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Outcome Stratified Analysis of Biomarker Trajectories for Patients With SARS-CoV-2 Infection.

ABSTRACT: Longitudinal trajectories of vital signs and biomarkers during admission remain poorly characterized for COVID-19 patients despite their potential to provide critical insights about disease progression. We studied 1884 patients with SARS-CoV2 infection from 3/4/2020-6/25/2020 within one Maryland hospital system and used a retrospective longitudinal framework with linear mixed-effects models to investigate relevant biomarker trajectories leading up to three critical outcomes: mechanical ventilation, discharge, and death. Trajectories of four vital signs (respiratory rate, SpO2/FiO2, pulse, and temperature) and four lab values (C-reactive protein (CRP), absolute lymphocyte count (ALC), estimated glomerular filtration rate (eGFR), and D-dimer) clearly distinguished the trajectories of COVID-19 patients. Prior to any ventilation, log-CRP, log-ALC, respiratory rate, and SpO2/FiO2 trajectories diverge approximately 8-10 days before discharge or death. Following ventilation, log-CRP, log-ALC, respiratory rate, SpO2/FiO2, and eGFR trajectories again diverge 10-20 days prior to death or discharge. Trajectories improved until discharge and remained unchanged or worsened until death. Our approach characterizes the distribution of biomarker trajectories leading up to competing outcomes of discharge versus death. Moving forward, this model can contribute to quantifying the joint probability of future biomarkers and outcomes provided clinical data up to a given moment.

SUBMITTER: Bowring MG

PROVIDER: S-EPMC8241476 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Characteristics and Outcome of SARS-CoV-2 Infection in Cancer Patients.

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| S-EPMC7665636 | biostudies-literature

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2021-09-20 | GSE167202 | GEO

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2013-07-31 | E-GEOD-47960 | biostudies-arrayexpress

SHAE003: SARS-CoV, SARS-dORF6 and SARS-BatSRBD infection of HAE cultures.

Project description:HAE cultures were infected with SARS-CoV, SARS-ddORF6 or SARS-BatSRBD and were directly compared to A/CA/04/2009 H1N1 influenza-infected cultures. Cell samples were collected at various hours post-infection for analysis. Time Points = 0, 12, 24, 36, 48, 60, 72, 84 and 96 hrs post-infection for SARS-CoV. Time Points = 0, 24, 48, 60, 72, 84 and 96 hrs post-infection forSARS-ddORF6 and SARS-BatSRBD. Time Points = 0, 6, 12, 18, 24, 36 and 48 hrs post-infection for H1N1. Done in triplicate/quadruplicate for RNA Triplicates/quadruplicates are defined as 3/4 different wells, plated at the same time and using the same cell stock for all replicates. Time matched mocks done in triplicate from same cell stock as rest of samples. Culture medium (the same as what the virus stock is in) will be used for the mock infections. Infection was done at an MOI of 2.

2013-07-31 | E-GEOD-47961 | biostudies-arrayexpress

SHAE004: SARS-CoV, SARS-dORF6 and SARS-BatSRBD infection of HAE cultures.

Project description:HAE cultures were infected with SARS-CoV, SARS-dORF6 or SARS-BatSRBD and were directly compared to A/CA/04/2009 H1N1 influenza-infected cultures. Cell samples were collected at various hours post-infection for analysis. Time Points = 0, 12, 24, 36, 48, 60, 72, 84 and 96 hrs post-infection for SARS-CoV, SARS-dORF6 and SARS-BatSRBD. Time Points = 0, 6, 12, 18, 24, 36 and 48 hrs post-infection for H1N1. Done in triplicate for RNA Triplicates are defined as 3 different wells, plated at the same time and using the same cell stock for all replicates. Time matched mocks done in triplicate from same cell stock as rest of samples. Culture medium (the same as what the virus stock is in) will be used for the mock infections. Infection was done at an MOI of 2 for SARS viruses and an MOI of 1 for H1N1.

