The Mechanism of Monolaurate Derived Glycolipids Inhibit Sindbis Virus Replication and Release.

Cough is a defensive respiratory manoeuvre that facilitates the clearance of inhaled irritants, pathogens and superfluous secretions (Morice, Dicpinigaitis, et al., ). However, when persistent or excessive, cough becomes maladaptive and pathological (Bali et al., ; Kubo et al., ; McGarvey et al., ). Clinically, pathological cough is defined by its duration: acute (<3 weeks), subacute (3–8 weeks) and chronic (>8 weeks) (Morice, Dicpinigaitis, et al., ). Acute and subacute cough are typically infective or inflammatory and are often self‐limiting, whereas chronic cough represents a more complex, burdensome condition. Chronic cough affects approximately 10% of the global adult population and is termed refractory chronic cough (RCC) when it persists despite exhaustive investigation and optimal treatment (Zhang & Morice, ). RCC is associated with a wide range of physical and psychosocial co‐morbidities, including syncope, chest pain, lethargy, depression and anxiety (Cho et al., ; Drake et al., ; French et al., ; Hirons et al., ; McGarvey et al., ; Morice, Dicpinigaitis, et al., ; Song et al., ). Chronic cough also carries a substantial economic burden, with a reported mean (SD) annual healthcare cost of approximately £1663 (£747) per person (Cho et al., ). Although chronic cough has long been viewed as a symptom of chronic respiratory conditions, such as asthma and COPD, it is now increasingly recognised as a distinct clinical entity (Zhang & Morice, ). RCC is not associated with any respiratory pathology and is increasingly believed to be secondary to neural dysfunction. RCC was associated with cough reflex hypersensitivity to tussive stimuli in early experimental and clinical reports (Kim et al., ; Singh et al., ). These observations led to the hypothesis that RCC is a neuropathic disorder mediated by cough reflex hypersensitivity (Zhang & Morice, ). However, cough is not solely a reflexive process; it can also be voluntarily initiated or suppressed. Indeed, recent functional neural imaging and physiological studies suggest that impaired central control diminished volitional suppression, which may contribute to the persistence of cough in RCC (Ando et al., ; Cho et al., ). These findings suggest that both peripheral sensory dysfunction and central neural dysregulation are important in its pathophysiology.