Clinical and Virological Characteristics of Hospitalized COVID-19 Patients in a German Tertiary Care Center during the First Wave of the SARS-CoV-2 Pandemic

Thibeault, Charlotte; Muehlemann, Barbara; Helbig, Elisa T; Mittermaier, Mirja; Lingscheid, Tilman; Tober‐Lau, Pinkus; Meyer-Arndt, Lil; Meiners, Leonie; Stubbemann, Paula; Haenel, Sascha S.; Jarcy, Laure Bosquillon de; Lippert, Lena J; Pfeiffer, Moritz; Stegemann, Miriam; Roehle, Robert; Wiebach, Janine; Hippenstiel, Stefan; Zöller, Thomas; Mueller-Redetzky, Holger; Uhrig, Alexander; Balzer, Felix; Kalle, Christoph von; Suttorp, Norbert; Jones, Terry C.; Drosten, Christian; Witzenrath, Martin; Sander, Leif Erik; Corman, Victor M.; Kurth, Florian

doi:10.1101/2020.12.12.20247726

Cited by 11 publications

(10 citation statements)

References 45 publications

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“…1,4 One study demonstrated a higher peak viral load and longer duration of viral shedding in 71 ventilated compared to 90 non-ventilated hospitalised patients, though initial viral loads were similar. 14 Like our findings, a large study of 3712 positive samples showed no association of viral load with age, and there has not been clear association of viral load with gender. 15 While not the focus of our study, quantitative SARS-CoV-2 results have been examined for associations with infectivity, most recently for the Delta SARS-CoV-2 variant for which Ct values on the day of first detection were lower compared to clade 19A/19B viruses (average Ct 24 versus 34 for an in-house ORF1ab gene assay).…”

Section: Discussioncontrasting

confidence: 58%

Clinical associations of SARS-CoV-2 viral load using the first WHO International Standard for SARS-CoV-2 RNA

2022

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SARS-CoV-2 viral load declines from the time of symptom onset; in some studies viral load is higher or persists longer in more severe COVID-19 infection, and viral load correlates with culture positivity. This was a retrospective cohort study of inpatients and outpatients during the first wave of COVID-19 infection in Western Australia, March to May 2020, of the relationship of SARS-CoV-2 viral load (using the First WHO International Standard for SARS-CoV-2 RNA) from symptom onset, by clinical subgroups determined from the public health database and hospital records, using regression analysis. We studied 320 samples from 201 COVID-19 cases: 181 mild, seven severe, 11 critical, and four cases who died (two were also critical cases). At symptom onset the mean viral load was 4.34 log 10 IU/mL (3.92–4.77 log 10 IU/mL 95% CI, cobas SARS-CoV-2 assay ORF1a Ct 28.9 cycles). The mean viral load change was –0.09 log 10 IU/mL/day (–0.12 to –0.06 95% CI). R 2 was 0.08 and residual standard deviation 2.68 log 10 IU/mL. Viral load at symptom onset was higher for those reporting fever compared to those not reporting fever. Viral load kinetics were not different for gender, age, shortness of breath, or those requiring oxygen. Mean viral load at usual release from isolation at 14 days was 2.5 log 10 IU/mL or day 20 was 1.8 log 10 IU/mL. Variability in respiratory sample SARS-CoV-2 viral load kinetics suggests viral loads will only have a role supporting clinical decision making, and an uncertain role for prognostication.

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Section: Discussioncontrasting

confidence: 58%

Clinical associations of SARS-CoV-2 viral load using the first WHO International Standard for SARS-CoV-2 RNA

2022

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“…Diagnosis was made based on detection of SARS-CoV-2 viral RNA using a reverse transcription-polymerase chain reaction (RT-PCR) test from nasopharyngeal swabs and/or detection of SARS-CoV-2 specific antibodies in the blood through enzyme-linked immunosorbent assay (ELISA). Sample collection took place during the first peak of the pandemic at six European Hospitals: Germany: Charite Universitaetsmedizin Berlin (3 sites, total 135 patients, DS1) [ 19 , 20 ]; Spain: Hospital Universitario de Valme, Sevilla (total 115 patients, first part of DS2), Hospital Universitario San Cecilio, Granada (total 18 patients, second part of DS2) and Switzerland: Kantonsspital Baden AG, Baden (total 20 patients, third part of DS2). All patients with COVID-19, who provided informed consent and were 18 years or older were included.…”