2013-07-31 | E-GEOD-47962 | biostudies-arrayexpress

Opposing activities of IFITM proteins in SARS-CoV-2 infection

Project description:Interferon-induced transmembrane proteins (IFITMs) restrict infections by many viruses, but a subset of IFITMs enhance infections by specific coronaviruses through currently unknown mechanisms. We show that SARS-CoV-2 Spike-pseudotyped virus and genuine SARS-CoV-2 infections are generally restricted by human and mouse IFITM1, IFITM2, and IFITM3, using gain- and loss-of-function approaches. Mechanistically, SARS-CoV-2 restriction occurred independently of IFITM3 S-palmitoylation, indicating a restrictive capacity distinct from reported inhibition of other viruses. In contrast, the IFITM3 amphipathic helix and its amphipathic properties were required for virus restriction. Mutation of residues within the IFITM3 endocytosis-promoting Yxx? motif converted human IFITM3 into an enhancer of SARS-CoV-2 infection, and cell-to-cell fusion assays confirmed the ability of endocytic mutants to enhance Spike-mediated fusion with the plasma membrane. Overexpression of TMPRSS2, which increases plasma membrane fusion versus endosome fusion of SARS-CoV-2, attenuated IFITM3 restriction and converted amphipathic helix mutants into infection enhancers. In sum, we uncover new pro- and anti-viral mechanisms of IFITM3, with clear distinctions drawn between enhancement of viral infection at the plasma membrane and amphipathicity-based mechanisms used for endosomal SARS-CoV-2 restriction.

| S-SCDT-EMBOJ-2020-106501 | biostudies-other

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Project description:The antiviral immune response to SARS-CoV-2 infection can limit viral spread and prevent development of pneumonic COVID-19. However, the protective immunological response associated with successful viral containment in the upper airways remain unclear. Here, we combine a multiomics approach with longitudinal sampling to reveal temporally resolved protective immune signatures in non-pneumonic and ambulatory SARS-CoV-2 infected patients and associate specific immune trajectories with upper airway viral containment. We see a distinct systemic rather than local immune state associated with viral containment, characterized by interferon stimulated gene (ISG) upregulation across circulating immune cell subsets in non-pneumonic SARS-CoV2 infection. We report reduced cytotoxic potential of Natural Killer (NK) and T cells, and an immune-modulatory monocyte phenotype with protective immunity in COVID-19. Together, we show protective immune trajectories in SARS-CoV2 infection, which have important implications for patient prognosis and the development of immunomodulatory therapies.

2022-01-17 | GSE193708 | GEO

Host methylation predicts SARS-CoV-2 infection and clinical outcome.

Project description:BackgroundSince the onset of the SARS-CoV-2 pandemic, most clinical testing has focused on RT-PCR1. Host epigenome manipulation post coronavirus infection2-4 suggests that DNA methylation signatures may differentiate patients with SARS-CoV-2 infection from uninfected individuals, and help predict COVID-19 disease severity, even at initial presentation.MethodsWe customized Illumina's Infinium MethylationEPIC array to enhance immune response detection and profiled peripheral blood samples from 164 COVID-19 patients with longitudinal measurements of disease severity and 296 patient controls.ResultsEpigenome-wide association analysis revealed 13,033 genome-wide significant methylation sites for case-vs-control status. Genes and pathways involved in interferon signaling and viral response were significantly enriched among differentially methylated sites. We observe highly significant associations at genes previously reported in genetic association studies (e.g. IRF7, OAS1). Using machine learning techniques, models built using sparse regression yielded highly predictive findings: cross-validated best fit AUC was 93.6% for case-vs-control status, and 79.1%, 80.8%, and 84.4% for hospitalization, ICU admission, and progression to death, respectively.ConclusionsIn summary, the strong COVID-19-specific epigenetic signature in peripheral blood driven by key immune-related pathways related to infection status, disease severity, and clinical deterioration provides insights useful for diagnosis and prognosis of patients with viral infections.

| S-EPMC8767772 | biostudies-literature

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