Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinN (1)


SARS-CoV-2 Proteins
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    Interferons and Multiple Sclerosis: Lessons from 25 Years of Clinical and Real-World Experience with Intramuscular Interferon-Beta-1a (Avonex)

    Authors: Stanley Cohan; Barry Hendin; Anthony Reder; Kyle Smoot; Robin Avila; Jason Mendoza; Bianca Weinstock-Guttman

    id:202101.0183/v1 Date: 2021-01-11 Source:

    Multiple sclerosis MESHD ( MS MESHD) is a chronic inflammatory demyelinating disease MESHD of the central nervous system. The interferons (IFNs) were discovered in 1957, and recombinant IFN-β-1b was approved by the US Food and Drug Administration as the first disease-modifying therapy (DMT) for MS MESHD in 1993. Since that time, clinical trials and real-world observational studies have demonstrated the effectiveness of IFN HGNC therapies. The pivotal intramuscular IFN-β HGNC-1a phase 3 trial was the first to demonstrate that a DMT could reduce accumulation of sustained disability in MS MESHD. Patient adherence to treatment is higher with intramuscular IFN-β-1a, given once weekly, than with subcutaneous formulations requiring multiple injections per week. Moreover, subcutaneous IFN-β HGNC-1a is associated with an increased incidence of injection site reactions and neutralizing antibodies compared with intramuscular administration. In recent years, revisions to MS MESHD diagnostic criteria have improved clinicians’ ability to identify patients with MS MESHD and have promoted the use of magnetic resonance imaging (MRI) for diagnosis and monitoring. MRI studies show that treatment with IFN-β-1a, relative to placebo, reduces T2 and gadolinium-enhancing lesions and gray matter atrophy MESHD. Since the approval of intramuscular IFN-β-1a, several high-efficacy therapies have been approved for MS MESHD, though the benefit of these high-efficacy therapies should be balanced against the increased risk of serious adverse events. For some subpopulations of patients, including pregnant women, the safety profile of IFN-β HGNC formulations may provide a particular benefit. In addition, the antiviral properties of IFNs may indicate therapeutic opportunities for IFN-β HGNC in the treatment of viral infections such as COVID-19 MESHD.


    Authors: Luca Elli; Federica Facciotti; Vincenza Lombardo; Alice Scricciolo; David S Sanders; Valentina Vaira; Donatella Barisani; Maurizio Vecchi; Andrea Costantino; Lucia Scaramella; Bernardo Dell'Osso; Luisa Doneda; Leda Roncoroni

    doi:10.1101/2020.12.15.20248039 Date: 2020-12-16 Source: medRxiv

    Objective. The SARS-CoV-2 pandemic has spread across the world causing a dramatic number of infections and deaths MESHD. No data are available about the effects of an infection in patients affected by celiac disease ( CD MESHD) in terms of the development of related symptoms and antibodies. We aimed to investigate the impact of the SARS-CoV-2 pandemic in celiac patients. Design. During a lockdown, the celiac patients living in the Milan area were contacted and interviewed about the development of COVID-19 MESHD symptoms as well as adherence to an anti-virus lifestyle and a gluten-free diet (GFD). They were also given a stress questionnaire to fill in. The development of anti-SARS-CoV-2 IgG and IgA (anti-RBD and N proteins PROTEIN) and the expression of the duodenal ACE2 HGNC receptor were investigated. When available, duodenal histology, anti-tissue transglutaminase IgA (tTGA), presence of immunologic comorbidities and adherence to the GFD were analysed as possible risk factors. Results. 362 celiac patients have been interviewed and 42 (11%) presented with COVID-19 MESHD symptoms. The presence of symptoms was not influenced by tTGA positivity, presence of duodenal atrophy MESHD or adherence to GFD. 37% of the symptomatic patients presented anti-SARS-CoV-2 immunoglobulins (Ig). Globally, 18% of celiac patients showed anti-SARS-CoV-2 Ig vs 25% of the non-celiac control (p=0.18). The values of anti-RBD IgG/IgA and anti-N IgG did not differ from the non-celiac controls. Celiac patients had a significant lower level of anti-N IgA. The ACE2 HGNC receptor was detected in the non-atrophic duodenal mucosa of celiac patients; atrophy MESHD was associated with a lower expression of the ACE2 HGNC receptor. Conclusion. CD MESHD patients have an anti-SARS-CoV-2 Ig positiveness and profile similar to non-celiac controls, except for anti-N IgA. The main celiac parameters and adherence to the GFD do not influence the development of a different Ig profile.

