SARS‐CoV‐2 viral load in nasopharyngeal swabs in the emergency department does not predict COVID‐19 severity and mortality

Borgne, Pierrick Le; Solis, Morgane; Séverac, François; Merdji, Hamid; Ruch, Yvon; Intern, Karine Alamé; Bayle, Eric; Hansmann, Yves; Bilbault, Pascal; Fafi‐Kremer, Samira; Meziani, Ferhat

doi:10.1111/acem.14217

Cited by 37 publications

(31 citation statements)

References 36 publications

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“…Our most striking observation was an approximately billion-fold variation in SARS-CoV-2 viral loads. While the predictive value of viral loads for clinical outcomes or treatment response is unclear, with several studies reporting significant [28][29][30][31][32][33], minimal [34,35] or no [36][37][38] associations with increased severity or mortality from COVID-19, we report significant independent associations of pre-treatment variables such as invasive ventilation and immunosuppression with higher viral loads in our cohort that may subsequently influence their response to treatment (Table 2A; Fig. 1C).…”

Section: Discussionmentioning

confidence: 67%

Virological Characterization of Critically Ill Patients With COVID-19 in the United Kingdom: Interactions of Viral Load, Antibody Status, and B.1.1.7 Infection

Ratcliff

Nguyen

Fish

et al. 2021

The Journal of Infectious Diseases

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Background Convalescent plasma containing neutralising antibody to SARS-CoV-2 is under investigation for COVID-19 treatment. We report diverse virological characteristics of UK intensive care patients enrolled in the Immunoglobulin Domain of the REMAP-CAP randomised controlled trial that potentially influence treatment outcomes. Methods SARS-CoV-2 RNA in nasopharyngeal swabs collected pre-treatment was quantified by PCR. Antibody status was determined by spike-protein ELISA. B.1.1.7 was differentiated from other SARS-CoV-2 strains using allele-specific probes or restriction site polymorphism (SfcI) targeting D1118H. Results Of 1274 subjects, 90% were PCR-positive with viral loads 118-1.7x10 11 IU/ml. Median viral loads were 40-fold higher in those seronegative for IgG antibodies (n=354; 28%) compared to seropositives (n=939; 72%). Frequencies of B.1.1.7 increased from <1% in early November, 2020 to 82% of subjects in January 2021. Seronegative individuals with wild-type SARS-CoV-2 had significantly higher viral loads than seropositives (medians 5.8x10 6 and 2.0 x10 5 IU/ml respectively; p=2x10 -15). However, viral load distributions were elevated in both seronegative and seropositive subjects infected with B.1.1.7 (4.0x10 6 and 1.6x10 6 IU/ml respectively). Conclusions High viral loads in seropositive B.1.1.7-infected subjects and resistance to seroconversion indicate less effective clearance by innate and adaptive immune responses. SARS-CoV-2 strain, viral loads and antibody status define subgroups for analysis of treatment efficacy.

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Section: Discussionmentioning

confidence: 67%

Virological Characterization of Critically Ill Patients With COVID-19 in the United Kingdom: Interactions of Viral Load, Antibody Status, and B.1.1.7 Infection

Ratcliff

Nguyen

Fish

et al. 2021

The Journal of Infectious Diseases

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“…Nonetheless, in our cohort, SARS-CoV-2 RNA levels were not associated with the clinical outcome at any time point. There are some controversial data regarding this issue, while some studies have not reported any association between SARS-CoV-2 viral load during acute infection and COVID-19 severity [11,12] others point out that elevated viral load could be used to identify patients at higher risk for morbidity or severe COVID-19 outcome [13,14]. The controversial results might be explained for the heterogeneity of the studies related to the different characteristics of the study population and/or the methodology used for SARS-CoV-2 quantification and sampling quality (i.e., normalization using copies/cells).…”

Section: Discussionmentioning

confidence: 99%

Elevated anti-SARS-CoV-2 antibodies and IL-6, IL-8, MIP-1β, early predictors of severe COVID-19

