preVIEW: COVID-19

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MeSH Disease

COVID-19 (127)

Inflammation (31)

Severe Acute Respiratory Syndrome (24)

Necrosis (20)

Coronavirus Infections (17)


HGNC Genes

tumor necrosis factor (127)

interleukin 6 (78)

interleukin 10 (28)

C-X-C motif chemokine ligand 8 (25)

interferon gamma (24)


SARS-CoV-2 proteins

ProteinS (11)

NSP5 (4)

ProteinN (2)

ProteinS1 (2)

NSP2 (1)


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    SARS-CoV-2 infection MESHD in the Syrian hamster model causes inflammation MESHD as well as type I interferon dysregulation MESHD in both respiratory and non-respiratory tissues including the heart and kidney

    Authors: Magen Francis; Una Goncin; Andrea Kroeker; Cynthia Swan; Robyn Ralph; Yao Lu; Athema Etzioni; Darryl Falzarano; Volker Gerdts; Steve Machtaler; Jason Kindrachuk; Alyson Ann Kelvin

    doi:10.1101/2021.04.07.438843 Date: 2021-04-08 Source: bioRxiv

    COVID-19 MESHD ( coronavirus disease 2019 MESHD) caused SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection MESHD is a disease affecting several organ systems. A model that captures all clinical symptoms of COVID-19 MESHD as well as long-haulers disease is needed. We investigated the host responses associated with infection in several major organ systems including the respiratory tract, the heart, and the kidneys after SARS-CoV-2 infection MESHD in Syrian hamsters. We found significant increases in inflammatory cytokines ( IL-6 HGNC, IL-1beta HGNC, and TNF HGNC) and type II interferons whereas type I interferons were inhibited. Examination of extrapulmonary tissue indicated inflammation MESHD in the kidney, liver, and heart which also lacked type I interferon upregulation. Histologically, the heart had evidence of mycarditis and microthrombi while the kidney had tubular inflammation MESHD. These results give insight into the multiorgan disease experienced by people with COVID-19 MESHD and possibly the prolonged disease in people with post-acute sequelae of SARS-CoV-2 (PASC).

    Relative expression of pro-inflammatory molecules in COVID-19 MESHD patients manifested disease severities.

    Authors: Shireen Nigar; SM Tanjil Shah; Ali Ahasan Setu; Sourav Dutta Dip; Habiba Ibnat; M. Touhid Islam; Selina Akter; Iqbal Kabir Jahid; Md. Anwar Hossain

    doi:10.1101/2021.04.01.21254770 Date: 2021-04-07 Source: medRxiv

    Aggressive immune response, due to over-expressed pro-inflammatory molecules, had been characterized in COVID-19 MESHD patients. Some of those mediators have a dual and opposite role on immune-systems to play behind differential disease severities. We investigated the expression of some cytokines and chemokines in COVID-19 MESHD patients in Bangladesh. We diagnosed the patients by detecting SARS-CoV-2 RNA in nasal swab samples by the real-time RT-PCR method. Thirty adult patients were preselected based on their disease severities and grouped into mild, moderate, and severe cases. Nine healthy volunteers participated in this study as control. Relative expression of nine cytokines/chemokine in total leukocytes was semi-quantified in SYBRgreen-based qRT-PCR. We performed statistical tests on transformed log data using SPSS 24.0. At the onset of symptoms (day-1), ACE2 HGNC (P < 0.05) and IL-6 HGNC (P > 0.05) were up-regulated in all COVID-19 MESHD groups, although expression levels did not significantly correlate with disease severities. However, expression of IL-6 HGNC, MCP-1 HGNC, MIP-1 HGNC, TNF- HGNC, RANTES HGNC, and ACE2 HGNC, on day-14, were positively correlated with disease severities. Relative viral load at day-1 showed no significant correlation with cytokine expression but had a significant positive correlation with RANTES HGNC and ACE2 HGNC expression on day-14 (P < 0.05). Male patients had a higher level of IL-6 HGNC than female patients on day-1 (P < 0.05). All COVID-19 MESHD patients showed up-regulated cytokines and chemokines on the day-14 compared to day-1 except TNF HGNC-. Female patients had higher expression of ACE2 HGNC and IL-12 on day-14. Up-regulated cytokines/chemokines at the convalescent stage, especially IL-6 HGNC, may target anti-cytokine therapy in post- COVID-19 MESHD patients management.

