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1.
Immunol Lett ; 243: 19-27, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1734546

ABSTRACT

The interest in the process of aging, and specifically in how aging affects the working of our immune system, has recently enormously grown among both specialists (immunologists and gerontologists) and representatives of other disciplines of health sciences. An obvious reason for this interest is the current pandemics of COVID-19, known to affect the elderly more than younger people. In this paper current knowledge about mechanisms and complex facets of human immune system aging is presented, stemming from the knowledge about the working of various parts of the immune system, and leading to understanding of immunological mechanisms of chronic, inflammatory, aging-related diseases and of COVID-19.


Subject(s)
Aging/physiology , Immune System/immunology , Inflammation/immunology , SARS-CoV-2/physiology , Aged , Animals , COVID-19 , Humans , Immunosenescence
2.
Int J Mol Sci ; 23(5)2022 Mar 06.
Article in English | MEDLINE | ID: covidwho-1732070

ABSTRACT

Almost two years have passed since the outbreak reported for the first time in Wuhan of coronavirus disease 2019 (COVID-19), due to severe acute respiratory syndrome (SARS)-CoV-2 coronavirus, rapidly evolved into a pandemic. This infectious disease has stressed global health care systems. The mortality rate is higher, particularly in elderly population and in patients with comorbidities such as hypertension, diabetes mellitus, cardiovascular disease, chronic lung disease, chronic renal disease, and malignancy. Among them, subjects with diabetes have a high risk of developing severe form of COVID-19 and show increased mortality. How diabetes contributes to COVID-19 severity remains unclear. It has been hypothesized that it may be correlated with the effects of hyperglycemia on systemic inflammatory responses and immune system dysfunction. Vitamin D (VD) is a modulator of immune-response. Data from literature showed that vitamin D deficiency in COVID-19 patients increases COVID-19 severity, likely because of its negative impact on immune and inflammatory responses. Therefore, the use of vitamin D might play a role in some aspects of the infection, particularly the inflammatory state and the immune system function of patients. Moreover, a piece of evidence highlighted a link among vitamin D deficiency, obesity and diabetes, all factors associated with COVID-19 severity. Given this background, we performed an overview of the systematic reviews to assess the association between vitamin D supplementation and inflammatory markers in patients with diabetes; furthermore, vitamin D's possible role in COVID-19 patients was assessed as well. Three databases, namely MEDLINE, PubMed Central and the Cochrane Library of Systematic Reviews, were reviewed to retrieve the pertinent data. The aim of this review is to provide insight into the recent advances about the molecular basis of the relationship between vitamin D, immune response, inflammation, diabetes and COVID-19.


Subject(s)
COVID-19/immunology , Diabetes Mellitus/immunology , Immune System/immunology , Inflammation/immunology , Obesity/immunology , Vitamin D/immunology , COVID-19/virology , Humans , Immune System/drug effects , Meta-Analysis as Topic , SARS-CoV-2/physiology , Systematic Reviews as Topic , T-Lymphocytes, Regulatory/drug effects , T-Lymphocytes, Regulatory/immunology , Vitamin D/administration & dosage , Vitamins/administration & dosage , Vitamins/immunology
3.
Nutrients ; 12(6)2020 May 27.
Article in English | MEDLINE | ID: covidwho-1725878

ABSTRACT

The coronavirus-disease 2019 (COVID-19) was announced as a global pandemic by the World Health Organization. Challenges arise concerning how to optimally support the immune system in the general population, especially under self-confinement. An optimal immune response depends on an adequate diet and nutrition in order to keep infection at bay. For example, sufficient protein intake is crucial for optimal antibody production. Low micronutrient status, such as of vitamin A or zinc, has been associated with increased infection risk. Frequently, poor nutrient status is associated with inflammation and oxidative stress, which in turn can impact the immune system. Dietary constituents with especially high anti-inflammatory and antioxidant capacity include vitamin C, vitamin E, and phytochemicals such as carotenoids and polyphenols. Several of these can interact with transcription factors such as NF-kB and Nrf-2, related to anti-inflammatory and antioxidant effects, respectively. Vitamin D in particular may perturb viral cellular infection via interacting with cell entry receptors (angiotensin converting enzyme 2), ACE2. Dietary fiber, fermented by the gut microbiota into short-chain fatty acids, has also been shown to produce anti-inflammatory effects. In this review, we highlight the importance of an optimal status of relevant nutrients to effectively reduce inflammation and oxidative stress, thereby strengthening the immune system during the COVID-19 crisis.


