Reliability of self-sampling for accurate assessment of respiratory virus viral and immunologic kinetics

Alpana Waghmare; Elizabeth M Krantz; Subhasish Baral; Emma Vasquez; Tillie Loeffelholz; E. Lisa Chung; Urvashi Pandey; Jane Kuypers; Elizabeth R Duke; Keith R Jerome; Alexander L Greninger; Daniel B Reeves; Florian Hladik; E Fabian Cardozo-Ojeda; Michael Boeckh; Joshua T Schiffer

is the (which was not peer-reviewed) The copyright holder for this preprint . https://doi.org/10.1101/2020.04.03.20051706 doi: medRxiv preprint Cytokines correlations according to cellular origin. We next examined the six participants 164 with HRV infection for any correlated cytokine patterns to infer cellular origin. Examples of high 165 positive correlations were noted among analytes associated with a cytotoxic T cell response 166 (granzyme B, perforin, TNFα, and IL-6), among several macrophage or epithelial cell derived 167 cytokines (MIP-1α, IL1α, IL-6, IL-12p70, IL-21), and among a cluster associated with Th2 168 responses (IL-5, IL-10, IL-17). The Th2 associated cytokines (IL-5, IL-10, IL-17) also correlated 169 with many of the cytolytic T cell and macrophage associated cytokines (Fig 3a) . HRV viral load 170 was only moderately correlated with a number of parameters, particularly granzyme B, perforin, 171 and IP10 which is a protein induced by IFNγ. This result suggests that HRV may not induce an 172 intense local molecular immune response in a dose-dependent fashion. Very similar results 173 occurred with inclusion of all samples from all participants in the cohort (Supp Fig 3a) . 174 175 We next examined cytokine correlations in the 2 persons infected with more inflammatory 176 respiratory viruses: RSV and MPV. We noted similar correlative trends in this data as with HRV. 177