The ability of the neonatal immune response to handle SARS-CoV-2 infection.
Ontology highlight
ABSTRACT:
SUBMITTER: Gotzinger F
PROVIDER: S-EPMC7826031 | biostudies-literature | 2021 Mar
REPOSITORIES: biostudies-literature
Publications
The ability of the neonatal immune response to handle SARS-CoV-2 infection.
Götzinger Florian F Santiago-Garcia Begoña B Fumadó-Pérez Victòria V Brinkmann Folke F Tebruegge Marc M
The Lancet. Child & adolescent health 20210121 3
Similar Datasets
Project description:SARS-CoV-2 infection results in impaired interferon response in severe COVID-19 patients. However, how SARS-CoV-2 interferes with host immune response is incompletely understood. Here, we sequenced small RNAs from SARS-CoV-2-infected human cells and identified a microRNA (miRNA) derived from a recently evolved region of the viral genome. We show that the virus-derived miRNA produces two miRNA isoforms in infected cells by the enzyme Dicer and they are loaded into Argonaute proteins. Moreover, the predominant miRNA isoform targets the 3´UTR of interferon-stimulated genes and represses their expression in a miRNA-like fashion. Finally, the two viral miRNA isoforms were detected in nasopharyngeal swabs from COVID-19 patients. We propose that SARS-CoV-2 can potentially employ a virus-derived miRNA to hijack the host miRNA machinery which can lead to evasion of the interferon-mediated immune response.
| S-SCDT-EMBOR-2021-54341-T | biostudies-other
Project description:Acute respiratory distress syndrome (ARDS) is a severe pulmonary disease, which is one of the major complications in COVID-19 patients. Dysregulation of the immune system and imbalances in cytokine release and immune cell activation are involved in SARS-CoV-2 infection. Here, the inflammatory, antigen, and auto-immune profile of patients presenting COVID-19-associated severe ARDS has been analyzed using functional proteomics approaches. Both, innate and humoral responses have been characterized through acute-phase protein network and auto-antibody signature. Severity and sepsis by SARS-CoV-2 emerged to be correlated with auto-immune profiles of patients and define their clinical progression, which could provide novel perspectives in therapeutics development and biomarkers of COVID-19 patients. Humoral response in COVID-19 patients' profile separates with significant differences patients with or without ARDS. Furthermore, we found that this profile can be correlated with COVID-19 severity and results more common in elderly patients.
| S-EPMC8831226 | biostudies-literature
Project description: Not available
| S-EPMC7798998 | biostudies-literature
Project description:COVID-19 pandemic has started in December 2019 in China and quickly extended to become a worldwide health and economic emergency issue. It is caused by the novel coronavirus; SARS-CoV-2. COVID-19 patients' clinical presentations vary from asymptomatic infection or flu like symptoms to serious pneumonia which could be associated with multiple organ failure possibly leading to death. It is understood that the immune response to SARS-CoV-2 includes all elements of the immune system which could altogether succeed in viral elimination and complete cure. Meanwhile, this immune response may also lead to disease progression and could be responsible for the patient's death. Many trials have been done recently to create therapies and vaccines against human coronavirus infections such as MERS or SARS, however, till now, there is some controversy about the effectiveness and safety of antiviral drugs and vaccines which have been developed to treat and prevent this disease and its management depends mainly on supportive care. The spike glycoprotein or protein S of SARS-CoV-2 is the main promoter that induces development of neutralizing antibodies; hence, many attempts of vaccines and antiviral drugs development have been designed to be directed specifically against this protein. While some of these attempts have been proved to be efficient in in vitro settings, only few of them have been proceeded to randomized animal trials and human studies which makes COVID-19 prevention an ongoing challenge. This review describes the natural immune response scenario during COVID-19 and the vaccines development trials to create efficient vaccines thus helping to build more effective approaches for prophylaxis and management.
