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Inhibition of the protein kinase CSNK2 with any of 30 specific and selective inhibitors representing different chemotypes, blocked replication of pathogenic human, bat, and murine β-coronaviruses. The potency of in-cell CSNK2A target engagement across the set of inhibitors correlated with antiviral activity and genetic knockdown confirmed the essential role of the CSNK2 holoenzyme in β-coronavirus replication. Spike protein endocytosis was blocked by CSNK2A inhibition, indicating that antiviral activity was due in part to a suppression of viral entry. CSNK2A inhibition may be a viable target for the development of anti-SARS-like β-coronavirus drugs.

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The classical view of conduction aphasia and the isolation syndrome holds that there is, respectively, preferential damage to, or sparing of, a (repetition) pathway between the posterior and anterior speech areas. This concept is deeply entrenched in neurological thinking, but is supported neither by clinical nor pathological evidence. These two disorders are explained from the standpoint of a more dynamic theory of language organization. This new approach has implications for our understanding of anatomical relationships "between" the speech areas.