    IL-6 HGNC and D-Dimer at Admission Predicts Cardiac Injury MESHD and Early Mortality during SARS-CoV-2 Infection MESHD

    Authors: Daoyuan Si; Beibei Du; Bo Yang; Lina Jin; Lujia Ni; Qian Zhang; Zhongfan Zhang; Mohammed Ali Azam; Patrick F.H Lai; Stephane Masse; Huan Sun; Xingtong Wang; Slava Epelman; Patrick R Lawler; Ping Yang; Kumaraswamy Nanthakumar

    doi:10.1101/2021.03.22.21254077 Date: 2021-03-29 Source: medRxiv

    BACKGROUND: We recently described mortality of cardiac injury MESHD in COVID-19 MESHD patients. Admission activation of immune, thrombotic MESHD biomarkers and their ability to predict cardiac injury MESHD and mortality patterns in COVID-19 MESHD is unknown. METHODS: This retrospective cohort study included 170 COVID-19 MESHD patients with cardiac injury MESHD at admission to Tongji Hospital in Wuhan from January 29-March 8, 2020. Temporal evolution of inflammatory cytokines, coagulation markers, clinical, treatment and mortality were analyzed. RESULTS: Of 170 patients, 60 (35.3%) died early (<21d) and 61 (35.9%) died after prolonged stay. Admission lab work that correlated with early death MESHD were elevate levels of interleukin 6 HGNC ( IL-6 HGNC) (p<0.0001), Tumor Necrosis Factor-a HGNC Tumor Necrosis Factor-a MESHD ( TNF-a HGNC) (p=0.0025), and C-reactive protein HGNC ( CRP HGNC) (p<0.0001). We observed the trajectory of biomarker changes after admission, and determined that early mortality had a rapidly increasing D-dimer, gradually decreasing platelet and lymphocyte counts. Multivariate and simple linear regression models showed that death risk was determined by immune and thrombotic MESHD pathway activation. Increasing cTnI HGNC levels were associated with those of increasing IL-6 HGNC (p=0.03) and D-dimer (p=0.0021). Exploratory analyses suggested that patients that received heparin has lower early mortality compared to those who did not (p =0.07), despite similar risk profile. CONCLUSIONS: In COVID-19 MESHD patients with cardiac injury MESHD, admission IL-6 HGNC and D-dimer predicted subsequent elevation of cTnI HGNC and early death MESHD, highlighting the need for early inflammatory cytokine-based risk stratification in patients with cardiac injury MESHD.

    Authors: Natalia G Sampaio; Lise Chauveau; Jonny Hertzog; Anne Bridgeman; Gerissa Fowler; Jurgen P Moonen; Maeva Dupont; Rebecca A Russel; Marko Noerenberg; Jan Rehwinkel

    doi:10.1101/2021.03.26.437180 Date: 2021-03-27 Source: bioRxiv

    Human cells respond to infection by SARS-CoV-2, the virus that causes COVID-19 MESHD, by producing cytokines including type I and III interferons (IFNs) and proinflammatory factors such as IL6 HGNC and TNF HGNC. IFNs can limit SARS-CoV-2 replication but cytokine imbalance contributes to severe COVID-19 MESHD. We studied how cells detect SARS-CoV-2 infection MESHD. We report that the cytosolic RNA sensor MDA5 HGNC was required for type I and III IFN induction in the lung cancer MESHD cell line Calu-3 upon SARS-CoV-2 infection MESHD. Type I and III IFN HGNC induction further required MAVS HGNC and IRF3 HGNC. In contrast, induction of IL6 HGNC and TNF HGNC was independent of the MDA5 HGNC- MAVS HGNC- IRF3 HGNC axis in this setting. We further found that SARS-CoV-2 infection MESHD inhibited the ability of cells to respond to IFNs. In sum, we identified MDA5 HGNC as a cellular sensor for SARS-CoV-2 infection MESHD that induced type I MESHD and III IFNs.

    The polymorphism L412F in TLR3 HGNC inhibits autophagy and is a marker of severe COVID-19 MESHD in males.

