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1.
Frontiers in immunology ; 13, 2022.
Article in English | EuropePMC | ID: covidwho-1918600

ABSTRACT

Background IgG anti-spike (S) antibodies arise after SARS-CoV-2 infection as well as vaccination. Levels of IgG anti-S are linked to neutralizing antibody titers and protection against (re)infection. Methods We measured IgG anti-S and surrogate neutralizing antibody kinetics against Wild Type (WT) and 4 Variants of Concern (VOC) in health care workers (HCW) 3 and 10 months after natural infection (“infection”, n=83) or vaccination (2 doses of BNT162b2) with (“hybrid immunity”, n=17) or without prior SARS-CoV-2 infection (“vaccination”, n=97). Results The humoral immune response in the “vaccination” cohort was higher at 3 months, but lower at 10 months, compared to the “infection” cohort due to a faster decline. The “hybrid immunity” cohort had the highest antibody levels at 3 and 10 months with a slower decline compared to the “vaccination” cohort. Surrogate neutralizing antibody levels (expressed as %inhibition of ACE-2 binding) showed a linear relation with log10 of IgG anti-S against WT and four VOC. IgG anti-S corresponding to 90% inhibition ranged from 489 BAU/mL for WT to 1756 BAU/mL for Beta variant. Broad pseudoneutralization predicted live virus neutralization of Omicron BA.1 in 20 randomly selected high titer samples. Conclusions Hybrid immunity resulted in the strongest humoral immune response. Antibodies induced by natural infection decreased more slowly than after vaccination, resulting in higher antibody levels at 10 months compared to vaccinated HCW without prior infection. There was a linear relationship between surrogate neutralizing activity and log10 IgG anti-S for WT and 4 VOC, although some VOC showed reduced sensitivity to pseudoneutralization.

2.
Viruses ; 14(6)2022 06 16.
Article in English | MEDLINE | ID: covidwho-1911639

ABSTRACT

The national vaccination campaign against SARS-CoV-2 started in January 2021 in Belgium. In the present study, we aimed to use national hospitalisation surveillance data to investigate the recent evolution of vaccine impact on the risk of COVID-19 hospitalisation. We analysed aggregated data from 27,608 COVID-19 patients hospitalised between October 2021 and February 2022, stratified by age category and vaccination status. For each period, vaccination status, and age group, we estimated risk ratios (RR) corresponding to the ratio between the probability of being hospitalised following SARS-CoV-2 infection if belonging to the vaccinated population and the same probability if belonging to the unvaccinated population. In October 2021, a relatively high RR was estimated for vaccinated people > 75 years old, possibly reflecting waning immunity within this group, which was vaccinated early in 2021 and invited to receive the booster vaccination at that time. In January 2022, a RR increase was observed in all age categories coinciding with the dominance of the Omicron variant. Despite the absence of control for factors like comorbidities, previous infections, or time since the last administered vaccine, we showed that such real-time aggregated data make it possible to approximate trends in vaccine impact over time.


Subject(s)
COVID-19 Vaccines , COVID-19 , Aged , Belgium/epidemiology , COVID-19/epidemiology , COVID-19/prevention & control , Hospitalization , Humans , SARS-CoV-2 , Vaccination
3.
Viruses ; 14(6)2022 06 09.
Article in English | MEDLINE | ID: covidwho-1884392

ABSTRACT

To mitigate the massive COVID-19 burden caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), several vaccination campaigns were initiated. We performed a single-center observational trial to monitor the mid- (3 months) and long-term (10 months) adaptive immune response and to document breakthrough infections (BTI) in healthcare workers (n = 84) upon BNT162b2 vaccination in a real-world setting. Firstly, serology was determined through immunoassays. Secondly, antibody functionality was analyzed via in vitro binding inhibition and pseudovirus neutralization and circulating receptor-binding domain (RBD)-specific B cells were assessed. Moreover, the induction of SARS-CoV-2-specific T cells was investigated by an interferon-γ release assay combined with flowcytometric profiling of activated CD4+ and CD8+ T cells. Within individuals that did not experience BTI (n = 62), vaccine-induced humoral and cellular immune responses were not correlated. Interestingly, waning over time was more pronounced within humoral compared to cellular immunity. In particular, 45 of these 62 subjects no longer displayed functional neutralization against the delta variant of concern (VoC) at long-term follow-up. Noteworthily, we reported a high incidence of symptomatic BTI cases (17.11%) caused by alpha and delta VoCs, although vaccine-induced immunity was only slightly reduced compared to subjects without BTI at mid-term follow-up.