Subject(s)
Coronavirus Infections , Diet , Immune System/immunology , Inflammation/immunology , Nutrients/immunology , Oxidative Stress/immunology , Pandemics , Pneumonia, Viral , Antioxidants , Betacoronavirus , COVID-19 , Coronavirus Infections/immunology , Humans , Inflammation/prevention & control , Nutritional Status/immunology , Pneumonia, Viral/immunology , SARS-CoV-2
4.
Int J Mol Sci ; 23(5)2022 Feb 28.
Article in English | MEDLINE | ID: covidwho-1715408

ABSTRACT

COVID-19, resulting from the SARS-CoV-2 virus, is a major pandemic that the world is fighting. SARS-CoV-2 primarily causes lung infection by attaching to the ACE2 receptor on the alveolar epithelial cells. However, the ACE2 receptor is also present in intestinal epithelial cells, suggesting a link between nutrition, virulence and clinical outcomes of COVID-19. Respiratory viral infections perturb the gut microbiota. The gut microbiota is shaped by our diet; therefore, a healthy gut is important for optimal metabolism, immunology and protection of the host. Malnutrition causes diverse changes in the immune system by repressing immune responses and enhancing viral vulnerability. Thus, improving gut health with a high-quality, nutrient-filled diet will improve immunity against infections and diseases. This review emphasizes the significance of dietary choices and its subsequent effects on the immune system, which may potentially impact SARS-CoV-2 vulnerability.


Subject(s)
COVID-19/immunology , Feeding Behavior , Immune System/immunology , Malnutrition/immunology , SARS-CoV-2/immunology , COVID-19/epidemiology , COVID-19/virology , Gastrointestinal Microbiome/immunology , Health Status , Humans , Models, Immunological , Nutritional Status , Pandemics , SARS-CoV-2/pathogenicity , Virulence/immunology
5.
Front Immunol ; 12: 747116, 2021.
Article in English | MEDLINE | ID: covidwho-1662579

ABSTRACT

The pandemic of coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 has caused a large number of deaths, and there is still no effective treatment. COVID-19 can induce a systemic inflammatory response, and its clinical manifestations are diverse. Recently, it has been reported that COVID-19 patients may develop myositis and interstitial pulmonary disease similar to dermatomyositis (DM). This condition is similar to the rapidly progressive interstitial lung disease associated with MDA5+ DM that has a poor prognosis and high mortality, and this poses a challenge for an early identification. Suppression of the immune system can protect COVID-19 patients by preventing the production of inflammatory cytokines. This article attempts to explore the possibility of a relationship between COVID-19 and DM in terms of the potential pathogenesis and clinical features and to analyze the therapeutic effect of the immunosuppressive drugs that are commonly used for the treatment of both DM and COVID-19.


Subject(s)
COVID-19/pathology , Dermatomyositis/pathology , COVID-19/immunology , Cytokines/immunology , Dermatomyositis/immunology , Humans , Immune System/immunology , Inflammation/immunology , Inflammation/pathology , Myositis/immunology , Myositis/pathology , SARS-CoV-2/immunology
6.
7.
Aging (Albany NY) ; 14(1): 73-108, 2022 01 11.
Article in English | MEDLINE | ID: covidwho-1622955

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly spread around the world and became a global pandemic in 2020. One promising drug target for SARS-CoV-2 is the transmembrane protease serine 2 (TMPRSS2). This study was designed to explore the expression status, prognostic significance and molecular functions of TMPRSS2 in lung cancer. TMPRSS2 expression was investigated using the TIMER, Oncomine, UALCAN, GEO, HPA and TCGA databases. The prognostic value of TMPRSS2 was examined using Cox regression and a nomogram. KEGG, GO and GSEA were performed to investigate the cellular function of TMPRSS2 in lung cancer. The relationship between TMPRSS2 and immune infiltration was determined using the TIMER and CIBERSORT algorithms. TMPRSS2 mRNA and protein expression was significantly reduced in lung cancer. Decreased TMPRSS2 expression and increased DNA methylation of TMPRSS2 were associated with various clinicopathological parameters in patients with lung cancer. Low TMPRSS2 mRNA expression also correlated with poor outcome in lung cancer patients. Moreover, a nomogram was constructed and exhibited good predictive power for the overall survival of lung cancer patients. KEGG and GO analyses and GSEA implied that multiple immune- and metabolism-related pathways were significantly linked with TMPRSS2 expression. Intriguingly, TMPRSS2 expression associated with immune cell infiltration in lung cancer. More importantly, TMPRSS2 expression was markedly decreased in SARS-CoV-infected cells. These findings indicate that TMPRSS2 may be a promising prognostic biomarker and therapeutic target for lung cancer through metabolic pathways and immune cell infiltration.