    Authors: Susanna Croci; Mary Anna Venneri; Stefania Mantovani; Chiara Fallerini; Elisa Benetti; Nicola Picchiotti; Federica Campolo; Francesco Imperatore; Maria Palmieri; Sergio Daga; Chiara Gabbi; Francesca Montagnani; Giada Beligni; Ticiana D.J. Farias; Miriam L. Carriero; Laura Di Sarno; Diana Alaverdian; Sigrid Aslaksen; Maria Vittoria Cubellis; Ottavia Spiga; Margherita Baldassarri; Francesca Fava; Paul J. Norman; Elisa Frullanti; Andrea M. Isidori; Antonio Amoroso; Francesca Mari; Simone Furini; Mario Mondelli; - GEN-COVID Multicenter Study; Mario Chiariello; Alessandra Renieri; Ilaria Meloni

    doi:10.1101/2021.03.23.21254158 Date: 2021-03-26 Source: medRxiv

    The polymorphism L412F in TLR3 HGNC has been associated with several infectious diseases MESHD. However, the mechanism underlying this association is still unexplored. Here, we show that the L412F polymorphism in TLR3 HGNC is a marker of severity in COVID-19 MESHD. This association increases in the sub-cohort of males. Impaired autophagy and reduced TNF HGNC production was demonstrated in HEK293 cells transfected with TLR3 HGNC-L412F plasmid and stimulated with specific agonist poly(I:C). A statistically significant reduced survival at 28 days was shown in L412F COVID-19 MESHD patients treated with the autophagy-inhibitor hydroxychloroquine (P=0.038). An increased frequency of autoimmune disorders MESHD as co-morbidity was found in L412F COVID-19 MESHD males with specific class II HLA haplotypes prone to autoantigen presentation. Our analyses indicate that L412F polymorphism makes males at risk of severe COVID-19 MESHD and provides a rationale for reinterpreting clinical trials considering autophagy pathways.

    Transcriptome analysis of PBMCs reveals distinct immune response in the asymptomatic and re-detectable positive COVID-19 MESHD patients

    Authors: Jiaqi Zhang; Dongzi Lin; Kui Li; Xiangming Ding; Lin Li; Yuntao Liu; Dongdong Liu; Jing Lin; Xiangyun Teng; Yizhe Li; Ming Liu; Xiaodan Wang; Dan He; Yaling Shi; Dawei Wang; Jianhua Xu

    doi:10.1101/2021.03.16.21251286 Date: 2021-03-24 Source: medRxiv

    The existence of asymptomatic and re-detectable positive COVID-19 MESHD patients presents the disease control challenges of COVID-19 MESHD. Most studies on immune response of COVID-19 MESHD have focused on the moderately or severely symptomatic patients, however little is known about the immune response in asymptomatic and re-detectable positive patients. Here we performed a comprehensive analysis of the transcriptomic profiles of PBMCs from 48 COVID-19 MESHD patients which include 8 asymptomatic, 13 symptomatic, 15 recovering and 12 RP MESHD patients. Our analysis revealed a down-regulation of IFN response and complement activation in the asymptomatic patients compared with the symptomatic, indicating a weaker immune response of the PBMCs in the asymptomatic patients. In addition, we observed a lower expression of the cytokines and chemokines in the PBMC of asymptomatic and symptomatic patients. In contrast, the cytokines and chemokines level in the RP patients are higher than the recovering. GSEA analysis showed the enrichment of TNFa HGNC/ NF-{kappa}B HGNC and influenza infection MESHD in the RP MESHD patients compared with the recovering patients, indicating a flu-like, hyper-inflammatory immune response in the PBMC of RP MESHD patients. Thus our findings could extend our understanding of host immune response during the progression COVID-19 MESHD disease and help the clinical management and the immunotherapy development for COVID-19 MESHD.

    Serological response to COVID-19 MESHD vaccination in IBD MESHD patients receiving biologics

    Authors: Serre-Yu Wong; Rebekah Dixon; Vicky Martinez Pazos; - ICARUS-IBD; Sacha Gnjatic; Jean-Frederic Colombel; Ken Cadwell