Subject(s)
COVID-19 , SARS-CoV-2 , Antibodies, Neutralizing , Antibodies, Viral , BNT162 Vaccine , Belgium , CD8-Positive T-Lymphocytes , COVID-19/epidemiology , COVID-19/prevention & control , Disease Progression , Follow-Up Studies , Health Personnel , Humans , Immunity, Cellular , Immunity, Humoral , Incidence , SARS-CoV-2/genetics , Vaccination
4.
Viruses ; 14(6)2022 05 31.
Article in English | MEDLINE | ID: covidwho-1869829

ABSTRACT

We report two clusters of SARS-CoV-2 B.1.617.2 (Delta variant) infections in a group of 41 Indian nursing students who travelled from New Delhi, India, to Belgium via Paris, France. All students tested negative before departure and had a second negative antigen test upon arrival in Paris. Upon arrival in Belgium, the students were quarantined in eight different houses. Four houses remained COVID-free during the 24 days of follow-up, while all 27 residents of the other four houses developed an infection during quarantine, including the four residents who were fully vaccinated and the two residents who were partially vaccinated. Genome sequencing revealed two distinct clusters affecting one and three houses, respectively. In this group of students, vaccination status did not seem to prevent infection nor decrease the viral load. No severe symptoms were reported. Extensive contact tracing and 3 months of nationwide genomic surveillance confirmed that these outbreaks were successfully contained and did not contribute to secondary community transmission in Belgium. These clusters highlight the importance of repeated testing and quarantine measures among travelers coming from countries experiencing a surge of infections, as all infections were detected 6 days or more after arrival.


Subject(s)
COVID-19 , SARS-CoV-2 , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/prevention & control , Humans , Quarantine , SARS-CoV-2/genetics , Students
5.
2021.
Preprint in English | Other preprints | ID: ppcovidwho-295467

ABSTRACT

Although the subject of intensive preclinical and clinical research, controversy on the protective vs. deleterious effect of interferon (IFN) in COVID-19 remains. Some apparently conflicting results are likely due to the intricacy of IFN subtypes (type I: IFN-alpha/beta, type III: IFN-lambda), timing and mode of administration (nebulized/subcutaneous) and clinical groups targeted (asymptomatic/mild, moderate, severe/critical COVID-19). Within the COntAGIouS (COvid-19 Advanced Genetic and Immunologic Sampling) clinical trial, we investigated endogenous type I and type III IFNs in nasal mucosa as possible predictors of clinical outcome in critical patients, as well as their correlation to SARS-CoV-2 viral load, using nCounter technology. We found that endogenous IFN-beta expression in the nasal mucosa predicts clinical outcome, independent of viral replication or Apache II score, and should be considered as a prognostic tool in a precision medicine approach of IFN therapy in COVID-19 clinical management.

6.
Nat Commun ; 12(1): 6243, 2021 10 29.
Article in English | MEDLINE | ID: covidwho-1493101

ABSTRACT

Understanding the pathology of COVID-19 is a global research priority. Early evidence suggests that the respiratory microbiome may be playing a role in disease progression, yet current studies report contradictory results. Here, we examine potential confounders in COVID-19 respiratory microbiome studies by analyzing the upper (n = 58) and lower (n = 35) respiratory tract microbiome in well-phenotyped COVID-19 patients and controls combining microbiome sequencing, viral load determination, and immunoprofiling. We find that time in the intensive care unit and type of oxygen support, as well as associated treatments such as antibiotic usage, explain the most variation within the upper respiratory tract microbiome, while SARS-CoV-2 viral load has a reduced impact. Specifically, mechanical ventilation is linked to altered community structure and significant shifts in oral taxa previously associated with COVID-19. Single-cell transcriptomics of the lower respiratory tract of COVID-19 patients identifies specific oral bacteria in physical association with proinflammatory immune cells, which show higher levels of inflammatory markers. Overall, our findings suggest confounders are driving contradictory results in current COVID-19 microbiome studies and careful attention needs to be paid to ICU stay and type of oxygen support, as bacteria favored in these conditions may contribute to the inflammatory phenotypes observed in severe COVID-19 patients.


Subject(s)
COVID-19/microbiology , Gastrointestinal Microbiome/genetics , Gastrointestinal Microbiome/physiology , Humans , Microbiota/physiology , SARS-CoV-2/pathogenicity , Transcriptome/genetics
8.
Nat Commun ; 11(1): 5838, 2020 11 17.
Article in English | MEDLINE | ID: covidwho-933686

ABSTRACT

Emergence of SARS-CoV-2 causing COVID-19 has resulted in hundreds of thousands of deaths. In search for key targets of effective therapeutics, robust animal models mimicking COVID-19 in humans are urgently needed. Here, we show that Syrian hamsters, in contrast to mice, are highly permissive to SARS-CoV-2 and develop bronchopneumonia and strong inflammatory responses in the lungs with neutrophil infiltration and edema, further confirmed as consolidations visualized by micro-CT alike in clinical practice. Moreover, we identify an exuberant innate immune response as key player in pathogenesis, in which STAT2 signaling plays a dual role, driving severe lung injury on the one hand, yet restricting systemic virus dissemination on the other. Our results reveal the importance of STAT2-dependent interferon responses in the pathogenesis and virus control during SARS-CoV-2 infection and may help rationalizing new strategies for the treatment of COVID-19 patients.


Subject(s)
Betacoronavirus/physiology , Coronavirus Infections/pathology , Coronavirus Infections/virology , Disease Models, Animal , Pneumonia, Viral/pathology , Pneumonia, Viral/virology , STAT2 Transcription Factor/metabolism , Signal Transduction , Animals , Betacoronavirus/pathogenicity , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/metabolism , Cricetinae , Immunity, Innate , Interferon Type I/genetics , Interferon Type I/metabolism , Lung/pathology , Lung/virology , Mice , Pandemics , Pneumonia, Viral/immunology , Pneumonia, Viral/metabolism , SARS-CoV-2 , STAT2 Transcription Factor/genetics , Virus Replication
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