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Cellular scent of influenza virus infection.

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.

SUBMITTER: Aksenov AA

PROVIDER: S-EPMC4104277 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature

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Cellular scent of influenza virus infection.

Aksenov Alexander A AA Sandrock Christian E CE Zhao Weixiang W Sankaran Shankar S Schivo Michael M Harper Richart R Cardona Carol J CJ Xing Zheng Z Davis Cristina E CE

Chembiochem : a European journal of chemical biology 20140409 7

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), H ...[more]

PMID: 24719290

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Project description:Highlights • Negative correlation of RV prevalence in suppressing influenza viruses is independent of meteorological effects.• A low odds of RV/IV co-detection infers a unique interference effect.• Sequential RV infection model demonstrates the inhibitory effect of RV on the replication of influenza A and B viruses. Background Influenza virus (IV) and the rhinovirus (RV) are the two most common circulating respiratory viruses circulating. Natural viral interference has been suggested between them. The effect of such at the population level has been described in temperate region, while its effect at the individual and cellular levels warrants further validation. In this study, we described the respiratory virus epidemiology and the co-infection landscape in the hospitalized population and investigated the distinct molecular pathways involved in the inhibition of virus replication. Methods Nasopharyngeal aspirates (NPAs) collected from patients during 2015 to 2019 were examined for the presence of respiratory viruses. The correlation of the monthly prevalence between all the tested respiratory viruses, the co-infection rate and the temporal interference of RV and IV were tested. The viral interference was validated in vitro by conducting sequential RV and IV infections in the well-differentiated primary human airway epithelial cells. The contributing molecular pathways were determined by transcriptome analysis. Findings A total of 112,926 NPAs were evaluated, and the Enterovirus/RV was the most prevalent respiratory virus detected. The negative correlation between EV/RV and IVs prevalence was independent of age and meteorological factors. Compare with other viruses, EV/RV had a significantly lower incidence of co-infection with IVs. Prior exposure to RV inhibited the replication of IV species A, B and oseltamivir-resistance stain in vitro. RV uniquely downregulated genes related to processing of viral mRNA, ribosomal proteins, translation and influenza infection. Interpretation Epidemiological surveillance and the sequential infection in vitro suggested viral interference between EV/RV and IV operates at the population, individual and cellular levels. Funding This study was supported by the 10.13039/501100012479General Research Fund (Ref: 24107017 and 14103119 to RWYC) and the Chinese University Direct Grant for Research (Ref: 2019·073 to RWYC). Graphical abstract Image, graphical abstract

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Cellular scent of influenza virus infection.

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Cellular scent of influenza virus infection.

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