Abstract

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 log10 IU/mL (3.92–4.77 log10 IU/mL 95% CI, cobas SARS-CoV-2 assay ORF1a Ct 28.9 cycles). The mean viral load change was –0.09 log10 IU/mL/day (–0.12 to –0.06 95% CI). R2 was 0.08 and residual standard deviation 2.68 log10 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 log10 IU/mL or day 20 was 1.8 log10 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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