Subject(s)
COVID-19/genetics , Immune System/immunology , Lung Neoplasms/genetics , SARS-CoV-2/physiology , Serine Endopeptidases/genetics , Adult , Aged , Aged, 80 and over , COVID-19/complications , COVID-19/immunology , COVID-19/virology , Female , Host-Pathogen Interactions , Humans , Lung Neoplasms/complications , Lung Neoplasms/immunology , Lung Neoplasms/mortality , Male , Metabolic Networks and Pathways , Middle Aged , SARS-CoV-2/genetics , Serine Endopeptidases/immunology , Young Adult
8.
Nat Immunol ; 22(12): 1479-1489, 2021 12.
Article in English | MEDLINE | ID: covidwho-1537327

ABSTRACT

The extreme diversity of the human immune system, forged and maintained throughout evolutionary history, provides a potent defense against opportunistic pathogens. At the same time, this immune variation is the substrate upon which a plethora of immune-associated diseases develop. Genetic analysis suggests that thousands of individually weak loci together drive up to half of the observed immune variation. Intense selection maintains this genetic diversity, even selecting for the introgressed Neanderthal or Denisovan alleles that have reintroduced variation lost during the out-of-Africa migration. Variations in age, sex, diet, environmental exposure, and microbiome each potentially explain the residual variation, with proof-of-concept studies demonstrating both plausible mechanisms and correlative associations. The confounding interaction of many of these variables currently makes it difficult to assign definitive contributions. Here, we review the current state of play in the field, identify the key unknowns in the causality of immune variation, and identify the multidisciplinary pathways toward an improved understanding.


Subject(s)
Evolution, Molecular , Genetic Variation , Immune System/physiology , Age Factors , Diet , Female , Gene-Environment Interaction , Host-Pathogen Interactions , Humans , Immune System/immunology , Immune System/metabolism , Male , Microbiota/immunology , Sex Factors , Species Specificity
9.
Front Immunol ; 12: 769543, 2021.
Article in English | MEDLINE | ID: covidwho-1520098

ABSTRACT

Many pathogens encode proteases that serve to antagonize the host immune system. In particular, viruses with a positive-sense single-stranded RNA genome [(+)ssRNA], including picornaviruses, flaviviruses, and coronaviruses, encode proteases that are not only required for processing viral polyproteins into functional units but also manipulate crucial host cellular processes through their proteolytic activity. Because these proteases must cleave numerous polyprotein sites as well as diverse host targets, evolution of these viral proteases is expected to be highly constrained. However, despite this strong evolutionary constraint, mounting evidence suggests that viral proteases such as picornavirus 3C, flavivirus NS3, and coronavirus 3CL, are engaged in molecular 'arms races' with their targeted host factors, resulting in host- and virus-specific determinants of protease cleavage. In cases where protease-mediated cleavage results in host immune inactivation, recurrent host gene evolution can result in avoidance of cleavage by viral proteases. In other cases, such as recently described examples in NLRP1 and CARD8, hosts have evolved 'tripwire' sequences that mimic protease cleavage sites and activate an immune response upon cleavage. In both cases, host evolution may be responsible for driving viral protease evolution, helping explain why viral proteases and polyprotein sites are divergent among related viruses despite such strong evolutionary constraint. Importantly, these evolutionary conflicts result in diverse protease-host interactions even within closely related host and viral species, thereby contributing to host range, zoonotic potential, and pathogenicity of viral infection. Such examples highlight the importance of examining viral protease-host interactions through an evolutionary lens.


Subject(s)
Immune System/immunology , Viral Proteases/immunology , Animals , Evolution, Molecular , Host Specificity/genetics , Host Specificity/immunology , Humans , Viral Proteases/genetics , Viral Proteins/genetics , Viral Proteins/immunology
10.
Nutrients ; 13(11)2021 Nov 05.
Article in English | MEDLINE | ID: covidwho-1502476

ABSTRACT

l-Arginine is involved in many different biological processes and recent reports indicate that it could also play a crucial role in the coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Herein, we present an updated systematic overview of the current evidence on the functional contribution of L-Arginine in COVID-19, describing its actions on endothelial cells and the immune system and discussing its potential as a therapeutic tool, emerged from recent clinical experimentations.