Codina

Viéitez

Gutiérrez‐Valencia

et al. 2021

Preprint

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Background: Viral and host immune kinetics during acute COVID-19 and after remission of acute symptoms need better characterization. Methods: SARS-CoV-2 RNA, anti-SARS-CoV-2 IgA, IgM, and IgG antibodies, and pro-inflammatory cytokines were measured in sequential samples among hospitalized COVID-19 patients during acute infection and 6 months following diagnosis. Results: 24 laboratory-confirmed COVID-19 patients with mild/moderate and severe COVID-19 were included. Most were males 83%, median age of 61 years. 21% were admitted to the ICU and 8 of them (33.3%) met criteria for severe COVID-19 disease. A delay in SARS-CoV-2 levels decline during the first 6 days of follow-up and viral load persistence until month 3 were related with severe COVID-19, but not viral load levels at the diagnosis. Higher levels of anti-SARS-CoV-2 IgA, IgM, IgG and the cytokines IL-6, IL-8 and MIP-1β at the diagnosis time were related with severe COVID-19 outcome. Higher levels of MIP-1β, IL-1β, MIP-1α and IFN-γ were observed at month 1-3 during mild/moderate disease compared to severe COVID-19. IgG persisted at low levels after 6 months of diagnosis. Conclusions: Higher concentrations of IgA, IgM, and IgG, and IL-6, IL-8 and MIP-1β are identified as early predictors of COVID-19 severity, but not SARS-CoV-2 RNA levels at diagnosis.

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“…In diseases caused by viral infections, viruses and hosts can contribute to disease heterogeneity. Studies have found that SARS-CoV-2 has limited genetic variation and stable evolution (17,18), suggesting that viral genetic variation and evolution might contribute to infectivity and fatality (19,20). However, not so much correlation is noted to the heterogeneity of COVID-19 (17,(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Cellular Immune Response to COVID-19 and Potential Immune Modulators

Zhou

2021

Front. Immunol.

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Coronavirus disease 2019 (COVID-19) is a respiratory infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Droplets and contacts serve as the main route of transmission of SARS-CoV-2. The characteristic of the disease is rather heterogeneous, ranging from no symptoms to critical illness. The factors associated with the outcome of COVID-19 have not been completely characterized to date. Inspired by previous studies on the relevance of infectious diseases, viral and host factors related to clinical outcomes have been identified. The severity of COVID-19 is mainly related to host factors, especially cellular immune responses in patients. Patients with mild COVID-19 and improved patients with severe COVID-19 exhibit a normal immune response to effectively eliminate the virus. The immune response in patients with fatal severe COVID-19 includes three stages: normal or hypofunction, hyperactivation, and anergy. Eventually, the patients were unable to resist viral infection and died. Based on our understanding of the kinetics of immune responses during COVID-19, we suggest that type I interferon (IFN) could be administered to patients with severe COVID-19 in the hypofunctional stage, intravenous immunoglobulin (IVIG) and glucocorticoid therapy could be administered in the immune hyperactivation stage. In addition, low molecular weight heparin (LMWH) anticoagulation therapy and anti-infective therapy with antibiotics are recommended in the hyperactivation stage.

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SARS‐CoV‐2 viral load in nasopharyngeal swabs in the emergency department does not predict COVID‐19 severity and mortality

Cited by 37 publications

References 36 publications

Virological Characterization of Critically Ill Patients With COVID-19 in the United Kingdom: Interactions of Viral Load, Antibody Status, and B.1.1.7 Infection

Virological Characterization of Critically Ill Patients With COVID-19 in the United Kingdom: Interactions of Viral Load, Antibody Status, and B.1.1.7 Infection

Elevated anti-SARS-CoV-2 antibodies and IL-6, IL-8, MIP-1β, early predictors of severe COVID-19

Cellular Immune Response to COVID-19 and Potential Immune Modulators

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