Abstract
BackgroundThe host response to influenza A infections is strongly influenced by host genetic factors. Animal models of genetically diverse mouse strains are well suited to identify host genes involved in severe pathology, viral replication and immune responses. Here, we have utilized a dual RNAseq approach that allowed us to investigate both viral and host gene expression in the same individual mouse after H1N1 infection.ResultsWe performed a detailed expression analysis to identify (i) correlations between changes in expression of host and virus genes, (ii) host genes involved in viral replication, and (iii) genes showing differential expression between two mouse strains that strongly differ in resistance to influenza infections. These genes may be key players involved in regulating the differences in pathogenesis and host defense mechanisms after influenza A infections. Expression levels of influenza segments correlated well with the viral load and may thus be used as surrogates for conventional viral load measurements. Furthermore, we investigated the functional role of two genes, Reg3g and Irf7, in knock-out mice and found that deletion of the Irf7 gene renders the host highly susceptible to H1N1 infection.ConclusionsUsing RNAseq analysis we identified novel genes important for viral replication or the host defense. This study adds further important knowledge to host-pathogen-interactions and suggests additional candidates that are crucial for host susceptibility or survival during influenza A infections.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1867-8) contains supplementary material, which is available to authorized users.
Highlights
The host response to influenza A infections is strongly influenced by host genetic factors
We recently demonstrated that these host responses can be studied comprehensively by measuring changes in the gene expression levels after infection [17, 18]
Global expression profiles are distinct in C57BL/6J and DBA/2J mice RNA was extracted from the lungs of C57BL/6J and DBA/ 2J mice infected with PR8M as described in [14], and gene expression was quantified using RNA sequencing (RNAseq) technology
Summary
The host response to influenza A infections is strongly influenced by host genetic factors. Animal models of genetically diverse mouse strains are well suited to identify host genes involved in severe pathology, viral replication and immune responses. We have utilized a dual RNAseq approach that allowed us to investigate both viral and host gene expression in the same individual mouse after H1N1 infection. Influenza A viruses have an adverse impact on human and animal health worldwide through seasonal epidemics, newly emerging pandemics, and reoccurring outbreaks in livestock. The most severe human pandemic in 1918 resulted in about 30 million fatal casualties [1]. We and others have shown in animal models that the genetic background of the host strongly influences mortality and morbidity after influenza infections.
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