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longhaulerbear · 2 days
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longhaulerbear · 4 days
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Results Compared with controls (n=20), severely symptomatic SARS-CoV-2-infected patients (n=28) had significantly less bacterial diversity (Shannon Index, p=0.0499; Simpson Index, p=0.0581), and positive patients overall had lower relative abundances of Bifidobacterium (p<0.0001), Faecalibacterium (p=0.0077) and Roseburium (p=0.0327), while having increased Bacteroides (p=0.0075). Interestingly, there was an inverse association between disease severity and abundance of the same bacteria.
Conclusion We hypothesise that low bacterial diversity and depletion of Bifidobacterium genera either before or after infection led to reduced proimmune function, thereby allowing SARS-CoV-2 infection to become symptomatic. This particular dysbiosis pattern may be a susceptibility marker for symptomatic severity from SARS-CoV-2 infection and may be amenable to preinfection, intrainfection or postinfection intervention.
The abundance of Bifidobacterium decreases with increasing age and body mass index (BMI)1 and Bifidobacterium is the active ingredient of many probiotics.
Additionally, Bifidobacterium have anti-inflammatory properties: Bifidobacterium animalis, B. longum and B. bifidum decrease the function of the ‘master switch’2 proinflammatory tumour necrosis factor-α (TNF-α), increase the anti-inflammatory cytokine IL-10 and promote the Th1 while inhibiting the Th2 immune response.8 In a mouse model of inflammatory bowel disease (IBD), B. bifidum and B. animalis reduced proinflammatory cytokines and restored intestinal barrier integrity.8
Evidence has accumulated to support a beneficial effect from supplementation with Bifidobacterium in numerous disease states.37 The numbers of commensal Bifidobacterium have been shown to decrease with age and obesity, major SARS-CoV-2 infection risk factors.
We demonstrate that patients with a more severe course of viral infection had decreased abundance of Bifidobacterium. However, it should be noted that there are no definitive studies concerning what constitutes a normal baseline abundance of Bifidobacterium in a ‘healthy’ individual.
Reduced Bifidobacterium abundance has been observed in the gut microbiome of patients with IBD, which has mechanisms involving IL-17.31 Furthermore, the direct endoscopic delivery of Bifidobacterium has been shown to be effective in promoting symptom resolution and mucosal healing in IBD—an effect likely to be associated with the anti-Th17 effect of Bifidobacterium.
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longhaulerbear · 4 days
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longhaulerbear · 5 days
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longhaulerbear · 6 days
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longhaulerbear · 7 days
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We report a previously unrecognized association between SARS-CoV-2 and acute appendicitis.
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longhaulerbear · 8 days
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Here, we present preliminary evidence that after COVID-19, SFN is responsive to treatment with IVIG and linked with neurovascular dysregulation and dysautonomia on iCPET. A larger clinical trial is indicated to further demonstrate the clinical utility of IVIG in treating postinfectious SFN.
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longhaulerbear · 8 days
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After acute infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a proportion of patients experience persistent symptoms beyond 12 weeks, termed Long Covid. Understanding the mechanisms that cause this debilitating disease and identifying biomarkers for diagnostic, therapeutic, and monitoring purposes are urgently required. We detected persistently high levels of interferon-γ (IFN-γ) from peripheral blood mononuclear cells of patients with Long Covid using highly sensitive FluoroSpot assays. This IFN-γ release was seen in the absence of ex vivo peptide stimulation and remains persistently elevated in patients with Long Covid, unlike the resolution seen in patients recovering from acute SARS-CoV-2 infection. The IFN-γ release was CD8+ T cell–mediated and dependent on antigen presentation by CD14+cells. Longitudinal follow-up of our study cohort showed that symptom improvement and resolution correlated with a decrease in IFN-γ production to baseline levels. Our study highlights a potential mechanism underlying Long Covid, enabling the search for biomarkers and therapeutics in patients with Long Covid.
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longhaulerbear · 8 days
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Persistent SARS-CoV-2 infections may act as viral reservoirs that could seed future outbreaks1,2,3,4,5, give rise to highly divergent lineages6,7,8 and contribute to cases with post-acute COVID-19 sequelae (long COVID)9,10. However, the population prevalence of persistent infections, their viral load kinetics and evolutionary dynamics over the course of infections remain largely unknown. Here, using viral sequence data collected as part of a national infection survey, we identified 381 individuals with SARS-CoV-2 RNA at high titre persisting for at least 30 days, of which 54 had viral RNA persisting at least 60 days. We refer to these as ‘persistent infections’ as available evidence suggests that they represent ongoing viral replication, although the persistence of non-replicating RNA cannot be ruled out in all. Individuals with persistent infection had more than 50% higher odds of self-reporting long COVID than individuals with non-persistent infection. We estimate that 0.1–0.5% of infections may become persistent with typically rebounding high viral loads and last for at least 60 days. In some individuals, we identified many viral amino acid substitutions, indicating periods of strong positive selection, whereas others had no consensus change in the sequences for prolonged periods, consistent with weak selection. Substitutions included mutations that are lineage defining for SARS-CoV-2 variants, at target sites for monoclonal antibodies and/or are commonly found in immunocompromised people.
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longhaulerbear · 8 days
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Here we show that BBB disruption is evident during acute infection and in patients with long COVID with cognitive impairment, commonly referred to as brain fog. Using dynamic contrast-enhanced magnetic resonance imaging, we show BBB disruption in patients with long COVID-associated brain fog. Transcriptomic analysis of peripheral blood mononuclear cells revealed dysregulation of the coagulation system and a dampened adaptive immune response in individuals with brain fog. Accordingly, peripheral blood mononuclear cells showed increased adhesion to human brain endothelial cells in vitro, while exposure of brain endothelial cells to serum from patients with long COVID induced expression of inflammatory markers. Together, our data suggest that sustained systemic inflammation and persistent localized BBB dysfunction is a key feature of long COVID-associated brain fog.
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longhaulerbear · 8 days
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longhaulerbear · 8 days
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Stewart and colleagues have shown that tilt table testing and standing testing are not equivalent in adolescents. Unfortunately, their study was not adequately powered to go further than that. Therefore, we still do not know what the equivalent standing HR threshold is for diagnosis of POTS in these adolescents who otherwise meet criteria for POTS by history plus tilt table test.
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longhaulerbear · 8 days
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People with EDS/HSD experience symptoms of acid reflux, dysphagia, and dysphonia to varying degrees with significant differences between hEDS than HSD. Awareness of the impact of EDS/HSD on throat symptoms will enable health care professionals to anticipate throat symptoms more readily in this population, providing individualized and effective management plans.
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longhaulerbear · 8 days
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with short- and long-term neurological complications. The variety of symptoms makes it difficult to unravel molecular mechanisms underlying neurological sequalae after coronavirus disease 2019 (COVID-19). Here we show that SARS-CoV-2 triggers the up-regulation of synaptic components and perturbs local electrical field potential.
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longhaulerbear · 8 days
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longhaulerbear · 15 days
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longhaulerbear · 23 days
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