| S-EPMC7846221 | biostudies-literature
Project description:SARS-CoV-2 infected pregnant women are at increased risk of severe COVID-19 than non-pregnant women and have a higher risk of adverse pregnancy outcomes like intrauterine/fetal distress and preterm birth. However, little is known about the impact of SARS-CoV-2 infection on maternal and neonatal immunological profiles. In this study, we investigated the inflammatory and humoral responses to SARS-CoV-2 in maternal and cord blood paired samples. Thirty-six pregnant women were recruited at delivery at Hospital Sant Joan de Déu, Barcelona, Spain, between April-August 2020, before having COVID-19 available vaccines. Maternal and pregnancy variables, as well as perinatal outcomes, were recorded in questionnaires. Nasopharyngeal swabs and maternal and cord blood samples were collected for SARS-CoV-2 detection by rRT-PCR and serology, respectively. We measured IgM, IgG and IgA levels to 6 SARS-CoV-2 antigens (spike [S], S1, S2, receptor-binding domain [RBD], nucleocapsid [N] full-length and C-terminus), IgG to N from 4 human coronaviruses (OC43, HKU1, 229E and NL63), and the concentrations of 30 cytokines, chemokines and growth factors by Luminex. Mothers were classified as infected or non-infected based on the rRT-PCR and serology results. Sixty-four % of pregnant women were infected with SARS-CoV-2 (positive by rRT-PCR during the third trimester and/or serology just after delivery). None of the newborns tested positive for rRT-PCR. SARS-CoV-2 infected mothers had increased levels of virus-specific antibodies and several cytokines. Those with symptoms had higher cytokine levels. IFN-α was increased in cord blood from infected mothers, and in cord blood of symptomatic mothers, EGF, FGF, IL-17 and IL-15 were increased, whereas RANTES was decreased. Maternal IgG and cytokine levels showed positive correlations with their counterparts in cord blood. rRT-PCR positive mothers showed lower transfer of SARS-CoV-2-specific IgGs, with a stronger effect when infection was closer to delivery. SARS-CoV-2 infected mothers carrying a male fetus had higher antibody levels and higher EGF, IL-15 and IL-7 concentrations. Our results show that SARS-CoV-2 infection during the third trimester of pregnancy induces a robust antibody and cytokine response at delivery and causes a significant reduction of the SARS-CoV-2-specific IgGs transplacental transfer, with a stronger negative effect when the infection is closer to delivery.
| S-EPMC9552073 | biostudies-literature
Project description:Coronavirus disease 2019 (COVID-19) has been a global pandemic, caused by a novel coronavirus strain with strong infectivity, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). With the in-depth research, the close relationship between COVID-19 and immune system has been dug out. During the infection, macrophages, dendritic cells, natural killer cells, CD8+ T cells, Th1, Th17, Tfh cells and effector B cells are all involved in the anti-SARS-CoV-2 responses, however, the dysfunctional immune responses will ultimately lead to the excessive inflammation, acute lung injury, even other organ failure. Thus, a detailed understanding of pertinent immune response during COVID-19 will provide insights in predicting disease outcomes and developing appropriate therapeutic approaches. In this review, we mainly clarify the role of immune cells in COVID-19 and the target-vaccine development and treatment.
