Background: Type I interferons (IFNs) are essential to the clearance of viral diseases, in part by initiating upregulation of IFN regulated genes (IRGs). A clear distinction between genes upregulated directly by virus and genes upregulated by secondary IFN production has not been made. Here we investigated the genes regulated by IFN-a2b compared to the genes regulated by SARS-CoV infection in ferrets.
Early gene expression events in ferrets in response to SARS coronavirus infection versus direct interferon-alpha2b stimulation.
Specimen part
View SamplesFerrets were experimentaly infected with influenza A/California/07/2009. RNA samples from lungs and lymph nodes were analyzed by Illumina sequencing.
Sequencing, annotation, and characterization of the influenza ferret infectome.
No sample metadata fields
View SamplesPandemic H1N1 influenza A Human infection leads to symptoms ranging from mild to severe with lower respiratory complications observed in a small but significant number of infected individuals. Microarray analysis of the lymph nodes from ferrets infected with A/California/07/2009 shows intense gene upregulation during days 3 and 5 post-infection, and followed by marked downregulation during days 7 and 14 post infection. Gene expression profiles during the upregulation phase show intense chemokine activity, cell replication and activation of the lymphocyte-related signaling pathways.
Sequencing, annotation, and characterization of the influenza ferret infectome.
Specimen part, Time
View SamplesTo further investigate the underlying mechanisms of severe acute respiratory syndrome (SARS) pathogenesis and evaluate the therapeutic efficacy of potential drugs and vaccines it is necessary to use an animal model that is highly representative of the human condition in terms of respiratory anatomy, physiology and clinical sequelae. The ferret, Mustela putorius furo, supports SARS-CoV replication and displays many of the symptoms and pathological features seen in SARS-CoV-infected humans. We have recently established a SARS-CoV infection-challenge ferret platform for use in evaluating potential therapeutics to treat SARS. The main objective of the current study was to extend our previous results and identify early host immune responses upon infection and determine immune correlates of protection upon challenge with SARS-CoV in ferrets.
Lack of innate interferon responses during SARS coronavirus infection in a vaccination and reinfection ferret model.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
HIV‐exposed seronegative commercial sex workers show a quiescent phenotype in the CD4+ T cell compartment and reduced expression of HIV‐dependent host factors.
No sample metadata fields
View SamplesUnderstanding why some indidivual resist HIV-1 infection despite continued exposure is an important goal for vaccine development.
HIV‐exposed seronegative commercial sex workers show a quiescent phenotype in the CD4+ T cell compartment and reduced expression of HIV‐dependent host factors.
No sample metadata fields
View SamplesThe 2009 H1N1 influenza pandemic has prompted a significant need for the development of efficient, single-dose, adjuvanted vaccines. Here we investigated the adjuvant potential of CpG oligodeoxynucleotide (ODN) when used with a human seasonal influenza virus vaccine in ferrets. We found that the CpG ODNadjuvanted vaccine effectively increased antibody production and activated type I interferon (IFN) responses compared to vaccine alone. Based on these findings, pegylated IFN- 2b (PEG-IFN) was also evaluated as an adjuvant in comparison to CpG ODN and complete Freunds adjuvant (CFA). Our results showed that all three vaccines with adjuvant added prevented seasonal human A/Brisbane/59/2007 (H1N1) virus replication more effectively than did vaccine alone. Gene expression profiles indicated that, as well as upregulating IFN-stimulated genes (ISGs), CpG ODN enhanced B-cell activation and increased Toll-like receptor 4 (TLR4) and IFN regulatory factor 4 (IRF4) expression, whereas PEG-IFN augmented adaptive immunity by inducing major histocompatibility complex (MHC) transcription and Ras signaling. In contrast, the use of CFA as an adjuvant induced limited ISG expression but increased the transcription of MHC, cell adhesion molecules, and B-cell activation markers. Taken together, our results better characterize the specific molecular pathways leading to adjuvant activity in different adjuvant-mediated influenza virus vaccinations.
Molecular characterization of in vivo adjuvant activity in ferrets vaccinated against influenza virus.
Specimen part, Treatment
View SamplesBackground: Pandemic H1N1 influenza A is a newly emerging strain of human influenza that is easily transmitted between people and has spread globally to over 116 countries. Human infection leads to symptoms ranging from mild to severe with lower respiratory complications observed in a small but significant number of infected individuals. Little is currently known about host immunity and Pandemic H1N1 influenza infections.
Modeling host responses in ferrets during A/California/07/2009 influenza infection.
Specimen part
View SamplesA global genomics approach was used to identify patterns of immune dysregulation during H5N1 influenza virus infection as the host response, in particular hyperchemokinemia, is thought to contribute to the extreme pathology associated with this disease.
Gene expression analysis of host innate immune responses during Lethal H5N1 infection in ferrets.
Specimen part
View SamplesNatural SIV infection of sooty mangabeys (SMs) does not progress to disease despite chronic virus replication. In contrast to pathogenic SIV infection of rhesus macaques (RMs), chronic SIV infection of SMs is characterized by low immune activation. To elucidate the mechanisms underlying this phenotype, we longitudinally assessed host gene expression in SIV-infected SMs and RMs. We found that acute SIV infection of SMs is consistently associated with a robust innate immune response, including widespread up-regulation of interferon-stimulated genes (ISGs). Our findings indicate that active immune regulatory mechanisms, rather than intrinsically attenuated innate immune responses, underlie the low immuneactivation of chronically SIV-infected SMs.
Global genomic analysis reveals rapid control of a robust innate response in SIV-infected sooty mangabeys.
Sex, Specimen part
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