    doi:10.1101/2021.03.17.21253848 Date: 2021-03-20 Source: medRxiv

    Objective The impact of medications on COVID-19 MESHD vaccine efficacy in IBD MESHD patients is unknown, as patients with immunosuppressed states and/or treated with immunosuppressants were excluded from vaccine trials. To address this, we evaluated serological responses to COVID-19 MESHD vaccination with the SARS-CoV-2 spike MESHD SARS-CoV-2 spike PROTEIN (S) mRNA BNT162b2 (Pfizer-BioNTech) and mRNA-1273 (NIH-Moderna) vaccines in IBD MESHD patients enrolled in an ongoing SARS-CoV-2 sero-survey at the Icahn School of Medicine at Mount Sinai in New York City. Design We obtained sera from 48 patients who had undergone vaccination with one or two vaccine doses. Sera were tested for SARS-CoV-2 anti-RBD total immunoglobulins and IgG (Siemens COV2T and sCOVG assays), anti-Spike IgG (in-house ELISA), and anti-nucleocapsid antibodies (Roche). Results All IBD MESHD patients (15/15) who completed two-dose vaccine schedules achieved seroconversion to high levels. Two IBD MESHD patients with history of COVID-19 MESHD infections and who were seropositive at baseline seroconverted to high levels after the first dose. Concurrent biologic use was 85% (41/48), including 33% of patients (16) on TNF HGNC antagonist monotherapy, 42% (17) on vedolizumab monotherapy, 6% (3) on vedolizumab combination therapy with thiopurine, and 8% (4) ustekinumab; 1 patient was receiving guselkumab for psoriasis MESHD. Three patients (6%) were on oral steroids at the time of vaccination. Conclusion IBD MESHD patients receiving biologics can seroconvert with robust serological responses after complete Pfizer-BioNTech and NIH-Moderna COVID-19 MESHD vaccination. In IBD-patients with previous SARS-CoV-2 seroconversion, a single dose of either vaccine can induce high index values, mirroring findings from the general population.

    Genetic variability associated with OAS1 HGNC expression in myeloid cells increases the risk of Alzheimer's disease MESHD and severe COVID-19 MESHD outcomes

    Authors: Naciye Magusali; Andrew C Graham; Thomas M Piers; Pantila Panichnantakul; Umran Yaman; Maryam Shoai; Regina H Reynolds; Juan A. Botia; Keeley J Brookes; Tamar Guetta-Baranes; Eftychia Bellou; Sevinc Bayram; Dimitra Sokolova; Mina Ryten; Carlo Sala Frigerio; Valentina Escott-Price; Kevin Morgan; Jennifer M Pocock; John Hardy; Dervis A Salih

    doi:10.1101/2021.03.16.435702 Date: 2021-03-18 Source: bioRxiv

    Genome-wide association studies of late-onset Alzheimer's disease MESHD ( AD MESHD) have highlighted the importance of variants associated with genes expressed by the innate immune system in determining risk for AD MESHD. Recently, we and others have shown that genes associated with variants that confer risk for AD MESHD are significantly enriched in transcriptional networks expressed by amyloid-responsive microglia. This allowed us to predict new risk genes for AD MESHD, including the interferon-responsive oligoadenylate synthetase 1 ( OAS1 HGNC). However, the function of OAS1 HGNC within microglia and its genetic pathway are not known. Using genotyping from 1,313 individuals with sporadic AD MESHD and 1,234 control individuals, we confirm that the OAS1 HGNC variant, rs1131454, is associated with increased risk for AD MESHD and decreased OAS1 HGNC expression. Moreover, we note that the same locus was recently associated with critical illness MESHD in response to COVID-19 MESHD, linking variants that are associated with AD MESHD and a severe response to COVID-19 MESHD. By analysing single-cell RNA-sequencing (scRNA-seq) data of isolated microglia from APPNL-G-F knock-in and wild-type C57BL/6J mice, we identify a transcriptional network that is significantly upregulated with age and amyloid deposition, and contains the mouse orthologue Oas1a, providing evidence that Oas1a plays an age-dependent function in the innate immune system. We identify a similar interferon-related transcriptional network containing OAS1 HGNC by analysing scRNA-seq data from human microglia isolated from individuals with AD MESHD. Finally, using human iPSC-derived microglial cells (h-iPSC-Mg), we see that OAS1 HGNC is required to limit the pro-inflammatory response of microglia. When stimulated with interferon-gamma HGNC ( IFN-{gamma} HGNC), we note that cells with lower OAS1 HGNC expression show an exaggerated pro-inflammatory response, with increased expression and secretion of TNF HGNC-. Collectively, our data support a link between genetic risk for AD MESHD and susceptibility to critical illness with COVID-19 MESHD centred on OAS1 HGNC and interferon signalling, a finding with potential implications for future treatments of both AD MESHD and COVID-19 MESHD, and the development of biomarkers to track disease progression.