    Short of Breath for the Long Haul: Diaphragm Muscle Dysfunction in Survivors of Severe COVID-19 MESHD as Determined by Neuromuscular Ultrasound

    Authors: Ellen Farr; Alexis R Wolfe; Swati Deshmukh; Leslie Rydberg; Rachna Soriano; James M Walter; Andrea J Boon; Lisa F Wolfe; Colin K. Franz

    doi:10.1101/2020.12.10.20244509 Date: 2020-12-11 Source: medRxiv

    Many survivors from severe coronavirus disease 2019 MESHD ( COVID-19 MESHD) suffer from persistent dyspnea MESHD and fatigue long MESHD after resolution of the active infection. In a cohort of 25 consecutive COVID-19 MESHD survivors admitted to an inpatient rehabilitation hospital (76% male), 80% of them had at least one sonographic abnormality of diaphragm muscle structure or function. Specifically, when compared to established normative data, 76% had reduced diaphragm thickening ratio (impaired contractility), and 20% patients had reduced diaphragm muscle thickness ( atrophy MESHD). These findings support neuromuscular respiratory dysfunction MESHD as a highly prevalent underlying cause for prolonged functional impairments after hospitalization for COVID-19 MESHD.

    Cytokine Signatures of End Organ Injury in COVID-19 MESHD

    Authors: Luis G. Gómez-Escobar; Katherine L. Hoffman; Justin J. Choi; Alain Borczuk; Steven Salvatore; Sergio L. Alvarez-Mulett; Manuel D. Galvan; Zhen Zhao; Sabrina E. Racine-Brzostek; He S. Yang; Heather Winona Stout-Delgado; Mary E Choi; Augustine MK Choi; Soo Jung Cho; Edward J. Schenck

    doi:10.21203/ Date: 2020-12-02 Source: ResearchSquare

    Increasing evidence has shown that Coronavirus disease MESHD 19 ( COVID-19 MESHD) severity is driven by a dysregulated immunologic response. We aimed to assess the differences in inflammatory cytokines in COVID-19 MESHD patients compared to contemporaneously hospitalized controls and then analyze the relationship between these cytokines and the development of Acute Respiratory Distress Syndrome MESHD ( ARDS MESHD), Acute Kidney Injury MESHD ( AKI MESHD) and mortality. In this cohort study of hospitalized patients, done between March third, 2020 and April first, 2020 at a quaternary referral center in New York City we included adult hospitalized patients with COVID-19 MESHD and negative controls. Serum specimens were obtained on the first, second, and third hospital day and cytokines were measured by Luminex. Autopsies of nine cohort patients were examined. We identified 90 COVID-19 MESHD patients and 51 controls. Analysis of 48 inflammatory cytokines revealed upregulation of macrophage induced chemokines, T-cell related interleukines and stromal cell producing cytokines in COVID-19 MESHD patients compared to the controls. Moreover, distinctive cytokine signatures predicted the development of ARDS MESHD, AKI MESHD and mortality in COVID-19 MESHD patients. Specifically, macrophage-associated cytokines predicted ARDS MESHD , T cell immunity related cytokines predicted AKI MESHD and mortality was  was associated with cytokines of activated immune pathways, of which IL-13 HGNC was universally correlated with ARDS MESHD, AKI MESHD and mortality. Histopathological examination of the autopsies showed diffuse alveolar damage MESHD with significant mononuclear inflammatory cell infiltration. Additionally, the kidneys demonstrated glomerular sclerosis MESHD, tubulointerstitial lymphocyte infiltration and cortical and medullary atrophy MESHD. These patterns of cytokine expression offer insight into the pathogenesis of COVID-19 MESHD disease, its severity, and subsequent lung and kidney injury MESHD suggesting more targeted treatment strategies. 