Section: Methodsmentioning

confidence: 99%

Increased risk of severe clinical course of COVID-19 in carriers of HLA-C*04:01

Weiner¹,

Suwalski²,

Holtgrewe³

et al. 2021

EClinicalMedicine

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Background Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, there has been increasing urgency to identify pathophysiological characteristics leading to severe clinical course in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Human leukocyte antigen alleles (HLA) have been suggested as potential genetic host factors that affect individual immune response to SARS-CoV-2. We sought to evaluate this hypothesis by conducting a multicenter study using HLA sequencing. Methods We analyzed the association between COVID-19 severity and HLAs in 435 individuals from Germany ( n = 135), Spain ( n = 133), Switzerland ( n = 20) and the United States ( n = 147), who had been enrolled from March 2020 to August 2020. This study included patients older than 18 years, diagnosed with COVID-19 and representing the full spectrum of the disease. Finally, we tested our results by meta-analysing data from prior genome-wide association studies (GWAS). Findings We describe a potential association of HLA-C*04:01 with severe clinical course of COVID-19. Carriers of HLA-C*04:01 had twice the risk of intubation when infected with SARS-CoV-2 (risk ratio 1.5 [95% CI 1.1–2.1], odds ratio 3.5 [95% CI 1.9–6.6], adjusted p -value = 0.0074). These findings are based on data from four countries and corroborated by independent results from GWAS. Our findings are biologically plausible, as HLA-C*04:01 has fewer predicted bindings sites for relevant SARS-CoV-2 peptides compared to other HLA alleles. Interpretation HLA-C*04:01 carrier state is associated with severe clinical course in SARS-CoV-2. Our findings suggest that HLA class I alleles have a relevant role in immune defense against SARS-CoV-2. Funding Funded by Roche Sequencing Solutions, Inc.

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“…Data collection was performed within the Pa-COVID-19 study, a prospective observational cohort study at Charité – Universitätsmedizin Berlin [ 5 , 6 ], approved by the local ethics committee (EA2/066/20), conducted according to the Declaration of Helsinki and Good Clinical Practice principles (ICH 1996), and registered in the German and WHO international clinical trials registry (DRKS00021688).…”

Section: Methodsmentioning

confidence: 99%

Impact of dexamethasone on SARS-CoV-2 concentration kinetics and antibody response in hospitalized COVID-19 patients: results from a prospective observational study

Mühlemann

Thibeault

Hillus

et al. 2021

Clinical Microbiology and Infection

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Objectives Dexamethasone has become standard of care for severe coronavirus disease 2019 (COVID-19), but its virological impact is poorly understood. The objectives of this work were to characterise the kinetics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) concentration in the upper respiratory tract (URT) and the antibody response in patients with (D + ) and without (D - ) dexamethasone treatment. Methods Data and biosamples from hospitalised patients with severe COVID-19, enrolled between March 4 th and December 11 th , 2020, in a prospective observational study, were analysed. SARS-CoV-2 virus concentration in serial URT samples was measured using RT-PCR. SARS-CoV-2-specific Immunoglobulin A and G (IgA and IgG) were measured in serum samples using S1-ELISA. Results We compared 101 immunocompetent patients who received dexamethasone according to the inclusion criteria and dosage determined in the RECOVERY trial to 93 immunocompetent patients with comparable disease severity from the first months of the pandemic, who had not been treated with dexamethasone or other glucocorticoids. We found no inter-group differences in virus concentration kinetics, duration of presence of viral loads >10 6 viral copies/mL (D + : median 17 days (IQR 13-24), D - : 19 days (IQR 13-29)), or time from symptom onset until seroconversion (IgA: D + : median 11.5 days (IQR 11-12), D - : 14 days (IQR 11.5-15.75); IgG: D + : 13 days (IQR 12-14.5), D - : 12 days (IQR 11-15)). Conclusion Dexamethasone does not appear to lead to a change in virus clearance or a delay in antibody response in immunocompetent patients hospitalised with severe COVID-19.

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Clinical and Virological Characteristics of Hospitalized COVID-19 Patients in a German Tertiary Care Center during the First Wave of the SARS-CoV-2 Pandemic

Cited by 11 publications

References 45 publications

Clinical associations of SARS-CoV-2 viral load using the first WHO International Standard for SARS-CoV-2 RNA

Clinical associations of SARS-CoV-2 viral load using the first WHO International Standard for SARS-CoV-2 RNA

Increased risk of severe clinical course of COVID-19 in carriers of HLA-C*04:01

Impact of dexamethasone on SARS-CoV-2 concentration kinetics and antibody response in hospitalized COVID-19 patients: results from a prospective observational study

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