ArticleBMC systems biology2013
Specific mutations in H5N1 mainly impact the magnitude and velocity of the host response in mice.
Article in BMC systems biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Enhanced neurotropism of bovine H5N1 compared to the Vietnam H5N1 isolate in C57BL/6J mice.Npj viruses · 2025Article
- Multi-platform omics analysis of Nipah virus infection reveals viral glycoprotein modulation of mitochondria.Cell reports · 2025Article
- A compendium of multi-omics data illuminating host responses to lethal human virus infections.Scientific data · 2024Article
- The Role of EGFR in Influenza Pathogenicity: Multiple Network-Based Approaches to Identify a Key Regulator of Non-lethal Infections.Frontiers in cell and developmental biology · 2019Article
- C57BL/6J and C57BL/6NJ Mice Are Differentially Susceptible to Inflammation-Associated Disease Caused by Influenza A Virus.Frontiers in microbiology · 2018Article
- Influenza-Omics and the Host Response: Recent Advances and Future Prospects.Pathogens (Basel, Switzerland) · 2017Review
- Systems biology approach: Panacea for unravelling host-virus interactions and dynamics of vaccine induced immune response.Gene reports · 2016Review
- Integrating Transcriptomic and Proteomic Data Using Predictive Regulatory Network Models of Host Response to Pathogens.PLoS computational biology · 2016Article
- Multi-task consensus clustering of genome-wide transcriptomes from related biological conditions.Bioinformatics (Oxford, England) · 2016Article
- Dynamic changes in host gene expression associated with H5N8 avian influenza virus infection in mice.Scientific reports · 2015Article
- Molecular pathogenesis of H5 highly pathogenic avian influenza: the role of the haemagglutinin cleavage site motif.Reviews in medical virology · 2015Review
- An Ultrasensitive Mechanism Regulates Influenza Virus-Induced Inflammation.PLoS pathogens · 2015Article
- New Metrics for Evaluating Viral Respiratory Pathogenesis.PloS one · 2015Article
- H7N9 and other pathogenic avian influenza viruses elicit a three-pronged transcriptomic signature that is reminiscent of 1918 influenza virus and is associated with lethal outcome in mice.Journal of virology · 2014Article
- A comprehensive collection of systems biology data characterizing the host response to viral infection.Scientific data · 2014Article
- Article
- Moving H5N1 studies into the era of systems biology.Virus research · 2013Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
backgroundInfluenza infection causes respiratory disease that can lead to death. The complex interplay between virus-encoded and host-specific pathogenicity regulators - and the relative contributions of each toward viral pathogenicity - is not well-understood.
resultsBy analyzing a collection of lung samples from mice infected by A/Vietnam/1203/2004 (H5N1; VN1203), we characterized a signature of transcripts and proteins associated with the kinetics of the host response. Using a new geometrical representation method and two criteria, we show that inoculation concentrations and four specific mutations in VN1203 mainly impact the magnitude and velocity of the host response kinetics, rather than specific sets of up- and down- regulated genes. We observed analogous kinetic effects using lung samples from mice infected with A/California/04/2009 (H1N1), and we show that these effects correlate with morbidity and viral titer.
conclusionsWe have demonstrated the importance of the kinetics of the host response to H5N1 pathogenesis and its relationship with clinical disease severity and virus replication. These kinetic properties imply that time-matched comparisons of 'omics profiles to viral infections give limited views to differentiate host-responses. Moreover, these results demonstrate that a fast activation of the host-response at the earliest time points post-infection is critical for protective mechanisms against fast replicating viruses.
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