| S-EPMC9727711 | biostudies-literature
Project description:ObjectiveWe aimed to characterize the evolution of humoral immune response up to 1 year after SARS-CoV-2 infection in healthcare workers (HCWs) during the first wave of COVID-19 in Paris.MethodsSerum samples from 92 HCWs were tested at month 0 (M0), M6, and M12 after SARS-CoV-2 infection for IgG targeting the nucleocapsid (N), IgG targeting the receptor-binding domain (RBD) of spike (S) protein, IgA targeting S, and anti-RBD neutralizing antibodies. After M6, 46 HCWs received a single dose of COVID-19 vaccine.ResultsWe observed a significant decrease in all SARS-CoV-2 immunologic markers at M6 post-infection: median decreases were 0.26 log binding antibody units/mL (M0: 1.9 (interquartile range (IQR) 1.47-2.27); M6: 1.64 (IQR 1.22-1.92)) for anti-RBD IgG; 4.10 (index) (M0: 4.94 (IQR 2.72-6.82); M6: 0.84 (IQR 0.25-1.55)) for anti-N IgG; 0.64 (index) (M0: 2.50 (IQR 1.18-4.62); M6: 1.86 (IQR 0.85-3.54)) for anti-S IgA; and 24.4% (M0: 66.4 (IQR 39.7-82.5); M6: 42.0 (IQR 16.8-68.8)) inhibition activity for the RBD neutralizing antibodies. Between M6 and M12, anti-RBD IgG level, anti-S IgA index, and anti-RBD neutralizing activity significantly increased among COVID-19 vaccinated HCWs, whereas they remained stable among unvaccinated HCWs. Anti-N IgG index significantly decreased between M6 and M12 among both vaccinated (median: 0.73 (IQR 0.23-1.11) at M6 and 0.52 (IQR 0.20-0.73) at M12) and unvaccinated HCWs (median: 0.79 (IQR 0.21-4.67) at M6 and 0.34 (IQR 0.24-2.78) at M12).DiscussionA steady decline in the anti-N IgG response was observed during the first year after SARS-CoV-2 infection among HCWs, whereas the anti-RBD IgG and the anti-S IgA responses remained stable and could be enhanced by COVID-19 vaccination.
| S-EPMC8928754 | biostudies-literature
Project description:Viral pandemics pose an imminent threat to humanity. The ongoing COVID-19 pandemic, caused by the SARS-CoV-2 virus, requires the urgent development of anti-viral therapies. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here, we offer an in-depth analysis of the host response to SARS-CoV-2 as it compares to other respiratory infections. Cell and animal models of SARS-CoV-2 infections, in addition to transcriptional profiling of a COVID-19 lung biopsy consistently revealed a unique and inappropriate inflammatory response defined by elevated chemokine expression in the absence of Type I and III interferons. Our identification of a muted transcriptional response to SARS-CoV-2 supports a model in which initial failure to rapidly respond to infection results in prolonged viral replication and an influx of proinflammatory cells that induce alveolar damage and manifest in COVID-19 lung pathology.
2020-03-25 | GSE147507 | GEO
Project description:SARS-CoV-2 infection results in impaired interferon response in patients with severe COVID-19. However, how SARS-CoV-2 interferes with host immune responses is incompletely understood. Here, we sequence small RNAs from SARS-CoV-2-infected human cells and identify a microRNA (miRNA) derived from a recently evolved region of the viral genome. We show that the virus-derived miRNA produces two miRNA isoforms in infected cells by the enzyme Dicer, which are loaded into Argonaute proteins. Moreover, the predominant miRNA isoform targets the 3'UTR of interferon-stimulated genes and represses their expression in a miRNA-like fashion. Finally, the two viral miRNA isoforms were detected in nasopharyngeal swabs from COVID-19 patients. We propose that SARS-CoV-2 can potentially employ a virus-derived miRNA to hijack the host miRNA machinery, which could help to evade the interferon-mediated immune response.
| S-EPMC8811647 | biostudies-literature
Project description:SARS CoV-2, a causative agent of human respiratory tract infection, was first identified in late 2019. It is a newly emerging viral disease with unsatisfactory treatments. The virus is highly contagious and has caused pandemic globally. The number of deaths is increasing exponentially, which is an alarming situation for mankind. The detailed mechanism of the pathogenesis and host immune responses to this virus are not fully known. Here we discuss an overview of SARS CoV-2 pathogenicity, its entry and replication mechanism, and host immune response against this deadly pathogen. Understanding these processes will help to lead the development and identification of drug targets and effective therapies.
| S-EPMC8096142 | biostudies-literature