Unknown,Transcriptomics,Genomics,Proteomics

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Antibody repertoire sequencing of blood and bone marrow plasma cell compartments following lymphocytic choriomeningitis virus infection

ABSTRACT: Antibody repertoire sequencing of blood and bone marrow plasma cell compartments following lymphocytic choriomeningitis virus infection. Heavy chain repertoires of 5 uninfected mice, 5 acutely infected mice and 5 chronically infected mice were longitudinally sequenced over 80 days. All samples are named according to the following scheme: dpi#_cohort$_R&.fastq.gz . dpi = days post infection = for all samples following the start of infection. Those samples starting with dm10 correspond to blood samples taken before the introduction of any virus. # = time point post virus infection cohort=acute (LCMV), chronic (LCMV), or naive (uninfected) animals $= mouse number, 1-5 R&=paired read, either R1 or R2 Those samples with \"bmpc\" in title correspond to sorted plasma cells (CD138hi, CD19lo) from bone marrow Example: dpi70_chronic3_R2.fastq.gz == blood repertoire 70 days post chronic LCMV infection in chronically-infected mouse#3

INSTRUMENT(S): Illumina MiSeq

ORGANISM(S): Mus musculus

SUBMITTER: Alexander Yermanos

PROVIDER: E-MTAB-8585 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Rhesus macaques (Macaca mulatta) infected with a lethal dose of lymphocytic choriomeningitis virus-strain WE (LCMV-WE) provide a model for Lassa fever virus infection of man. Like Lassa fever in human beings, disease begins with flu-like symptoms but can progress to morbidity fairly rapidly. Previously, we profiled the blood transcriptome of LCMV-infected monkeys (M. Djavani et al. J. Virol. 2007: PMID 17522210) showing distinct pre-viremic and viremic stages that discriminated between virulent and benign infections. In the present study, changes in liver gene expression from macaques infected with virulent LCMV-WE were compared to gene expression in uninfected monkeys as well as to monkeys that were infected but not diseased. We observed gene expression changes that occurred before the viremic stage of the disease, and could potentially serve as biomarkers that discriminate between exposure to a hemorrhagic fever virus and exposure to a benign virus. Based on a functional pathway analysis of differentially expressed genes, virulent LCMV-WE had a much broader effect on liver cell function than non-virulent virus. During the first few days of infection, virulent virus impacted gene expression associated with the generation of energy, such as fatty acid metabolism and glucose metabolism, with the complement and coagulation cascades, and with steroid metabolism, MAPK signaling and cell adhesion. For example, the energy profile resembled that of an organism entering starvation: acetyl-CoA carboxylase, a key enzyme of fatty acid synthesis, was shut down and gene products involved in gluconeogenesis were up-regulated. In conclusion, this study identifies several potential gene markers of LCMV-WE-associated liver disease and contributes to the database of gene expression changes correlated with LCMV pathogenesis in primates. 6 groups: uninfected controls, LCMV-WE infected (pre-viremic; day 1 to day 3), LCMV-WE infected (viremic; day 4 to day 7), LCMV-WE infected (post-viremic; day 8 to day 12), LCMV-Armstrong (LCMV-ARM; non-virulent strain) infected, and LCMV-ARM/LCMV-WE infected but not diseased. Each sample is from the liver of a different rhesus macaque.

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Antibody repertoire sequencing of blood and bone marrow plasma cell compartments following lymphocytic choriomeningitis virus infection

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