    The Novel Severe Acute Respiratory Syndrome Coronavirus 2(SARS-CoV-2) Directly Decimates Human Spleens and Lymph Nodes

    Authors: yongwen chen; Zeqing Feng; Bo Diao; Rongshuai Wang; Gang Wang; Chenhui Wang; Yingjun Tan; Liang Liu; Changsong Wang; Ying Liu; Yueping Liu; Zilin Yuan; Liang Ren; Yuzhang Wu

    doi:10.1101/2020.03.27.20045427 Date: 2020-03-31 Source: medRxiv

    While lymphocytopenia MESHD is a common characteristic of patients infected by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the mechanisms responsible for this depletion are unclear. Through careful inspection of the spleens and lymph nodes (LNs) from six cases with postmortem examinations, we observed that SARS-CoV-2 could directly infect secondary lymphoid organs to induce cell death. Immunohistochemistry demonstrated ACE2 HGNC ( angiotensin-converting enzyme 2 HGNC), the potential receptor of SARS-CoV-2, expresses on tissue-resident CD169+ macrophages in spleens and LNs. Immunofluorescent staining confirmed that viral nucleocaspid protein (NP) can be found in ACE2 HGNC+ cells, CD169+ macrophages, but not in CD3+ T cells or B220+ B cells in spleens and LNs. SARS-CoV-2 infection MESHD induces severe tissue damage including lymph follicle depletion, splenic nodule atrophy MESHD, histiocyte hyperplasia MESHD and lymphocyte reductions. Moreover, in situ TUNEL staining illustrated that viral infection leads to severe lymphocyte apoptosis, which might be mediated by viral antigens inducing Fas upregulation. Furthermore, SARS-CoV-2 also triggers macrophages to produce IL-6 HGNC, a proinflammatory cytokine that directly promotes lymphocyte necrosis MESHD. Collectively, these results demonstrate that SARS-CoV-2 directly neutralizes human spleens and LNs through infecting tissue- resident CD169+ macrophages.

    Clinical Pathology of Critical Patient with Novel Coronavirus Pneumonia ( COVID-19 MESHD)

    Authors: Weiren Luo; Hong Yu; Jizhou Gou; Xiaoxing Li; Yan Sun; Jinxiu Li; Lei Liu

    id:202002.0407/v4 Date: 2020-03-09 Source:

    Background Critical patients with novel coronavirus pneumonia MESHD ( COVID-19 MESHD) have worse outcome and high mortality. However, the histopathology of critical patient with COVID-19 MESHD remains undisclosed. Methods We performed the whole lung biopsy, and described the pathological changes of critical COVID-19 MESHD patient done with transplant by HE staining, immunohistochemistry and special staining observed under the microscopy. Findings The whole lungs displayed diffuse congestive appearance and partly haemorrhagic necrosis MESHD on gross examination. The haemorrhagic necrosis MESHD was prominently present in outer edge of the right lower lung. The cut surfaces of the lung displayed severe congestive and haemorrhagic changes. The main pathological changes showed massive pulmonary interstitial fibrosis MESHD, and partly hyaline degeneration MESHD, variable degrees of hemorrhagic pulmonary infarction MESHD. Small vessels hyperplasia MESHD, vessel wall thickening, lumen stenosis, occlusion and microthrombosis MESHD formation. Focal monocytes, lymphocytes and plasma cells infiltrating into pulmonary interstitium. Bronchiolitis and alveolitis MESHD with proliferation, atrophy MESHD, desquamation MESHD and squamous MESHD metaplasia of epithelial cells. Atrophy MESHD, vacuolar degeneration, proliferation, desquamation MESHD and squamous MESHD metaplasia in alveolar epithelial MESHD cells. Alveolar MESHD cavity congestion was prominent, and contained mucus, edema MESHD fluid, desquamated epithelial cells, and inflammatory cells. We also found several multinucleate giant cells and intracytoplasmic viral inclusion bodies. Special stains including Masson stain, sirius red staining, reticular fibers staining indicated massive pulmonary interstitial fibrosis MESHD. Immunohistochemistry showed positive for immunity cells including CD3, CD4 HGNC, CD8 HGNC, CD20 HGNC, CD79a HGNC, CD5 HGNC, CD38 HGNC and CD68 HGNC. Interpretation We demonstrate the pathological findings of critical patient with COVID-19 MESHD, which might provide a deep insight of the pathogenesis and severity of this disease.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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