Subject(s)
Arginine/metabolism , COVID-19/metabolism , Endothelial Cells/metabolism , Immune System/metabolism , SARS-CoV-2/pathogenicity , Animals , Arginine/therapeutic use , COVID-19/drug therapy , COVID-19/immunology , COVID-19/virology , Endothelial Cells/drug effects , Endothelial Cells/immunology , Endothelial Cells/virology , Host-Pathogen Interactions , Humans , Immune System/drug effects , Immune System/immunology , Immune System/virology , Nitric Oxide/metabolism , SARS-CoV-2/immunology
11.
Immunology ; 164(4): 722-736, 2021 12.
Article in English | MEDLINE | ID: covidwho-1494730

ABSTRACT

Bruton's tyrosine kinase (BTK) is a TEC kinase with a multifaceted role in B-cell biology and function, highlighted by its position as a critical component of the B-cell receptor signalling pathway. Due to its role as a therapeutic target in several haematological malignancies including chronic lymphocytic leukaemia, BTK has been gaining tremendous momentum in recent years. Within the immune system, BTK plays a part in numerous pathways and cells beyond B cells (i.e. T cells, macrophages). Not surprisingly, BTK has been elucidated to be a driving factor not only in lymphoproliferative disorders but also in autoimmune diseases and response to infection. To extort this role, BTK inhibitors such as ibrutinib have been developed to target BTK in other diseases. However, due to rising levels of resistance, the urgency to develop new inhibitors with alternative modes of targeting BTK is high. To meet this demand, an expanding list of BTK inhibitors is currently being trialled. In this review, we synopsize recent discoveries regarding BTK and its role within different immune cells and pathways. Additionally, we discuss the broad significance and relevance of BTK for various diseases ranging from haematology and rheumatology to the COVID-19 pandemic. Overall, BTK signalling and its targetable nature have emerged as immensely important for a wide range of clinical applications. The development of novel, more specific and less toxic BTK inhibitors could be revolutionary for a significant number of diseases with yet unmet treatment needs.


Subject(s)
Agammaglobulinaemia Tyrosine Kinase/metabolism , B-Lymphocytes/enzymology , Immune System/enzymology , Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors , Animals , Autoimmune Diseases/drug therapy , Autoimmune Diseases/enzymology , Autoimmune Diseases/immunology , B-Lymphocytes/drug effects , B-Lymphocytes/immunology , COVID-19/drug therapy , COVID-19/enzymology , COVID-19/immunology , Humans , Immune System/drug effects , Immune System/immunology , Lymphoproliferative Disorders/drug therapy , Lymphoproliferative Disorders/enzymology , Lymphoproliferative Disorders/immunology , Molecular Targeted Therapy , Protein Kinase Inhibitors/therapeutic use , Receptors, Antigen, B-Cell/metabolism , Receptors, Chemokine/metabolism , Signal Transduction , Toll-Like Receptors/metabolism
12.
Expert Rev Gastroenterol Hepatol ; 15(11): 1281-1294, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1470080

ABSTRACT

INTRODUCTION: Human gut microbiota plays a crucial role in providing protective responses against pathogens, particularly by regulating immune system homeostasis. There is a reciprocal interaction between the gut and lung microbiota, called the gut-lung axis (GLA). Any alteration in the gut microbiota or their metabolites can cause immune dysregulation, which can impair the antiviral activity of the immune system against respiratory viruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2. AREAS COVERED: This narrative review mainly outlines emerging data on the mechanisms underlying the interactions between the immune system and intestinal microbial dysbiosis, which is caused by an imbalance in the levels of essential metabolites. The authors will also discuss the role of probiotics in restoring the balance of the gut microbiota and modulation of cytokine storm. EXPERT OPINION: Microbiota-derived signals regulate the immune system and protect different tissues during severe viral respiratory infections. The GLA's equilibration could help manage the mortality and morbidity rates associated with SARS-CoV-2 infection.


