6.
Health Promot Perspect ; 10(3): 166-167, 2020.
Article in English | MEDLINE | ID: covidwho-831311
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