Cellular scent of influenza virus infection - PubMed (original) (raw)

Cellular scent of influenza virus infection

Alexander A Aksenov et al. Chembiochem. 2014.

Abstract

Volatile organic compounds (VOCs) emanating from humans have the potential to revolutionize non-invasive diagnostics. Yet, little is known about how these compounds are generated by complex biological systems, and even less is known about how these compounds are reflective of a particular physiological state. In this proof-of-concept study, we examined VOCs produced directly at the cellular level from B lymphoblastoid cells upon infection with three live influenza virus subtypes: H9N2 (avian), H6N2 (avian), and H1N1 (human). Using a single cell line helped to alleviate some of the complexity and variability when studying VOC production by an entire organism, and it allowed us to discern marked differences in VOC production upon infection of the cells. The patterns of VOCs produced in response to infection were unique for each virus subtype, while several other non-specific VOCs were produced after infections with all three strains. Also, there was a specific time course of VOC release post infection. Among emitted VOCs, production of esters and other oxygenated compounds was particularly notable, and these may be attributed to increased oxidative stress resulting from infection. Elucidating VOC signatures that result from the host cells response to infection may yield an avenue for non-invasive diagnostics and therapy of influenza and other viral infections.

Keywords: breath analysis; esters; gas chromatography; influenza; mass spectrometry; volatile organic compounds.

© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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Figures

Figure 1

Figure 1

GC/MS analysis of volatile organic compounds produced by C1R cells infected with H1N1 at MOI 10 and incubated for 24 h. A representative chromatogram from 12 replicates is shown. Inset: detail illustrates the high information content in the experimental data.

Figure 2

Figure 2

Overlay of GC chromatograms differentiates between uninfected C1R cells and those infected as indicated and incubated for 48 h. Peak C1 (Tables 1, 2, S1, and S2) was identified as 2-methoxy-ethanol. Representative chromatograms of 12 replicates are shown. The p value p ≤ 0.05 was used throughout.

Figure 3

Figure 3

Overlay of GC chromatograms shows abundance differences at different incubation times. C1R cells were infected and incubated as indicated. Peak C12 (Tables 1, 2, S1, and S2) was identified as 3,7-dimethyloctan-3-ol, and is evident after 48 h incubation with H9N2 and H6N2 strains, but essentially not present under all other conditions. Representative chromatograms of 12 replicates are shown. Appearance of peak C12 was consistent with observed morphological changes in cells only after 48 h incubation. The p value _p_≤ 0.05 was used throughout.

Figure 4

Figure 4

Work flow: C1R cells were placed into 12 vials and incubated. Vials were infected with influenza virus (n = 9 total, gray; n = 3 H9N2, n = 3 H6N2, and n = 3 H1N1, MOI 10) or untreated (controls; n = 3, white). After re-suspension in medium and further incubation, vials were removed at either 24 h (n = 9 gray and n = 3 white) or 48 h (n = 9 gray and n = 3 white). All vials underwent the same VOC sampling. All experiments were repeated four times. The H1N1 experiment at MOI 1 was conducted independently (n = 12 at 24-hours, n = 12 at 48-hours). Totals: virus-infected 96; controls 24; VOC chromatograms 120.

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