Project description:HeLa cells were serum starved and preincubated with DMSO (vehicle) and infected with CVB3. Following infection, virus was removed and fresh media containing 10% fetal bovine serum was added for the remainder of the infectious process. At 0, 30 minutes, 1, 3, 5, 7 and 9 hours following CVB3 infection, RNA was isolated, processed and hybridized to GeneChip®s. Keywords: time-course
Project description:HeLa cells were serum starved and either preincubated with DMSO (vehicle), preincubated with U0126 (10µM in DMSO) and infected with CVB3 (MOI 10), or preincubated with DMSO (vehicle) and infected with CVB3. Following infection, virus was removed and fresh media containing 10% fetal bovine serum was added for the remainder of the infectious process. At 0, 30 minutes, 3 and 9 hours following CVB3 infection (N=3 plates per time point), RNA was isolated, processed and hybridized to GeneChip®s (N=3 per sample) Keywords: time-course
Project description:HeLa cells were serum starved and preincubated with DMSO (vehicle) and infected with CVB3. Following infection, virus was removed and fresh media containing 10% fetal bovine serum was added for the remainder of the infectious process. At 0, 30 minutes, 1, 3, 5, 7 and 9 hours following CVB3 infection, RNA was isolated, processed and hybridized to GeneChip®s.
Project description:HeLa cells were serum starved and either preincubated with DMSO (vehicle), preincubated with U0126 (10µM in DMSO) and infected with CVB3 (MOI 10), or preincubated with DMSO (vehicle) and infected with CVB3. Following infection, virus was removed and fresh media containing 10% fetal bovine serum was added for the remainder of the infectious process. At 0, 30 minutes, 3 and 9 hours following CVB3 infection (N=3 plates per time point), RNA was isolated, processed and hybridized to GeneChip®s (N=3 per sample)
Project description:We infected two strains of mice, 129S1/SvImJ and 129X1/SvJ, with coxsackievirus type b3 (CVB3) at a dose of 500 pfu/g. 129S1 mice developed increased cardiopathology despite equal viral replication. We hypothesized that the increased cardiopathology might result from an ongoing pathologic host response that we could characterize by global expression profiling. Gene expression was assessed in hearts from 129S1 and 129X1 mice that were uninfected or infected for 6 days. Total RNA obtained from hearts of 3 129S1 and 3 129X1 that were infected or uninfected with CVB3(H3) at 500pfu/g and collected at day 6 post infection
Project description:Viruses are obligate intracellular parasites that reshape the ultrastructure, composition and metabolism of host cells to suit their specific needs, although disparate viruses may modify their host in different ways. Such changes may be specifically induced by the virus to support the infection or be part of cellular antiviral responses or stress responses. Here, using state-of-the-art quantitative (phospho)proteomics, we reveal the unique proteome and phosphoproteome dynamics that occur in the host cells infected with the enterovirus coxsackievirus B3 (CVB3).
Project description:We infected two strains of mice, 129S1/SvImJ and 129X1/SvJ, with coxsackievirus type b3 (CVB3) at a dose of 500 pfu/g. 129S1 mice developed increased cardiopathology despite equal viral replication. We hypothesized that the increased cardiopathology might result from an ongoing pathologic host response that we could characterize by global expression profiling. Gene expression was assessed in hearts from 129S1 and 129X1 mice that were uninfected or infected for 6 days.
Project description:The pathogenesis of viral myocarditis is a multifactorial process involving host genetics, viral genetics and the environment in which they interact. Here, we used a model of infection with Coxsackievirus B3 to characterize the contribution of host genetics to viral myocarditis. We determined heart CVB3 load in mice from a classical intercross between progenitors A/J (H2a) and B10.A-H2a (B10.A) of different genetic backgrounds but with a common H2 haplotype. Here we compare whole genome expression patterns in infected and uninfected A/J and B10.A mice in order to determine which gene expression programs are common or distinct to each strain. Total RNA obtained from hearts of 3 AJ, 3 B10.A(H2a), 3 CSS3 and 3 B6.chr3AJ that were infected or uninfected with CVB3(CG) at 400pfu/g and collected at day 4 post infection.
