Inflammation induced by influenza virus impairs innate control of human pneumococcal carriage

Simon P. Jochems; Fernando Marcon; Beatriz F. Carniel; Mark Holloway; Elena Mitsi; Emma Smith; Jenna F. Gritzfeld; Carla Solórzano; Jesús Reiné; Sherin Pojar; Elissavet Nikolaou; Esther L. German; Angie Hyder-Wright; Helen Hill; Caz Hales; Wouter A.A de Steenhuijsen Piters; Debby Bogaert; Hugh Adler; Seher Zaidi; Victoria Connor; Jamie Rylance; Helder I. Nakaya; Daniela M. Ferreira

To test whether this was specific for LAIV infection, we measured IP-10 in nasal washes from an 102 independent cohort in which a subset of subjects had asymptomatic viral upper respiratory tract 103 infection before Spn inoculation. These comprised rhinovirus (n=12), coronavirus (n=5), respiratory 104 syncytial virus (n=2) and parainfluenzavirus (n=1) 29 . The predominant virus, rhinovirus, was 105 recently shown to associate with increased pneumococcal acquisition and transmission 30 . In these 106 virus-infected subjects, levels of IP-10 were increased (Fig S2) , and baseline IP-10 levels 107 correlated with increased pneumococcal density also in this second cohort (r = 0.32, p = 0.02, Fig 108 1e ). While the correlation was modest in this validation cohort suggesting that other host and 109 environmental factors are involved, this is the first time a biomarker predicting Spn density has 110 been identified.