Host factors: Implications in immunopathogenesis of COVID-19.
Ontology highlight
ABSTRACT:
SUBMITTER: Jafarpour R
PROVIDER: S-EPMC8505027 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Following the outbreak of the COVID-19 pandemic, millions of people around the world have been affected with SARS-CoV-2 infection. In addition to the typical symptoms, thrombotic events, lymphopenia, and thrombocytopenia have been reported in COVID-19 patients. Immune thrombocytopenic purpura (ITP) is one of the thrombotic events that occur in some COVID-19 patients. Hyperinflammation, cytokine storms, and immune dysregulation in some patients are the cause to the main COVID-19 complications such as ALI (acute lung injury), acute respiratory distress syndrome (ARDS), and multiple organ failure. Disruption in the differentiation of T-cells, enhanced differentiation of Th17 and Th1, cell death (pyroptosis), hyper-inflammation and dysfunction of inflammatory neutrophils and macrophages, and hyperactivity of NLRP3-inflammasome are among the important factors that may be the cause to COVID-19-induced ITP. This study aimed to give an overview of the findings on the immunopathogenesis of ITP and COVID-19-induced ITP. Further studies are required to better understand the exact immunopathogenesis and effective treatments for ITP, especially in inflammatory disorders.
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Project description:BackgroundThe ACE2 protein acts as a gateway for SARS-CoV-2 in the host cell, playing an essential role in susceptibility to infection by this virus. Genetics and epigenetic mechanisms related to the ACE2 gene are associated with changes in its expression and, therefore, linked to increased susceptibility to infection. Although some variables such as sex, age, and obesity have been described as risk factors for COVID-19, the molecular causes involved in the disease susceptibility are still unknown.AimTo evaluate the ACE2 gene expression profiles and their association with epigenetic mechanisms and demographic or clinical variables.MethodsIn 500 adult volunteers, the mRNA expression levels of the ACE2 gene in nasopharyngeal swab samples and its methylation status in peripheral blood samples were quantified by RT-qPCR and qMSP, respectively. The existence of significant differences in the ACE2 gene expression and its determinants were evaluated in different study groups according to several demographic or clinical variables such as sex, age, body mass index (BMI), smoking, SARS-CoV-2 infection, and presence of underlying diseases such as type II diabetes mellitus (DM2), asthma and arterial hypertension (AHT).ResultsOur results show that ACE2 gene overexpression, directly involved in susceptibility to SARS-CoV-2 infection, depends on multiple host factors such as male sex, age over 30 years, smoking, the presence of obesity, and DM2. Likewise, it was determined that the ACE2 gene expression is regulated by changes in the DNA methylation patterns in its promoter region.ConclusionsThe ACE2 gene expression is highly variable, and this variability is related to habits such as smoking and demographic or clinical variables, which details the impact of environmental and host factors on our epigenome and, therefore, in susceptibility to SARS-CoV-2 infection.
| S-EPMC9420046 | biostudies-literature
Project description:The Coronavirus Disease-2019 (COVID-19) imposed public health emergency and affected millions of people around the globe. As of January 2021, 100 million confirmed cases of COVID-19 along with more than 2 million deaths were reported worldwide. SARS-CoV-2 infection causes excessive production of pro-inflammatory cytokines thereby leading to the development of "Cytokine Storm Syndrome." This condition results in uncontrollable inflammation that further imposes multiple-organ-failure eventually leading to death. SARS-CoV-2 induces unrestrained innate immune response and impairs adaptive immune responses thereby causing tissue damage. Thus, understanding the foremost features and evolution of innate and adaptive immunity to SARS-CoV-2 is crucial in anticipating COVID-19 outcomes and in developing effective strategies to control the viral spread. In the present review, we exhaustively discuss the sequential key immunological events that occur during SARS-CoV-2 infection and are involved in the immunopathogenesis of COVID-19. In addition to this, we also highlight various therapeutic options already in use such as immunosuppressive drugs, plasma therapy and intravenous immunoglobulins along with various novel potent therapeutic options that should be considered in managing COVID-19 infection such as traditional medicines and probiotics.
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Project description:Post-acute sequelae of COVID-19 (PASC) represent an emerging global crisis. However, quantifiable risk-factors for PASC and their biological associations are poorly resolved. We executed a deep multi-omic, longitudinal investigation of 309 COVID-19 patients from initial diagnosis to convalescence (2-3 months later), integrated with clinical data, and patient-reported symptoms. We resolved four PASC-anticipating risk factors at the time of initial COVID-19 diagnosis: type 2 diabetes, SARS-CoV-2 RNAemia, Epstein-Barr virus viremia, and specific autoantibodies. In patients with gastrointestinal PASC, SARS-CoV-2-specific and CMV-specific CD8+ T cells exhibited unique dynamics during recovery from COVID-19. Analysis of symptom-associated immunological signatures revealed coordinated immunity polarization into four endotypes exhibiting divergent acute severity and PASC. We find that immunological associations between PASC factors diminish over time leading to distinct convalescent immune states. Detectability of most PASC factors at COVID-19 diagnosis emphasizes the importance of early disease measurements for understanding emergent chronic conditions and suggests PASC treatment strategies.
