PMC:7519301 / 30374-31141 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7519301","sourcedb":"PMC","sourceid":"7519301","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7519301","text":"Correlating in vitro findings with clinical phenotypes can be complicated. During the Ebola outbreak of 2013–2016, some fixed mutations were suspected to confer an advantage to the virus. Specifically, an A82V mutation in the glycoprotein, which, like S for SARS-CoV-2, is critical for the virus entry into host cells, was associated with an increase in infectivity (44–46). Yet, effects varied across cell types (47), and no phenotypic differences were associated with the mutations when viruses were evaluated in vivo in mouse and nonhuman primate models (48), highlighting the difficulty in linking biological mechanisms to outcomes at the population level. So far, no causal association has been identified between the presence of D614G and disease severity 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