No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2
Lucy van Dorp; Damien Richard; Cedric Tan; Liam P. Shaw; Mislav Acman; François Balloux · 2020 · Nature Communications
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
COVID-19 is caused by the coronavirus SARS-CoV-2, which jumped into the human population in late 2019 from a currently uncharacterised animal reservoir. Due to this recent association with humans, SARS-CoV-2 may not yet be fully adapted to its human host. This has led to speculations that SARS-CoV-2 may be evolving towards higher transmissibility. The most plausible mutations under putative natural selection are those which have emerged repeatedly and independently (homoplasies). Here, we formally test whether any homoplasies observed in SARS-CoV-2 to date are significantly associated with inc
Abstract by Lucy van Dorp; Damien Richard; Cedric Tan; Liam P. Shaw; Mislav Acman; François Balloux, Nature Communications (2020) — licensed CC BY 4.0.
About to run something similar?
Run an AI Precheck on your own design to catch failure modes like this one before you spend the time. Your first desk check is free.
Related failures
A Randomized Trial of Intraarterial Treatment for Acute Ischemic Stroke
Negative / Null Result ReportDuodenal Infusion of Donor Feces for Recurrent Clostridium difficile
Negative / Null Result ReportStenting versus Endarterectomy for Treatment of Carotid-Artery Stenosis
Negative / Null Result ReportEffects of Combination Lipid Therapy in Type 2 Diabetes Mellitus
Replication FailureA Randomized Trial of Bevacizumab for Newly Diagnosed Glioblastoma
Negative / Null Result ReportSpironolactone for Heart Failure with Preserved Ejection Fraction
WASTE indexes this work — it does not host or republish it. Failure-type classification is automated and approximate.
Metadata source: OpenAlex · DOI 10.1038/s41467-020-19818-2