2022-02-01 | E-MTAB-10129 | biostudies-arrayexpress
Project description:A cytokine storm is a hyperinflammatory state secondary to the excessive production of cytokines by a deregulated immune system. It manifests clinically as an influenza-like syndrome, which can be complicated by multi-organ failure and coagulopathy, leading, in the most severe cases, even to death. The term cytokine storm was first used in 1993 to describe the graft-versus-host disease following allogeneic hematopoietic stem cell transplantation. It was then reused to define the adverse syndromes secondary to the administration of immunostimulating agents, such as anti-CD28 antibodies or bioengineered immune cells, i.e., CAR T-cell therapy. Currently, the concept of cytokine storm has been better elucidated and extended to the pathogenesis of many other conditions, such as sepsis, autoinflammatory disease, primary and secondary hemophagocytic lymphohistiocytosis, and multicentric Castleman disease. Moreover, cytokine storm has recently emerged as a key aspect in the novel Coronavirus disease 2019, as affected patients show high levels of several key pro-inflammatory cytokines, such as IL-1, IL-2, IL-6, TNF-α, IFN-γ, IP-10, GM-CSF, MCP-1, and IL-10, some of which also correlate with disease severity. Therefore, since the onset of the pandemic, numerous agents have been tested in the effort to mitigate the cytokine storm in COVID-19 patients, some of which are effective in reducing mortality, especially in critically ill patients, and are now becoming standards of care, such as glucocorticoids or some cytokine inhibitors. However, the challenge is still far from being met, and other therapeutic strategies are being tested in the hope that we can eventually overcome the disease.
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Project description:Coronavirus disease 2019 (COVID-19) infection which is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has led to a "public health emergency of international concern" (PHEIC). The infection is highly contagious, has a high mortality rate, and its pathophysiology remains poorly understood. Pulmonary inflammation with substantial lung damage together with generalized immune dysregulation are major components of COVID-19 pathogenesis. The former component, lung damage, seems to be at least in part a consequence of immune dysregulation. Indeed, studies have revealed that immune alteration is not merely an association, as it might occur in systemic infections, but, very likely, the core pathogenic element of COVID-19. In addition, precise management of immune response in COVID-19, i.e. enhancing anti-viral immunity while inhibiting systemic inflammation, may be key to successful treatment. Herein, we have reviewed current evidence related to different aspects of COVID-19 immunology, including innate and adaptive immune responses against the virus and mechanisms of virus-induced immune dysregulation. Considering that current antiviral therapies are chiefly experimental, strategies to do immunotherapy for the management of disease have also been reviewed. Understanding immunology of COVID-19 is important in developing effective therapies as well as diagnostic, and prophylactic strategies for this disease.
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Project description:The COVID-19 pandemic caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) poses an unprecedented challenge to humanity. SARS-CoV-2 infections range from asymptomatic to severe courses of COVID-19 with acute respiratory distress syndrome (ARDS), multiorgan involvement and death. Risk factors for disease severity include older age, male sex, increased BMI and pre-existing comorbidities. Ethnicity is also relevant to COVID-19 susceptibility and severity. Host genetic predisposition to COVID-19 is now increasingly recognized and whole genome and candidate gene association studies regarding COVID-19 susceptibility have been performed. Several common and rare variants in genes related to inflammation or immune responses have been identified. We summarize research on COVID-19 host genetics and compile genetic variants associated with susceptibility to COVID-19 and disease severity. We discuss candidate genes that should be investigated further to understand such associations and provide insights relevant to pathogenesis, risk classification, therapy response, precision medicine, and drug repurposing.
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Project description:RNA-Seq was used to study changes in gene expression in saliva samples from 266 human subjects after SARS-COV-2 infection, vaccination, or combined infection and vaccination (breakthrough). Approximately equal numbers of males and females, matched for age, were profiled after subjects tested positive for COVID-19 by PCR and sequencing of the variant. In addition to samples from uninfected controls with and without vaccination, samples from infected subjects with and without vaccination that represent eight major SARS-COV-2 lineages are included: epsilon, iota, alpha, delta, omicron BA.1, omicron BA.2, omicron BA.4, and omicron BA.5. Stranded single-end sequencing was performed using standard Illumina protocols. Reads were quantified to hg38 human transcriptome using Salmon after adapter trimming. Quantified reads were filtered to remove features with fewer than one count in 80% of the samples, and normalized using TPM, followed by quantile and log2 transformation.
2023-09-19 | GSE212191 | GEO
Project description:Due to COVID 19 (Corona virus disease)pandemic, majority of surgeries, including surgery for cancer patients got delayed across the globe. Surgeries were limited to emergency set up only. At our institute we tried to perform colorectal cancer surgeries through out the pandemic, albeit in less numbers, as we thought cancer in itself is an emergency setting. we are planning to analyse the prospectively managed database of this particular group of patients over a period of last six 6 months and look out at 30 day post operative morbidity and mortality. Besides we will try to analyse the implications of our decision to carry on with cancer surgeries in terms of number of health care workers who got infected while being involved in primary care of these patients.
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Project description:The severe cases of Coronavirus Disease 2019 (COVID-19) frequently exhibit excessive inflammatory responses, acute respiratory distress syndrome (ARDS), coagulopathy, and organ damage. The most striking immunopathology of advanced COVID-19 is cytokine release syndrome or "cytokine storm" that is attributable to the deficiencies in immune regulatory mechanisms. CD4+FoxP3+ regulatory T cells (Tregs) are central regulators of immune responses and play an indispensable role in the maintenance of immune homeostasis. Tregs are likely involved in the attenuation of antiviral defense at the early stage of infection and ameliorating inflammation-induced organ injury at the late stage of COVID-19. In this article, we review and summarize the current understanding of the change of Tregs in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and discuss the potential role of Tregs in the immunopathology of COVID-19. The emerging concept of Treg-targeted therapies, including both adoptive Treg transfer and low dose of IL-2 treatment, is introduced. Furthermore, the potential Treg-boosting effect of therapeutic agents used in the treatment of COVID-19, including dexamethasone, vitamin D, tocilizumab and sarilumab, chloroquine, hydroxychloroquine, azithromycin, adalimumab and tetrandrine, is discussed. The problems in the current study of Treg cells in COVID-19 and future perspectives are also addressed.
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