Subject(s)
COVID-19/immunology , Dysbiosis/immunology , Gastrointestinal Microbiome/immunology , Immune System/immunology , Pneumonia, Viral/immunology , Humans , SARS-CoV-2
13.
Nutrients ; 13(10)2021 Sep 29.
Article in English | MEDLINE | ID: covidwho-1444284

ABSTRACT

There is an ongoing need for new therapeutic modalities against SARS-CoV-2 infection. Mast cell histamine has been implicated in the pathophysiology of COVID-19 as a regulator of proinflammatory, fibrotic, and thrombogenic processes. Consequently, mast cell histamine and its receptors represent promising pharmacological targets. At the same time, nutritional modulation of immune system function has been proposed and is being investigated for the prevention of COVID-19 or as an adjunctive strategy combined with conventional therapy. Several studies indicate that several immunonutrients can regulate mast cell activity to reduce the de novo synthesis and/or release of histamine and other mediators that are considered to mediate, at least in part, the complex pathophysiology present in COVID-19. This review summarizes the effects on mast cell histamine of common immunonutrients that have been investigated for use in COVID-19.


Subject(s)
COVID-19/immunology , Histamine/immunology , Immune System/immunology , Mast Cells/immunology , Nutritional Physiological Phenomena/immunology , Signal Transduction/immunology , Humans , SARS-CoV-2
14.
Immunology ; 164(4): 722-736, 2021 12.
Article in English | MEDLINE | ID: covidwho-1429802

ABSTRACT

Bruton's tyrosine kinase (BTK) is a TEC kinase with a multifaceted role in B-cell biology and function, highlighted by its position as a critical component of the B-cell receptor signalling pathway. Due to its role as a therapeutic target in several haematological malignancies including chronic lymphocytic leukaemia, BTK has been gaining tremendous momentum in recent years. Within the immune system, BTK plays a part in numerous pathways and cells beyond B cells (i.e. T cells, macrophages). Not surprisingly, BTK has been elucidated to be a driving factor not only in lymphoproliferative disorders but also in autoimmune diseases and response to infection. To extort this role, BTK inhibitors such as ibrutinib have been developed to target BTK in other diseases. However, due to rising levels of resistance, the urgency to develop new inhibitors with alternative modes of targeting BTK is high. To meet this demand, an expanding list of BTK inhibitors is currently being trialled. In this review, we synopsize recent discoveries regarding BTK and its role within different immune cells and pathways. Additionally, we discuss the broad significance and relevance of BTK for various diseases ranging from haematology and rheumatology to the COVID-19 pandemic. Overall, BTK signalling and its targetable nature have emerged as immensely important for a wide range of clinical applications. The development of novel, more specific and less toxic BTK inhibitors could be revolutionary for a significant number of diseases with yet unmet treatment needs.


Subject(s)
Agammaglobulinaemia Tyrosine Kinase/metabolism , B-Lymphocytes/enzymology , Immune System/enzymology , Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors , Animals , Autoimmune Diseases/drug therapy , Autoimmune Diseases/enzymology , Autoimmune Diseases/immunology , B-Lymphocytes/drug effects , B-Lymphocytes/immunology , COVID-19/drug therapy , COVID-19/enzymology , COVID-19/immunology , Humans , Immune System/drug effects , Immune System/immunology , Lymphoproliferative Disorders/drug therapy , Lymphoproliferative Disorders/enzymology , Lymphoproliferative Disorders/immunology , Molecular Targeted Therapy , Protein Kinase Inhibitors/therapeutic use , Receptors, Antigen, B-Cell/metabolism , Receptors, Chemokine/metabolism , Signal Transduction , Toll-Like Receptors/metabolism
15.
FEBS J ; 288(17): 4992-4995, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1393881

ABSTRACT

In this Editorial, we highlight the contents of The FEBS Journal's second Special Issue focussed on COVID-19. The issue covers a variety of aspects related to COVID-19, ranging from the most recent improvements in therapies and the significant impact of rapidly developed COVID-19 vaccines to the emergence of variants of SARS-CoV-2, the role of the immune system in the various stages of the disease and the impact of the disease in different organs. We hope that this collection of articles will give readers an informative and critical perspective on recent advances in understanding and treating COVID-19.


