The SARS-CoV-2 virus infects cells of the airway and lungs in humans causing the disease
COVID-19. This disease is characterized by
cough,
shortness of breath, and in severe cases causes
pneumonia and
acute respiratory distress syndrome (ARDS) which can be fatal. Bronchial alveolar lavage fluid (BALF) and plasma from mild and severe cases of
COVID-19 have been profiled using
protein measurements and bulk and single cell
RNA sequencing. Onset of
pneumonia and ARDS can be rapid in
COVID-19, suggesting a potential neuronal involvement in pathology and mortality. We sought to quantify how immune cells might interact with sensory innervation of the lung in
COVID-19 using published data from patients, existing
RNA sequencing datasets from human dorsal root ganglion neurons and other sources, and a genome-wide
ligand-receptor pair database curated for pharmacological interactions relevant for neuro-immune interactions. Our findings reveal a landscape of
ligand-receptor interactions in the lung caused by SARS-CoV-2
viral infection and point to potential interventions to reduce the burden of
neurogenic inflammation in
COVID-19 disease. In particular, our work highlights opportunities for clinical trials with existing or under development
rheumatoid arthritis and other (e.g. CCL2, CCR5 or EGFR inhibitors) drugs to treat high risk or severe
COVID-19 cases.