This is a Twitter summary from the 2018 WSAAI meeting. This summary was compiled from the tweets posted by @MatthewBowdish, an allergist/immunologist, who attended the 2018 Western Society of Allergy, Asthma and Immunology (WSAAI) meeting. The tweets were labeled #WSAAI. The text was edited and modified by me.
Larry Borish on "Rhinovirus-Induced Asthma Exacerbations: How it happens and implications for treatment."
September and May Epidemics of Asthma Exacerbations in Kids in North America - 80% are due to rhinovirus: https://twitter.com/MatthewBowdish/status/956232214806609921
Rhinovirus is truly the perfect pathogen because it doesn't ever kill its host and it doesn't make you so sick that you have to stay home, allowing for easier spread.
Rhinovirus occurs year-round: https://twitter.com/MatthewBowdish/status/956233009757282305
But it's not just the rhinovirus leading to exacerbations, it's the rhinovirus infection occurring during the allergy seasons (Fall: ragweed/Alternaria; Spring: grass pollen)).
Most asthma exacerbation in children and adolescents occur in association with rhinovirus infection. This trend reflects concomitant presence of allergic sensitization to aeroallergens expressed at the time of infection.
Two schools of thoughts on why rhinovirus associated with asthma exacerbations: https://twitter.com/MatthewBowdish/status/956235171988213760
Humoral mechanisms of RV-induced upper respiratory rhinitis during lower respiratory asthma exacerbations: https://twitter.com/MatthewBowdish/status/956236188389552128
In studies using rhinovirus challenges, symptoms are worse in allergic asthmatics and last longer despite receiving similar viral loads.
Dr Borish points out that when he does studies using nasal epithelial cells, he grows them up in culture and then studies are done on the great(x5)-grandchildren cells. How do those cells remember they are asthmatic epithelial cells and make IL25, IL33 and TSLP?
Image source: Molecular surface of a rhinovirus, Wikipedia, GNU Free Documentation License.