Subject(s)
COVID-19 Vaccines/therapeutic use , COVID-19/epidemiology , SARS-CoV-2/genetics , COVID-19/therapy , COVID-19/virology , Disease Management , Humans , Immune System/immunology , SARS-CoV-2/pathogenicity
16.
Viruses ; 13(9)2021 09 02.
Article in English | MEDLINE | ID: covidwho-1390789

ABSTRACT

SARS-CoV-2 uses ACE2 and TMPRSS2 to gain entry into the cell. However, recent studies have shown that SARS-CoV-2 may use additional host factors that are required for the viral lifecycle. Here we used publicly available datasets, CoV-associated genes, and machine learning algorithms to explore the SARS-CoV-2 interaction landscape in different tissues. We found that in general a small fraction of cells express ACE2 in the different tissues, including nasal, bronchi, and lungs. We show that a small fraction of immune cells (including T cells, macrophages, dendritic cells) found in tissues also express ACE2. We show that healthy circulating immune cells do not express ACE2 and TMPRSS2. However, a small fraction of circulating immune cells (including dendritic cells, monocytes, T cells) in the PBMC of COVID-19 patients express ACE2 and TMPRSS2. Additionally, we found that a large spectrum of cells (in tissues and circulation) in both healthy and COVID-19-positive patients were significantly enriched for SARS-CoV-2 factors, such as those associated with RHOA and RAB GTPases, mRNA translation proteins, COPI- and COPII-mediated transport, and integrins. Thus, we propose that further research is needed to explore if SARS-CoV-2 can directly infect tissue and circulating immune cells to better understand the virus' mechanism of action.


Subject(s)
COVID-19/etiology , Disease Susceptibility , Host-Pathogen Interactions/genetics , Host-Pathogen Interactions/immunology , SARS-CoV-2/physiology , Virus Internalization , COVID-19/blood , Dendritic Cells/immunology , Dendritic Cells/metabolism , Gene Expression Profiling , Gene Expression Regulation , High-Throughput Nucleotide Sequencing , Humans , Immune System/immunology , Immune System/metabolism , Immunity, Innate , Macrophages/immunology , Macrophages/metabolism , Single-Cell Analysis
17.
Front Immunol ; 11: 631743, 2020.
Article in English | MEDLINE | ID: covidwho-1389175

ABSTRACT

The concept of trained immunity has recently emerged as a mechanism contributing to several immune mediated inflammatory conditions. Trained immunity is defined by the immunological memory developed in innate immune cells after a primary non-specific stimulus that, in turn, promotes a heightened inflammatory response upon a secondary challenge. The most characteristic changes associated to this process involve the rewiring of cell metabolism and epigenetic reprogramming. Under physiological conditions, the role of trained immune cells ensures a prompt response. This action is limited by effective resolution of inflammation and tissue repair in order to restore homeostasis. However, unrestrained activation of innate immune cells contributes to the development of chronic inflammation and tissue destruction through the secretion of inflammatory cytokines, proteases and growth factors. Therefore, interventions aimed at reversing the changes induced by trained immunity provide potential therapeutic approaches to treat inflammatory and autoimmune diseases like rheumatoid arthritis (RA). We review cellular approaches that target metabolism and the epigenetic reprogramming of dendritic cells, macrophages, natural killer cells, and other trained cells in the context of autoimmune inflammatory diseases.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Autoimmune Diseases/drug therapy , Autoimmunity/drug effects , Biological Products/therapeutic use , Immune System/drug effects , Inflammation/drug therapy , Animals , Autoimmune Diseases/genetics , Autoimmune Diseases/immunology , Autoimmune Diseases/metabolism , COVID-19/drug therapy , COVID-19/immunology , Energy Metabolism/drug effects , Epigenesis, Genetic/drug effects , Humans , Immune System/immunology , Immune System/metabolism , Immunity, Innate/drug effects , Immunologic Memory/drug effects , Inflammation/genetics , Inflammation/immunology , Inflammation/metabolism , Signal Transduction
18.
Dtsch Med Wochenschr ; 146(16): 1085-1090, 2021 Aug.
Article in German | MEDLINE | ID: covidwho-1366846