    SARS-CoV-2 spike PROTEIN protein induces inflammation MESHD via TLR2 HGNC-dependent activation of the NF-κB pathway

    Authors: Shahanshah Khan; Mahnoush S. Shafiei; Christopher Longoria; John Schoggins; Rashmin C. Savani; Hasan Zaki

    doi:10.1101/2021.03.16.435700 Date: 2021-03-17 Source: bioRxiv

    Pathogenesis of COVID-19 MESHD is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation MESHD is poorly understood. Here we investigated direct inflammatory functions of major structural proteins of SARS-CoV-2. We observed that spike (S) protein PROTEIN potently induces inflammatory cytokines and chemokines including IL-6 HGNC, IL-1b HGNC, TNFa HGNC, CXCL1 HGNC, CXCL2 HGNC, and CCL2 HGNC, but not IFNs in human and mouse macrophages. No such inflammatory response was observed in response to membrane (M), envelope (E), and neucleocapsid ( N) proteins PROTEIN. When stimulated with extracellular S protein PROTEIN, human lung epithelial cells A549 also produce inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein PROTEIN intracellularly are non-inflammatory, but elicit an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein PROTEIN triggers inflammation MESHD via activation of the NF-kB pathway in a MyD88 HGNC-dependent manner. Further, such an activation of the NF-kB pathway is abrogated in Tlr2 HGNC-deficient macrophages. Consistently, administration of S protein PROTEIN induces IL-6, TNF-a, and IL-1b in wild-type, but not Tlr2-deficient mice. Together these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection MESHD and suggest that TLR2 could be a potential therapeutic target for COVID-19 MESHD.

    Soluble angiotensin-converting enzyme 2 HGNC is transiently elevated in COVID-19 MESHD and correlates with specific inflammatory and endothelial markers

    Authors: Annika Lundstrom; Louise Ziegler; Sebastian Havervall; Ann-Sofie Rudberg; Fien Von Meijenfeldt; Ton Lisman; Nigel Mackman; Per Sanden; Charlotte Thalin

    doi:10.1101/2021.03.03.21252841 Date: 2021-03-05 Source: medRxiv

    RationaleAngiotensin-converting enzyme 2 ( ACE2 HGNC) is the main entry receptor of severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), but how SARS-CoV-2 interactions with ACE2 HGNC influences the renin-angiotensin system (RAS) in Coronavirus disease 2019 MESHD ( COVID-19 MESHD) is unknown. ObjectiveTo measure circulating ACE2 HGNC and ACE HGNC levels in COVID-19 MESHD patients and investigate association with risk factors, outcome and inflammatory markers. Methods and resultsSoluble ACE2 HGNC (sACE2) and sACE concentrations were measured by ELISA in plasma samples from 114 hospital-treated COVID-19 MESHD patients and 10 healthy controls. Follow-up samples after four months were available for 58/114 patients. Von Willebrand MESHD Von Willebrand HGNC factor ( VWF HGNC), factor VIII ( fVIII HGNC), D-dimer, interleukin 6 ( IL-6 HGNC), tumor necrosis MESHD factor and plasminogen activator inhibitor 1 ( PAI-1 HGNC) had previously been determined. Levels of sACE2 were higher in COVID-19 MESHD patients than in healthy controls, median 5.0 (interquartile range 2.8-11.8) ng/ml versus 1.4 (1.1-1.6) ng/ml, p < 0.0001. sACE2 was higher in men than women, but were not affected by other risk factors for severe COVID-19 MESHD. sACE 2 decreased to 2.3 (1.6-3.9) ng/ml at follow-up, p < 0.0001, but remained higher than in healthy controls, p=0.012. Follow-up sACE2 levels were higher with increasing age, BMI, total number of comorbidities, for patients with diabetes MESHD and patients on RAS-inhibition. sACE was marginally lower during COVID-19 MESHD compared with at follow-up, 57 (45-70) ng/ml versus 72 (52-87) ng/ml, p=0.008. Levels of sACE2 and sACE did not differ depending on survival or disease severity (care level, respiratory support). sACE2 during COVID-19 MESHD correlated with VWF HGNC, fVIII HGNC and D-dimer, while sACE correlated with IL-6 HGNC, TNF HGNC and PAI-1 HGNC. ConclusionssACE2 was transiently elevated in COVID-19 MESHD, likely due to increased shedding from infected cells. sACE2 and sACE during COVID-19 MESHD differed distinctly in their correlations with markers of inflammation MESHD and endothelial dysfunction, suggesting release from different cell types and/or vascular beds.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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