ABSTRACT

Since the end of 2019 a new coronavirus, SARS-CoV-2, first identified in Wuhan, China, is spreading around the world partially associated with a high death toll. Besides hygienic measurements to reduce the spread of the virus vaccines have been confected, partially based on the experiences with Ebola virus vaccine, based on recombinant human or chimpanzee adenovirus carrying the spike protein and its ACE2 receptor binding domain (RBD). Further vaccines are constructed by spike protein coding mRNA incorporated in lipid nano vesicles that after entry in human cells produce spike protein. Both vaccine types induce a strong immune response that lasts for months possibly for T-cell immunity a few years. Due to mutations in the coronavirus genome in several parts of the world variants selected, that were partially more pathogenic and partially easier transmissible - variants of concern (VOC). Until now vaccinees are protected against the VOC, even when protection might be reduced compared to the Wuhan wild virus.An open field is still how long the vaccine induced immunity will be sufficient to prevent infection and/or disease; and how long the time period will last until revaccination will be required for life saving protection, whether a third vaccination is needed, and whether revaccination with an adenovirus-based vaccine will be tolerated.


Subject(s)
COVID-19 Vaccines/immunology , COVID-19/prevention & control , Immune System/physiology , SARS-CoV-2/immunology , Vaccination/standards , COVID-19/epidemiology , COVID-19/physiopathology , Humans , Immune System/immunology , Immunity, Cellular , Immunity, Humoral , Time Factors
19.
Mol Genet Metab ; 135(2): 115-121, 2022 02.
Article in English | MEDLINE | ID: covidwho-1356494

ABSTRACT

INTRODUCTION: The impact of SARS-CoV-2 in rare disease populations has been underreported. Gaucher disease (GD) is a prototype rare disease that shares with SARS-CoV-2 a disruption of the lysosomal pathway. MATERIALS-METHODS: Retrospective analysis of 11 patients with Type 1 GD who developed COVID-19 between March 2020 and March 2021. RESULTS: Seven male and 4 female patients with Type 1 GD developed COVID-19. One was a pediatric patient (8 years old) while the remainder were adults, median age of 44 years old (range 21 to 64 years old). Two patients required hospitalization though none required intensive care or intubation. All 11 patients recovered from COVID-19 and there were no reported deaths. CONCLUSIONS: Our case series suggests that GD patients acquired COVID-19 at a similar frequency as the general population, though experienced a milder overall course despite harboring underlying immune system dysfunction and other known co-morbidities that confer high risk of adverse outcomes from SARS-CoV-2 infection.


Subject(s)
COVID-19/immunology , Gaucher Disease/immunology , Gaucher Disease/virology , Immune System/immunology , Rare Diseases/immunology , SARS-CoV-2/immunology , Adult , COVID-19/virology , Child , Comorbidity , Female , Hospitalization , Humans , Male , Middle Aged , Pandemics/prevention & control , Retrospective Studies , Young Adult
20.
J Interferon Cytokine Res ; 41(7): 244-257, 2021 07.
Article in English | MEDLINE | ID: covidwho-1316789

ABSTRACT

Severe Acute Respiratory Syndrome-Coronavirus (SARS-CoV-2), which initiated as an endemic from China, converted into a pandemic disease worldwide within a couple of months' time. This has led researchers from all over the world to come together to find and develop possible curative or preventive strategies, including vaccine development, drug repurposing, plasma therapy, drug discovery, and cytokine-based therapies. Herein, we are providing, a summarized overview of immunopathology of the SARS-CoV-2 along with various therapeutic strategies undertaken to COVID-19 with a vision for their possible outcome. High levels of proinflammatory cytokines such as interleukin (IL)-7, G-CSF, IP-10, TNF-α, monocyte chemoattractant protein-1 (MCP-1), and IL-2 in severe cases of COVID-19 have been observed. Immune responses play significant roles in the determination of SARS-CoV-2 pathogenesis. Thus, exploring the underlying mechanism of the immune system response to SARS-CoV-2 infection would help in the prediction of disease course and selection of intensive care and therapeutic strategy. As an effort toward developing possible therapeutics for COVID-19, we highlighted different types of vaccines, which are under clinical trials, and also discussed the impact of genome variability on efficacy of vaccine under development.


Subject(s)
COVID-19 Vaccines/immunology , COVID-19/immunology , Immune System/immunology , Immunity, Innate/immunology , SARS-CoV-2/immunology , COVID-19/drug therapy , COVID-19/epidemiology , COVID-19 Vaccines/therapeutic use , Communicable Disease Control/methods , Communicable Disease Control/statistics & numerical data , Global Health/statistics & numerical data , Humans , Immune System/drug effects , Immunity, Innate/drug effects , Mutation , Pandemics/prevention & control , SARS-CoV-2/drug effects , SARS-CoV-2/genetics
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